Archive for the ‘Male Genetics’ Category

Facial hair, like scalp hair, grows in stages and understanding it may help you maximize your beard-growing potential.

A full beard can take 2 to 4 months to grow, as facial hair tends to grow between 0.3 and 0.5 millimeters (mm) every 24 hours. This works out to between one third and one half an inch per month.

Many factors can affect the growth of your beard, but there are some lifestyle strategies you can try to enhance your beard growth. Read on to learn more about what influences beard growth and if it can be influenced.

Once you stop shaving, you can expect facial hair to grow in stages. Hair may grow fuller and faster in certain areas, especially at first. Be patient, though, as this is a normal growth pattern for most guys.

Your ethnicity, age, genetics, and hormones not to mention various medical conditions can all affect whether your beard comes in faster or slower, or in all the places you desire.

If your beard seems to be taking a long time to grow in, one of the following factors may be at play.

You may remember guys in high school who seemed to have a full beard before they got their drivers license. Theyre the exception, not the rule.

Typically, full beard growth is possible starting at around age 18, but for many men, that time may not arrive until theyre 30. So, if youre not getting the beard growth you want, it may be because its not your time.

Certain ethnic groups tend to be more hirsute than others. Chinese men, for example, generally have less facial hair than white men, and men of Mediterranean descent generally have thicker beards.

Beyond your ethnic origins, your direct family traits have much to do with whether you can grow a full beard. Likewise, your genetics also determine the texture of your hair, your likelihood of going bald, and so forth.

For clues about your beards future, look to your male relatives. While theres no guarantee that a dad with a full beard will have a son who can pull off the same thing, hair patterns do tend to be hereditary.

Low levels of testosterone can make it more difficult to grow a beard. Talk with your doctor about taking supplements or trying testosterone therapy to help combat low testosterone.

If you want to grow your beard faster, there are a few strategies worth trying. Understand, however, that these tips may not work for everyone.

For general health, its recommended you have a balanced diet that includes fruits, vegetables, whole grains, and lean proteins, while avoiding processed food and added sugars.

For healthy hair growth, some key nutrients should have a place in your diet, including:

Too much stress and too little sleep can cause countless health problems, not to mention affect your beard growth.

Aim for 7 to 8 hours of sleep each night, and try strategies such as meditation or deep-breathing techniques to help de-stress.

Its not uncommon for guys to have thicker hair around their mouths and parts of their sideburns but a little less on their cheeks.

One way to help mask thinner (or zero) growth in those spots is to let the hair around them grow longer. You can hide those sparse spots a little with longer beard hair nearby.

Hair growth, whether its on your scalp or your face, is subject to many changes in your health.

Underlying medical conditions such as alopecia barbae or alopecia areata can cause hair loss from your beard or make it harder to grow a beard that isnt patchy or thin in places.

Alopecia areata is the more common condition. It occurs when the bodys immune system mistakenly attacks healthy hair follicles. When beard alopecia areata develops, men are usually middle-aged and hair loss is typically along the jawline.

Unusual conditions, such as prolactinoma a noncancerous tumor of the pituitary gland can also result in thin or missing facial hair.

Conversely, a noncancerous birthmark called Beckers nevus can sometimes cause excessive, coarse hair to form at the site of the birthmark.

The time it takes to grow a beard not to mention the look of the final product varies from person to person.

If youre trying to grow a full beard, plan on waiting a couple of months before you reach your goal. That means being patient and watching for signs of medical conditions that may affect your beard growth.

If youre concerned about a lack of beard growth, talk with your doctor or a dermatologist.

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How Long Does It Take to Grow a Beard? Tips, Genetics, and More - Healthline

The latestrelease from Database of WM Research, The Global Male Breast Cancer Market opportunities and current market scenario, providing insights and updates about the corresponding segments like Male Breast Cancers MarketSize, Share, Growth, Manufacturers, Regions, Type, and Application, Forecast to 2027.The report provides detailed assessment of key market dynamics and comprehensive information about the structure of theMale Breast Cancer industry. This market study contains exclusive insights into how the globalMale Breast Cancer market is predicted to grow during the forecast period.

In addition, the statistical research for the Male Breast Cancer Report focuses onproduct specifications, costs, capacity, marketing channels, and market players.Upstream raw materials, downstream demand analysis, and end-user industry listings have been systematically studied with vendors in this market. Product flows and distribution channels were also presented in this research report.

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The outbreak of the pandemicCOVID-19changed the market scenario on the global platform. Many of the regions are facing the biggest economic crisis owing to the lockdowns that were implemented due to the outspread of the coronavirus infection. As the only solution that has been found to contracting this disease is social distancing many countries have implemented strong regulations in regards with people gatherings. Owing to this many of the businesses are working with only 30% of its employees thus not able to bring the maximum production.

Thiscan affect the global economy in 3 main ways: by directly affecting production and demand, by creating supply chain and market disturbance, and by its financial impact on firms and financial markets.

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Market Attributes

Details

Market size value in 2020

USDXX Million

Revenue forecast in 2027

USDXX Million

Growth Rate

CAGR of XX % from 2020 to 2027

Base year for estimation

2019

Historical data

2016 2019

Forecast period

2020 2027

Report coverage

Revenue Forecast, Company Ranking, Competitive Landscape, Growth Factors, And Trends

Country scope

U.S., Canada, Mexico, U.K., Germany, France, Italy, China, India, Japan, Brazil, Argentina, Saudi Arabia, South Africa

Key companies profiled

Pfizer, Roche, GlaxoSmithKline, Sanofi, Novartis, Bayer, Bristol-Myers Squibb, Eli Lilly, AstraZeneca, Teva Pharmaceutical, Sun Pharmaceutical, BioNumerik Pharmaceuticals, Seattle Genetics, Accord Healthcare Customization Available

Medication, Chemotherapy, Others

Section 1: Market Introduction

This section deals with the Male Breast Cancer market definition or the market along with the target audience of the market. Later in the chapters, the research methodologies and the market tools that were used for the market analysis is mentioned.

Section 2: Male Breast Cancer Market DROC

The flow of this section is: Male Breast Cancer market growth factors and limitations. In the later chapters, the Male Breast Cancer market opportunities and challenges are described. All the points mentioned within the report are updated based on the COVID-19 situation.

Section 3: Conclusion and Observations

Last section of the report includes comments and observations by the research analysts and the market experts for the Male Breast Cancer market.

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Strategic and COVID-19 Analysis of Male Breast Cancer Market with Profiles like- Pfizer, Roche, GlaxoSmithKline, Sanofi, Novartis - re:Jerusalem

The Global Male Breast Cancer Treatment market research report comprises the description of allmajor aspects concerning the Male Breast Cancer Treatment market. It provides thehelpful information that focuses on the key aspects and features linked to the market current and forecast growth trends, and clarify it with the help of appropriate statistics. The global market research report also includes the in-depth information regarding the leading market. Competing with one another as well as developing industries in terms of value, the volume of sales, demand, and quality of products and services.

The report assesses the key opportunities in the market and outlines the factors that are and will be driving the growth of the Male Breast Cancer Treatmentindustry. Growth of the overall Male Breast Cancer Treatmentmarket has also been forecasted for the period 2020-2025, taking into consideration the previous growth patterns, the growth drivers and the current and future trends.

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Impact of COVID-19:

Male Breast Cancer Treatment Market report analyses the impact of Coronavirus (COVID-19) on the Male Breast Cancer Treatment industry. Since the COVID-19 virus outbreak in December 2019, the disease has spread to almost 180+ countries around the globe with the World Health Organization declaring it a public health emergency. The global impacts of the coronavirus disease 2019 (COVID-19) are already starting to be felt, and will significantly affect the Male Breast Cancer Treatment market in 2020.

COVID-19 can affect the global economy in 3 main ways: by directly affecting production and demand, by creating supply chain and market disturbance, and by its financial impact on firms and financial markets.

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The major players profiled in this report include

Market Segments and Sub-segments Covered in the Report are as per below:

Based on Product TypeMale Breast Cancer Treatmentmarket is segmented into

Based on ApplicationMale Breast Cancer Treatmentmarket is segmented into

Regional Coverage of theMale Breast Cancer TreatmentMarket:

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Male Breast Cancer Treatment Market Analysis -Worldwide Opportunities, Revenue, Production, Demand and Geographical Forecast To 2027 - Eurowire

Science has enabled physicians to predict the likelihood of a woman getting breast cancer, much in the same way that meteorologists determine where and when a tornado will touch down and Amazon ensures you receive your order quickly. Predictive modeling, when coupled with powerful tools such as genetic testing, helps doctors prevent breast cancer or detect it early when it is most curable.

Miami Cancer Institutephysicians are at the forefront of these data-driven advances, working to prevent cancer as much as they are focused on curing it. Recently the Institute opened theBreast Cancer Prevention Clinicspecifically for those with a genetic predisposition to breast cancer or another underlying issue that makes them more susceptible. This concept ofprevivorship promotes fighting breast cancer before ever getting it.

In this clinic we will tailor a prevention plan for these patients, saidJane Mendez, M.D., chief of breast surgery at Miami Cancer Institute, so that instead of becoming a breast cancer survivor, they can continue as aprevivor. Meaning that even though you have the increased predisposition to breast cancer, we keep it at that.

With Breast Cancer Awareness Month in October, Dr. Mendez, sat down with Jonathan Fialkow, M.D., deputy medical director and chief of cardiology at Miami Cardiac & Vascular Institute, for a recent episode of theBaptist HealthTalk podcast, Breast Cancer: Risks, Prevention and Previvors. They discussed the latest breast cancer advances, as well as the basics such as screening guidelines and prevention recommendations.

Below are edited excerpts from their conversation. You can also access this and other Baptist HealthTalk podcast episodes in their entirety on your computer or smartphone or viaApple PodcastsandGoogle Podcasts.

Dr. Fialkow:

Lets start out by talking about what would be risk factors that would make a woman more likely to get breast cancer? What are the things weve identified that we want to pay attention to?

Dr. Mendez:

The two main risk factors for breast cancer are being a woman and getting older. So, even though wed like to forget about breast cancer the older we get, the more concerned we need to be about it. To that, you can add other factors such as family history as well as some environmental factors, some hormonal factors, and some of those are modifiable and some are not.

Dr. Fialkow:

What would the average person be told to do regarding screenings, mammograms, etc.?

Dr. Mendez:

For an average woman with no significant risk factors, the recommendation is a baseline mammogram anytime between age 30 to 40, and, then, provided there are no abnormalities, an annual mammogram starting at age 40. And we know the denser the breast tissue, the more important it is to complement that with a breast ultrasound. Its part of doing a more thorough evaluation.

Dr. Fialkow:

You mentioned some of the non-modifiable risk factors, things you cant change. One is family history, which speaks to genetics. Can you unpack that a bit?

Dr. Mendez:

I want to make it clear that only 10 percent of breast cancers occur in women who have a family history of breast cancer and 5 percent have an identifiable mutation or something in the genetic makeup that really predisposes them to breast cancer. At the time of our initial consultation, or as part of our follow-up, we ask very specific questions about family history. Who was the relative? Is this your mother, your sister? Also we would want to know about any male breast cancer in the family or any other cancers in the family. We ask about ovarian cancer because thats related to the BRCA genes, which are the most prevalent genes associated with breast cancer. But we also ask about colon cancer, prostate cancer, pancreas, stomach cancer, because we know that certain genetic mutations are also associated with the gene. It helps us stratisfy the risk so we can determine who might benefit from a genetic consultation and actual genetic testing.

Dr. Fialkow:

If someone is high risk, what is the next step?

Dr. Mendez:

We have models to help us calculate. One that is most commonly used is the Tyrer-Cuzick Eighth Edition model, where it takes a lot of these factors in consideration. It gives us a percentage probability of that woman developing breast cancer within 10 years and during their lifetime. If someone indeed has high risk, usually greater than 20 percent, in addition to the increased surveillance, we will follow that patient with a breast MRI.

Dr. Fialkow:

During COVID-19 were seeing a decrease in women getting their mammograms. Can you speak to how important it is to maintain your screening, your routine screening process?

Dr. Mendez:

Its very important to maintain the screening. Early detection is key for improved outcomes and improved survival. In addition to screening, its important to know your family history and your body. I cannot underscore the importance also of breast self-exam. I can assure patients that the imaging centers are following COVID-19 guidelines in terms of safety. I encourage all women to go and seek their mammogram so that we can attend to their needs and continue with prevention.

Dr. Fialkow:

Can we talk a little about the Breast Cancer Prevention Clinic at Miami Cancer Institute?

Dr. Mendez:

In this clinic we are trying to identify a very specific patient population at increased risk of breast cancer because of their family history, certain pathologic conditions, previous radiation or because they have been identified to have some of these high-risk mutations. We will tailor a prevention plan, including genetic consultation if needed, and nutrition and exercise plans so that they can monitor all of the different components that are critical in order to maintain a healthy lifestyle. Instead of becoming a breast cancer survivor, they can continue as aprevivor. So thats a great concept.

Dr. Fialkow:

Theres also aBenign Breast Cancer Clinic. Could you speak a little about the benefit of that?

Dr. Mendez:

This clinic focuses on non-cancerous conditions. We make sure that in their clinical exam, everything is normal, as well as in their imaging. These are women who might be having breast pain or cysts or other benign conditions and need to be reassured by an expert so that they can move on, and, receive proper follow-up when needed.

Dr. Fialkow:

And how about survivorship programs?

Dr. Mendez:

Its not only about surviving the breast cancer, but also living your life with good quality and any adjustments. Currently in the United States we have 3 million breast cancer survivors because of all the advances and technology. We have a whole program of survivorship, everything from psychological support to yoga classes, to acupuncture, to nutrition and obviously healing. Whatever is needed to keep the patient not only cancer-free, but with great quality of life.

Tags: breast cancer, breast cancer awareness month, Miami Cancer Institute

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Previvorship: How to Beat Cancer Before It Happens - Baptist Health South Florida

An international team of scientists from China, Taiwan and the United States has successfully sequenced and analyzed the genomes of the Chinese banyan tree (Ficus microcarpa), which is famous for its extraordinary aerial roots; Ficus hispida, a related fig species lacking aerial roots; and Eupristina verticillata, a wasp coevolving with the banyan tree. Theyve identified regions in the banyan trees genome that promote the development of its unusual aerial roots and enhance its ability to signal its wasp pollinator, and found a sex-determining region in Ficus hispida.

Zhang et al. reveal the genomic changes that allow the Chinese banyan tree (Ficus microcarpa) to produce roots that spring from its branches. Image credit: Gang Wang.

Understanding the evolutionary history of Ficus species and their wasp pollinators is important because their ability to produce large fruits in a variety of habitats makes them a keystone species in most tropical forests, said Professor Ray Ming, a researcher at the University of Illinois, Urbana-Champaign.

To better understand their evolutionary developments, Professor Ming and colleagues analyzed the genomes of the two fig species, Ficus microcarpa and Ficus hispida, along with that of Eupristina verticillata, a wasp that pollinates Ficus microcarpa.

When we sequenced the trees genomes, we found more segmental duplications in the genome of the banyan tree than in Ficus hispida, the fig without the aerial roots, Professor Ming said.

Those duplicated regions account for about 27% of the genome.

The duplications increased the number of genes involved in the synthesis and transport of auxins, a class of hormones that promote plant growth.

The duplicated regions also contained genes involved in plant immunity, nutrition and the production of volatile organic compounds that signal pollinators.

The levels of auxin in the aerial roots are five times higher than in the leaves of trees with or without aerial roots, Professor Ming said.

The elevated auxin levels appear to have triggered aerial root production. The duplicated regions also include genes that code for a light receptor that accelerates auxin production.

When the researchers studied the genome of the Eupristina verticillata wasp and compared it with those of other related wasps, they observed that the wasps were retaining and preserving genes for odorant receptors that detect the same smelly compounds the fig trees produce.

These genomic signatures are a signal of coevolution between the fig trees and the wasps.

The authors also discovered a Y chromosome-specific gene that is expressed only in male plants of Ficus hispida and three other fig species that produce separate male and female plants, a condition known as dioecy.

This gene had been duplicated twice in the dioecious genomes, giving the plants three copies of the gene, Professor Ming said.

But Ficus species that have male and female flowers together on one plant have only one copy of this gene.

This strongly suggests that this gene is a dominant factor affecting sex determination.

The results were published in the journal Cell.

_____

Xingtan Zhang et al. Genomes of the Banyan Tree and Pollinator Wasp Provide Insights into Fig-Wasp Coevolution. Cell, published online October 8, 2020; doi: 10.1016/j.cell.2020.09.043

Original post:
Researchers Sequence Genomes of Two Fig Species and Pollinator Wasp | Genetics - Sci-News.com

Norman Swan: One of the mysteries surrounding COVID-19, the disease that is caused by SARS-CoV-2, is why some people experience severe life-threatening disease and others don't. Age, male gender and having other problems like diabetes, heart and lung disease and probably obesity, are risk factors. But what about individual differences in people's immune systems? Well, two recent studies have found that to be the case in a significant percentage of people with serious COVID-19 disease. One study looked for genetic patterns and found an effect on immune messages called interferons. There are about 18 interferons in the body and they act like volume controls and orchestra conductors in the immune system once it has been alerted to an attack by a virus. The second study found antibodies against interferon in some people. This has huge implications for a better understanding of the immune system, not to mention more targeted therapies for people with COVID-19. Professor Paul Hertzog is one of Australia's leading experts on interferons. Paul is head of the Centre for Innate Immunity and Infectious Disease at the Hudson Institute in Melbourne.

Paul Hertzog: This study, initiated by Jean-Laurent Casanova who is based at the Rockefeller, and Helen Su at NIH, they've set up actually a global network looking for patients who might have genetic predispositions to getting extremely ill with the Covid SARS-CoV-2 virus. And it is really the first output of that global network of people who are doing the searches.

So firstly it's really the first substantial report that there is a genetic susceptibility of this disease. It's something that we always suspected but this really proves it. And more particularly what is unusual and fascinating is that most of the culprits they found were actually lying in different components of the interferon signalling system.

Norman Swan: They found a relatively consistent genetic problem in people when they looked at their genes, and these genes seem to code for the interferons in some shape or form.

Paul Hertzog: Yes, they identified 12 genes that we knew were involved in susceptibility to infections, particularly respiratory infections, and they happen to be in the interferon pathway, but involved in the production of it, or the response to it. And so they really looked where the light was and they said, well, can we find deficiency in any of these 12 genes? They actually found deficiencies in quite a high proportion of patients, about 3% of them. So I'm sure there are many more to cover because this was really just a very targeted look.

Norman Swan: So 3% doesn't sound too high.

Paul Hertzog: With a million people dying, I think it's a lot of human beings. And I think it is just the tip of the iceberg.

Norman Swan: People have been talking about interferons now for a while, and in fact interferons have been trialled as a treatment for people with COVID-19 disease even prior to these studies coming out. What's the net effect of these genetic abnormalities or these genetic differences?

Paul Hertzog: I suppose what they might enable us to do, Norman, is to use what you would call a precision medicine approach where we can identify people who would benefit and who would not benefit from this. So, for example, if a person has a defect which means they are unable to respond to interferon, and some of these genes are involved in that, it's absolutely pointless giving them interferon therapeutically because they just would not be able to respond. On the flipside, if we identify patients who can't make it and some of the genes are involved in the making of the interferon, then they are more likely to benefit from therapeutic administration of interferon.

Norman Swan: So where does this research go next? Presumably it's a simple test or what?

Paul Hertzog: I think that's a simple test. As I said, I think it might enable us to identify groups of patients who are likely to respond to interferon than those who don't. And if we can talk for a minute about the other paper which involves the identification of autoantibodies to interferon, that's probably in fact a far more fascinating study because autoantibodies, some of your listeners might recognise, are usually associated with autoimmune diseases like lupus where something goes wrong with the immune system, instead of recognising a foreign antigen it turns on itself, and these rogue antibodies can cause disease. So what they found in their second study was that 10% of the patients they looked at, which is a staggering number really, produced antibodies to these type I interferons and would negate its effect. That population of patients won't be able to respond. That has a number of implications. Secondly,

Norman Swan: Before you get to the implications, is the assumption that the autoantibodies pre-existed the infection or were created by the virus?

Paul Hertzog: Their study was nearly 1,000 patients, so there were probably about 100 of them and that they found these autoantibodies. I think in about 10 or 12 of them that they had the opportunity in the samples there to look before they had obvious signs of disease, and some of them did have pre-existing antibodies, but that's just a small proportion of those patients, I think it needs a much bigger study but it tells us that some of them certainly can predate. And that's interesting for a number of reasons because it identifies an underlying condition that we never would have thought of. And the other thing is those patients have no previous signs of other respiratory or susceptibility to viral infections, which raises the question whether this is fairly specific to COVID-19.

Norman Swan: And it also raises a question which a lot of people, at least to my Coronacast podcast ask, if I've got rheumatoid arthritis or Multiple Sclerosis or scleroderma or SLE, one of the other autoimmune diseases, doesn't make me more susceptible to COVID-19? Do any of the other autoantibodies that are around in the community affect interferons in this way?

Paul Hertzog: A really interesting question that has complicated answers, and the answers are yes and no. There are some autoimmune conditions where similar autoantibodies to interferons have been seen. But there are others like lupus where the opposite seems to happen. In lupus it seems a large part of the disease is driven by interferon, and in fact there was a large trial headed by an Australian clinician from Monash, Eric Morand last year that identified blocking antibodies to interferon that actually look like they will have beneficial effects in lupus, so that's quite the opposite effect.

Norman Swan: So this discovery of autoantibodies which might actually be quite significant in a reasonable percentage of people, is there a therapy there?

Paul Hertzog: Good question. Not obviously. It's probably may lieagain, if you're thinking interferon therapy it clearly wouldn't work and less there is some specificity in the antibodies that you could get around. I think there are ways of screening it out. For example, you wouldn't want the samples of those serum in your convalescent serum preparation, so I think there are practical outcomes like that.

Norman Swan: Oh yes, that's right, so if you're taking serum from these people to give to other people and you give them autoantibodies you can make them worse.

Paul Hertzog: Right, so it's another screening test for that. There are B cell and antibody depletion therapies that are used in other autoimmune diseases, and that might be in the area that could be looked at in these patients.

Norman Swan: So what's next for your research, given all this?

Paul Hertzog: Well, it provides us with an opportunity. For us it's yet another example of the importance of the interferon system. We are currently collaborating with Jean-Laurent Casanova in a number of these mutations prior to Covid and we will continue that. What we'll do is drill down to try and find out the mechanism whereby some of these mutations in the interferon system are working, and in fact whether some of them that haven't yet been identified as loss of function and disease contributing might in fact be so.

Norman Swan: Paul, thanks for joining us.

Paul Hertzog: My pleasure, thanks a lot.

Norman Swan: Professor Paul Hertzog is head of the Centre for Immunity and Infectious Disease at the Hudson Institute in Melbourne.

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Could genetics explain the mystery of severe coronavirus? - ABC News

How can you make this type of research information into news you can use? Thats a real challenge.

About a year ago, I thought I saw a path to greater use of genetic information by consumers. An ambitious company named Veritas Genetics was offering full genome sequencing to U.S. customers for $599 US. They told me they were planning to expand to Canada. Veritas is backed by considerable brainpower, including its co-founder, Harvard professor George Church, often called the father of synthetic biology.

A full human genome sequence is about three billion base pairs, containing your complete genetic blueprint. By contrast, companies like Ancestry and 23andme only look at certain parts of the genome that provide information about ancestral roots and common medical conditions.

What Veritas seemed to lack is financial backing. This was complicated by the fact that many of its investors were from China, which raised red flags because of possible U.S. regulations. Privacy experts have also told us to be very careful about where our genetic data goes once it leaves our mouth as a bit of spittle. Veritas has suspended their U.S. whole genome testing, laid off some staff, and is currently focusing on COVID-19 tests.

Competitors are cropping up, and theres no doubt you will eventually be able to download your complete gene sequence and scan it for interesting findings. There are already tools out there like OpenSNP that can work with the information you can download from 23andme, deCODEme or FamilyTreeDNA. It can answer questions like am I a fast metabolizer of caffeine?

Read more from the original source:
Keenan: Thinking well beyond COVID-19 - Calgary Herald

One upside of the COVID-19 disruption is that many people have a bit more time if only because theyre not commuting, looking for a parking space, going for after-work drinks, etc. Ive been encouraging my students to pick up a fun new activity to make good use of this time bonus. Ive chosen to try to learn to draw and am making a start on it. Well, at least Ive bought some instructional books and supplies. Wish me luck!

One activity that we could all benefit from is paying attention to our long-term health. After all, youre far more likely to die from cancer or heart disease than from COVID-19. There are some concrete steps you can take to improve your long term health prospects. If youve been putting off a visit to your doctor for a physical, this might be a good time, even if its a telehealth visit. Some procedures like that dreaded prostate exam do require the hands-on approach. But youd be amazed at how much you and your doctor can sort out over the phone and with lab tests.

To see whats included in a good physical, have a look at the Preventive Care Checklist on the website of the College of Family Physicians of Canada (cfp.ca). It was recently updated, and I learned a lot from it, including that at my age I should be getting the pneumococcal 23-valent polysaccharide vaccine.

Discoveries also highlight the importance of knowing more about our genetic heritage. In a first-of-its-kind genomic study, researchers at Vanderbilt University Medical Center led by William D. Dupont and Joan P. Breyer studied prostate cancer patients with family histories of the disease. They note that prostate cancer heritability is twice that of breast cancer, at roughly 58 per cent. Their latest research focused on the detailed genetic makeup of chromosome 8, which is known to be related to prostate cancer. The Vanderbilt scientists found three mutations that helped protect us from prostate cancer, and four that raised the danger, in one case by 22-fold.

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Keenan: Thinking well beyond COVID-19 - Edmonton Journal

Named Cardamine inseuta, was first spotted in 1972 in the Urnerboden region after the land in the area went from being a forest to a grassland. Now, researchers at the University of Zurich (UZH) have narrowed down the two species of the plants that merged to create the hybrid that is thriving.

One is Cardamine amara, which grows in and around streams and the other is Cardamine rivularis, which inhabits moist, not wet, areas.

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It is the combination of genetic traits from its parents that enabled the new species to grow in a district environmental niche, said Rei Shimizu-Inatsugi, co-author of the study published in Frontiers in Genetics.

The best of both worldsC. inseuta is a so-called triploid plant. It means that it has three sets of chromosomes. Two come from C. rivularis and one set from C. amara.

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From its other parent, C. amara, the new species inherited the trait of submergence tolerance. That means that even if surrounded by water, C. inseuta would survive rather than drown.

Depending on the environmental situation, the plant activates a different set of genes it inherited from its two parent species, said Shimizu-Inatsugi.

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Andrea Ghez is the fourth woman to win the Nobel Prize for Physics found the first signs of the supermassive black hole at the center of the Milky Way

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Scientists unravel the mystery behind new plant species found in the Swiss Alps, which only took 150 years to - Business Insider India

Mathew Knowles, the father of music powerhouses Beyonc Knowles-Carter and Solange Knowles, on Saturday penned an opinion piece encouraging men to get tested for breast cancer.

Knowles wrote the op-ed for USA Today on the one-year anniversary of sharing his diagnosisof Stage 1A breast cancer and called for an inclusive term that doesnt embarrass men or prevent them from seeking the care they need.

It wasnt comforting to walk into my first oncology appointment through doors that read Womens Breast Clinic and to be greeted with the question, am Ihere for my wife? Knowles wrote. Since Ive shared my diagnosis, countless men have secretly shared their male chest cancer diagnosis with me, as they were too ashamed to talk openly about having breast cancer.

The music executive told Good Morning America last year that breast cancer affected several women in his family, including his aunt and cousins.

After his scheduled mastectomy, he learned that he had the BRCA2 gene mutation that put him at a higher risk of breast, prostate and pancreatic cancers and melanoma.

Im grateful to say Im cancer-free today and have the knowledge to make important lifestyle choices that hopefully keep me in remission, such as getting a mammogram every six months, Knowles wrote. Im perhaps even more grateful this discovery spurred my kids to take their own medical genetic tests to learn their own risks and better inform the decisions they make my newfound knowledge also became theirs.

He has since partnered with a medical genetics company, Invitae, and encouraged readers to get screenings done for gene mutations.

Its foolish that so few of us take advantage of this information thats more affordable and accessible than ever. Who doesn't want to be able to get ahead of potentially life-changing diseases or health conditions? Knowledge is power, he wrote.

There will be approximately 2,620 new cases of invasive breast cancer diagnosed in men in the year 2020, according to the American Cancer Society.

Breast cancer is about 100 times less common among white men than among white women.It is about 70 times less common among Black men than Black women, and Black men typically have a worse prognosis.

Go here to see the original:
Beyonc's father in op-ed urges men to get tested for breast cancer | TheHill - The Hill

Its one of the most important genes in biology: Sry, the gene that makes males male. Development of the sexes is a crucial step in sexual reproduction and is essential for the survival of almost all animal species.

Today in the journal Science, my international collaborators and I report the surprise discovery of an entirely new part of the Sry gene in mice a part we had no idea existed.

I co-discovered Sry in 1990. It is the gene on the Y (male) chromosome that leads to the development of male characteristics in mice, humans and most other mammals. Since then, Sry has been the subject of intense study worldwide because of its fundamental role in mammalian biology.

We have come to understand, in some detail, how Sry acts to trigger a cascade of gene activity that results in the formation of testes, instead of ovaries, in the embryo. Testes then stimulate the formation of other male characteristics.

But its clear we dont have all the answers just yet. Our results published today take us one step further in the right direction.

For 30 years, we have understood the Sry gene is made up of one exon, a segment of a gene used to code for amino acids, the building blocks of proteins. This can be compared to a computer file consisting of one contiguous block of data, on a hard disk.

Our newest research reveals theres actually a second exon in mouse Sry. This is like finding a whole new separate block of previously hidden data.

The mouse genome, like the human genome, has been extensively characterised due to the availability of advanced DNA sequencing and related technologies. Researchers commonly assume all the genes and all the parts of the genes have already been discovered.

But earlier this year, scientists in Japan uncovered what looked like a new piece of the Sry gene in mice. New sequencing approaches revealed what appeared to be two versions of Sry: a short, single-exon form and a longer, two-exon form. They called this two-exon version Sry-T.

They collaborated with my group at the University of Queensland and removed the new exon using CRISPR, a gene editing tool that lets researchers alter DNA precisely. Together we discovered this prevented Sry from functioning: XY mice (which would normally develop as males) developed as females instead.

Conversely, adding Sry-T to fertilised XX mouse eggs (which would normally develop as females) resulted in males.

Importantly, although human Sry does not have the added exon, our discovery may reveal new functions that might be shared between mouse and human Sry.

The DNA sequence of the new exon in Sry-T may point us towards discovering some of the genes and proteins that interact with Sry, something that has been elusive up till now.

And interactions we find in mice may also occur in humans. Studying what human Sry interacts with may help explain some cases of differences in human sex development, otherwise known as intersex development. This is a common but poorly understood group of mostly genetic conditions that arise in humans.

Currently, we dont know the genetics behind a large proportion of intersex conditions. This is partly because we dont yet know all the genes involved in the human sex development pathway.

Read more: Sex, genes, the Y chromosome and the future of men

Scientifically, this discovery is a bit like discovering a new cell type in the body, or a new asteroid in the Kuiper belt. As with many scientific discoveries, it challenges what we thought we knew and raises many questions.

What is the function of the new exon in Sry-T?

Currently, we only have part of the answer. It turns out the first exon of Sry, the one we already knew about, contains instability sequences at its end. These are sequences that cause proteins to fray and degrade.

An important function of the newly discovered second exon is to mask the instability sequences, seal the end of the Sry protein and prevent it from degrading. In other words, this second exon is crucial to the development of male babies.

Whats more, this protection mechanism represents an unusual and intriguing evolutionary mechanism that has acted to help stop vulnerable Y-chromosome genes from literally falling apart.

But its early days yet. The challenge now is to understand whether there are more functions hidden within the newly discovered exon.

If so, this information may provide some of the missing links that have stood in the way of our full understanding of how Sry works at a molecular level and of how males and females come to be.

Read more: Why education about gender and sexuality does belong in the classroom

Read more:
We discovered a missing gene fragment that's shedding new light on how males develop - The Conversation AU

Although rare, men get breast cancer too.

According to the National Breast Cancer Foundation, in 2020, an estimated 2,620 men will be diagnosed with breast cancer this year in the U.S. and approximately 520 will die.

The American Society of Clinical Oncology reports that the 5-year survival rate for men with breast cancer is 84%, with individual survival rates dependent upon various factors, including the stage of the disease when it is first diagnosed. If the cancer is located only in the breast, the 5-year survival rate of men with breast cancer increases to 96%. About 47% of cases are diagnosed at this localized stage. If the cancer has spread to the regional lymph nodes, the 5-year survival rate is 83%.

Breast cancer in men is usually detected as a hard lump underneath the nipple and areola. The mortality rate is higher in men than women because awareness among men is sadly lacking. Men are generally less likely to assume a lump is breast cancer, which may keep them from seeking medical advice. Any delay in seeking treatment can diminish the likelihood of a positive outcome.

Most men diagnosed with breast cancer are over the age of 50.

Here are some important facts about male breast cancer from the American Cancer Society:

Breast cancer is about 100 times less common among white men than among white women; and about 70 times less common among Black men than Black women

As with Black women, Black men with breast cancer tend to have a worse prognosis

For men, the lifetime risk of getting breast cancer is about 1 in 833

Breast cancers can start from different parts of the breast

The most common types of breast cancer are ductal carcinoma in situ, invasive ductal carcinoma, and invasive lobular carcinoma

Breast cancer can spread when the cancer cells get into the blood or lymph system and are carried to other parts of the body

Risk factors for breast cancer in men include the following:

Age The risk of male breast cancer increases as a man ages. The average age of men diagnosed with breast cancer is 72.

Genetics Men with a mutation in the BRCA2 gene have an increased risk of breast cancer.

Klinefelter syndrome This is a congenital condition that affects approximately 1 in 1,000 men. Men with Klinefelter syndrome are more likely to get breast cancer than other men.

Radiation exposure Any man whose chest has been treated with radiation is at an increased risk of developing breast cancer.

Alcohol Excessive consumption of alcoholic beverages increases the risk of breast cancer in men.

Liver disease Men with severe liver disease, such as cirrhosis, run an elevated risk of developing benign male breast growth.

Obesity Studies have shown that obesity is a factor for male breast cancer.

The American Cancer Society encourages men who are or may be at a high risk for male breast cancer to discuss how to manage that risk with their doctor. The American Society of Clinical Oncology goes one step further and urges men to become familiar with the feel of their breast and chest wall tissue, so they can talk with their doctor if they notice any lump or change.

Following is a list of possible symptoms of breast cancer:

A lump or swelling, which is often (but not always) painless

Skin dimpling or puckering

Nipple retraction (turning inward)

Redness or scaling of the nipple or breast skin

Discharge from the nipple

For more information about male breast cancer, visit http://www.nationalbreastcancer.org or http://www.cancer.org.

See original here:
Male breast cancer rare, but men should learn risk factors, signs and symptoms - Tampa Bay Newspapers

European wildcats, thought to be extinct 50 or so years ago in the Jura mountains, have since recolonised part of their former territory. This resurgence in an area occupied by domestic cats has gone hand-in-hand with genetic crosses between the two species. The hybridisation between wild and domesticated organisms is known to endanger the gene pool of wild species. In a study to be published in the journal Evolutionary Applications, a team of biologists from the University of Geneva (UNIGE), in collaboration with the University of Zurich and the University of Oxford, modelled the interactions between the two species to predict the future of the wildcat in the mountainous region of the Swiss Jura. The different scenarios modelled by the scientists show that within 200 to 300 years --a very short time in evolutionary terms-- hybridisation will entail the irreversible genetic replacement of wildcats, making it impossible to distinguish them from their domestic cousins, as is already the case in Scotland and Hungary.

Although the European wildcat (Felis silvestris) or forest cat was once very common, it fell victim to intensive hunting in the 19th and 20th centuries and to the massive deforestation that cut back its natural habitat, resulting in its disappearance in some parts of Europe. In Switzerland, the wildcat was deemed practically extinct, with no trace found for 25 years from 1943 to 1968. Thanks to a federal law that has protected the animal since 1962, the wildcat has recolonised the forests and meadows in the Jura range, where it lives side-by-side with the domestic cat (Felis catus) in particular. Although considered two species --or as different subspecies by some-- wildcats and domestic cats can interbreed and have hybrid, fertile kittens. These have the genome of both species and may give birth to offspring carrying the recombinant genes of each species. These hybridisations pose a new threat to the wildcat, since they prompt gene transfers based on a mechanism known as genetic introgression. This mechanism can quickly result in the dissemination of the genes of the more abundant species in the genome of the rarer species. The risk exists in the short term that the genome of the domestic cat will gradually replace the gene of the wildcat, which is markedly less plentiful than its domestic cousin, leading to the extinction of the wildcat.

Recolonising the territory

Scientists from UNIGE and the University of Zurich demonstrated in earlier studies that there is a greater introgression of the wildcat genome by the domestic cat genes than vice versa. The demographic and territorial expansion of wildcats over the last 50 years was identified as the most likely cause of these introgressions, which tallies with observations in the field. This conclusion was reached using bioinformatic simulation models factoring in ecological and genetic characteristics. It was estimated that about 5-10% of contacts between wild and domestic cats produced hybrid kittens. Following these discoveries, the computer model was refined in order to make projections and define the urgency for intervening and preserving the species.

The only solution: stop crossbreeding

The variable factors in the model incorporated in the new article, whose last author is Mathias Currat, senior researcher at the UNIGE Department of Genetics and Evolution, are the hybridisation rate, competition for resources in the environment and the size of the populations. Irrespective of the scenario put forward while acting on these variables, a very strong introgression of the domestic cat's genome into the genome of the wildcat is predicted. Mathias sounds a warning: "This is strongest with population sizes comparable to today's, but is still very high even if we consider more favourable conditions for the wildcat, such as an increase in its population size or a competitive advantage over the domestic cat in the regions where they coexist." Juan Montoya-Burgos, laboratory director in the Department of Genetics and Evolution at UNIGE, and co-author of the study, warns: "The model leads to an irreversible genetic replacement resulting in the ultimate disappearance of the wildcat. Only the end of crossbreeding between the two species predicts the conservation of the wild species."

Action needed now

It follows that the wildcat remains an endangered species in spite of the positive signs of its recent expansion. The dynamic model put forward in the UNIGE study, which combines the demographic and spatial growth of the wildcat populations, can be used to predict the future of the species. Based on the various scenarios, wildcats will be assimilated to domestic cats in as little as 200 to 300 years, as is already the case in Scotland and Hungary. "A hybridisation event has a proportionally much greater impact on the wildcat population, which consists of a few hundred individuals, than in the domestic population, which numbers over one million individuals in Switzerland", points out Mathias Currat.

One initiative suggested by the authors is to drastically reduce the opportunities for hybridisation on the fringes of the wildcat territories. Campaigns to sterilise domestic cats living near farms or close to forests are just one of the proposals. Females should be the primary target since domestic females mate more readily with male wildcats than male domestic cats with wild females. "Early interventions are likely to be less costly both financially and in environmental terms. If we stay passive, the threat to weigh on wildcats in the Jura risks being irreversible," concludes Juan Montoya-Burgos.

Link:
Wildcats threatened by their domestic cousins - Science Codex

Mosquitoes are probably most people's least favorite insect.

Mosquito-borne diseases include malaria, yellow fever, and the Zika virus all of which can cause extreme sickness, birth defects, or death. Per year, malaria is responsible for the deaths of over 400,000 people, while dengue fever causes about 20,000, according to the World Health Organization.

Vaccines have been in development for dengue fever, malaria, and Zika, but production can be very slow and result in low efficacy. Drugs can help, but can be expensive. Insecticides are successful in the short term, but mosquitoes can become resistant, and mass-release insecticide can have health impacts on plants and wildlife.

Instead, othershave focused their attention on treating the mosquitos, not the symptoms:genetically modifying mosquitos themselves to only produce sterile offspring, effectively wiping out an entire population of insects. Modern genetic modification techniques are fast, and work at thescale of genes but they mimic the plant breedingfocused on phenotype humans have been doing since the beginning of history (like, say, selective breeding of crops, which humans have been doing since agriculture was invented).

There are two general approaches to producing genetically modified mosquitoes: 1) modifying the reproductive ability of male mosquitoes so that they cannot produce offspring, and 2) modifying both male and female mosquitoes so that they are resistant to diseases or incapable of transmitting them to other species. Oxitec, the biotechnology company behind a genetically modified (GM) mosquito Aedes aegypti, has tested the first approach to GM mosquito releases in field trials in parts of Brazil, the Cayman Islands, and Malaysia. These male mosquitoes mate with a female, exchanging a gene mutation that causes the larvae to die unless they are given an antibiotic. These trials have shown to reduce mosquito populations from 80-95%, reducing dengue fever cases by 91%.

GM mosquitoes are successful in reducing mosquito populations, and reducing disease spread. But there are still many scientific questions that haven't been fully answered, including concern over public health, mosquito resistance risks, and environmental consequences associated with genetic modification of a wild-living organism. Many people believe that genetic modification goes against the natural order of the world, or that we don't know the full range of possible outcomes for releasing modified organisms into the environment.

And the skeptics have a point: GM crops, initially thought to reduce our need for pesticide applications, have resulted in increased herbicide applications in the face of the development of resistant weeds and insect pests. In the case of genetically modified corn targeting the European corn borer pest, known as Bt corn, resistance has driven an increase in pesticide use by about 7% over a 15 year period.

A map showing dengue spread in the US as of August 2020, with outbreaks in Puerto Rico, Texas, Florida, and Wisconsin, among others

Via CDC

Studies testing the safety of GM crops are widespread, but the public often sees these announcements coming from huge corporations like General Mills, aiming at selling a GM product. In a 2014 Pew Research Center survey, only 37% of adults felt that GM foods were safe to eat, and only 26% felt GM foods were safe to eat if they stated they had less scientific knowledge than their peers. And yet, multiple science and health organizations have deemed GM crops as safe for human consumption.

But what does all of this uncertainty about GM crops mean for GM mosquitoes? Oxitec is currently the first and only company to be approved to release genetically modified mosquitoes, beginning in 2009 (though not announced until 2010) with the release of 3 million genetically modified mosquitoes in the Cayman Islands in response to high levels of pesticide resistance in the mosquito population. In 2015, in response to an increase in Zika virus in the country, Brazil's National Biosafety Committee approved the release of GM mosquitoes in Juazeiro, in northeast Brazil. The trials were successful, with Oxitec concluding the modified mosquitoes reduced dengue fever mosquito populations by 95%.

It's important to note that Oxitec was not the first to alter the genetics of insects for population control. The genetic approach to render insects infertile or resistant to disease is based on the Sterile Insect Technique (SIT). SIT was developed in the 1930s as a way to reduce insect populations. The technique renders male insects sterile by exposing them to extremely high levels of radiation, before releasing them to mate with females. The technique has great success, eradicating multiple pest species such as the screwworm in the 1950s and reducing pink bollworm moth populations in California beginning in 1967.

A workflow describing proposed stages for developing, testing, and releasing genetically modified mosquitos

Via WHO

Following the success of the initial trials, Oxitec had another GM mosquito release in Jacobina, Bahia, Brazil in 2015. About 450,000 mosquitoes were released each week for 27 months, developed using a strain from Cuba outcrossed with a strain from Mexico. The Brazil trials had little-to-no pushback in the region, with many residents believing the GM mosquito resulted in a drop in dengue fever cases and limiting the success of Zika virus spread.

Oxitec applied to the EPA in the United States to release the modified insect containing a gene in GM male mosquitoes that would spread to and kill offspring in the larval stage in 2012, after outbreaks in 2009 and 2010 of dengue fever in the Florida Keys. But when the public found out about the potential experiment, a petition on Change.org gathered over 100,000 signatures against the project (it's at over 235,000 today). Many skeptics reference Oxitec's rush to use GM mosquitoes in the field in their initial Cayman Island trials without properly consulting the public.

Oxitec scrapped their original release mechanism which would allow female mosquitoes to escape from the release capsule due to public pressure. Instead, they developed a newly branded version of the mosquito technology, coining it "friendly mosquito technology." The new GM mosquito is programmed to only release males from an Oxitec capsule placed in water, and not the biting females. The "safe" name refers to the fact that male mosquitoes do not bite, so the company's release would not increase numbers of female-biting mosquitoes.

A map showing Aedes aegypti's range in the United States and Indigenous reservations

Via CDC

But environmental groups are still unhappy. Many believe the engineered mosquitoes are still putting Floridians at risk, and worry that spreading modified genes from male mosquitoes into the wild mosquito population could cause cascading effects on the food chain. Birds, insects, and mammals all feed on mosquitoes; environmentalists are concerned about any affect the genes could have on these organisms. Many scientists have speculated about whether the elimination of the mosquito would have any impact on other creatures, but others are hesitant to promote the purposeful extinction of a species.

There are also other options for reducing diseases spread by mosquitoes. A non-profit organization in Brazil known as Eliminate Dengue is working to breed mosquitoes that are less likely to spread disease. The group is focused on breeding mosquitoes to carry on a parasite widely found and naturally occurring in mosquitoes, Wolbachia, which has been shown to inhibit the mosquito's ability to spread viruses such as dengue fever or chikungunya. Eliminate Dengue, funded through the Gates Foundation, has released these mosquitoes in 40 areas worldwide. The parasite stays in the population, reducing the need to release modified mosquitoes year after year.

The majority of scientists believe that GM mosquitoes pose no human health risks. However, the possibility of hybridization between GM mosquitoes and wild mosquitoes, passing the genetically modified genetics to wild populations and into the ecosystem, is concerning to many.

The potential good may outweigh the potential bad. But with EPA approval and test releases of genetically modified mosquitoes planned for the Florida Keys and Texas, the future is already here. Only time and data will tell.

More:
You should be excited that scientists are releasing 750 million genetically modified mosquitoes this year - Massive Science

The last seven months or so have been an interesting time to be alive. Lets face it, its not often that we see our grandparents scratching their heads and saying theyve never seen anything like it. From COVID-19 to politics, 2020 has been one of those years that will be referred to in history lessons for decades, if not centuries, to come. Of course all of that upheaval also comes with a record-breaking amount of personal stress, too, manifesting itself in our bodies in all sorts of ways. For a lot of modern men, that tension is working its way out literally through hair loss.

Its perfectly normal to experience some hair loss. Hair goes through phases just like the rest of us. Without getting too technical, theres a growth phase, a transition phase, and a resting phase. Hair can grow for anywhere from five to seven years, depending on your genetics. That transitional phase, on the other hand, only lasts about ten days. The resting phase (the technical term is telogen) can last as long as three months, but thats the point where slowly but surely the hair starts to loosen and come out. After about three months the whole process starts all over again. Usually.

Those of us with Male Pattern Baldness will lose hair due to genetics. The hair follicle starts to shrink and, after a while, that whole growth process just dies out. (Dont despair, there is hope for that.)

Beyond genetics, though the stress of our current times including the stress on your body if you have actually contracted COVID may also lead to premature hair loss. (Editors note: We truly hope that hair loss is the only thing you have to cope with, should you be ill.) In fact, according to Dr Dayal Mukherjee, MD, at The Aura Clinic London, Psychological factors such as stress, anxiety or any significant traumatic episode, may trigger or exacerbate certain types of hair loss.

Dr. Craig Ziering is a hair restoration specialist with clinics in Newport and Beverly Hills, CA, Las Vegas, and New York City. He refers to this circumstance as telogen effluvium. Sure, it sounds like something sticky from Ghostbusters, but its actually the technical term for hair loss that happens after stress. And these past seven months or so have been all about stress.

The coronavirus itself can cause inflammation, so people who are already hypersensitive may find that its bad for their hair, Ziering tells The Manual. Weve even been seeing patients who arent sick suddenly losing more hair than usual. Men particularly are suffering because they are still, traditionally, seen as the head of the household. If they get even a little sick it can cause emotional stress. How will they provide for their families? Compound that with fluctuations in the stock market. Guys who own small businesses may feel it even more because they feel the stress of providing for their families as well as for their employees.

Ziering goes on to point out that a lot of things can unmask underlying genetic hair loss that a patient might not normally experience until later in life. Men who are treated for cancer, for instance, may lose their hair temporarily, but it will grow back. If there is underlying Male Pattern Baldness, however, that may exacerbate hair loss into a more permanent condition.

Sometimes its as simple as giving the patient a sense of control. Everything else in his life is spiraling beyond his power, now its his hair, too? Its about breaking that cycle., says Ziering.

Sometimes that cycle may be as simple as using hair products that are healthier for your hair and scalp. Buildup from styling products can actually clog hair follicles, accelerating that telegenic effluvium response. Here are some of the best natural styling products weve tried.

Dr. Mukherjees comment sparked British grooming brand No Gunk to launch its lighthearted campaign, Dont Be a Receder Peter, in September. The accompanying video shows a young, healthy-haired man transformed into an aged, bald one from using preparations with harsh chemicals and those that leave residue behind. No Gunk is in favor of natural ingredients like lava clay, shea butter, and argan oil.

Winner of 2020 Grooming Awards, Jack Henrys rockstar product only contains four main ingredients beeswax, coconut oil, bentonite clay, and lavender oil to easily shape hair without damaging follicles.

Lots of drugstore shampoos contain some artificial ingredients that can further cause hair damage. Not so with Verbs vegan shampoo, which is infused with hydrating moringa and sunflower seed extracts to thoroughly clean your mane. Plus, its free of harmful sulfates and parabens, and its cruelty-free.

If youve tried changing products and are still experiencing rapid hair loss, dont waste any time getting to a doctor. If a serious hair loss problemis diagnosed in time, it may be reversible within three to six months.

Dr. Ziering starts with topical medications like minoxidil or finasteride, an easy at-home treatment. In some cases he may move on to oral finasteride, which blocks DHT. DHT is a type of testosterone that works wonders for men when were going through puberty, but is not so friendly to your follicles when you get older.

We also use laser therapy, where the patient wears a cap that stimulates the mitochondria, improving cell growth, says Ziering. Finally we also do exosomes injections, which is a form of stem cell therapy. The treatment nourishes the hair and basics all helps wimpy hair grow thicker.

Finally, if it comes down to it, actual surgery may be an option, and doctors like Ziering can help with hair restoration and transplants.

Maybe the most important part of stress-related hair loss is to keep things in perspective.

Im a medical doctor. I deal with the patient as a whole, says Dr. Ziering. Its important to remember that we are all in this together. Find something thats good for your body: Meditation, exercise, rest, yoga, or whatever makes you feel better. Eat a high protein diet with fresh super greens and legumes. Dont keep stress bottled up! Find somebody that you can talk to and share your feelings. Dont be ashamed if its time to do something about losing your hair. Do whats necessary to break that stressful cycle and feel like youre doing something positive for yourself.

Link:
How To Treat Stress-Related Hair Loss During COVID-19 - The Manual

OWINGS MILLS, Md., Sept. 24, 2020 /PRNewswire/ --Chesapeake Urology, an affiliate of United Urology Group, recently welcomed three new physicians to its growing team of specialists and general urologists. The addition of David A. Levy, M.D., Devang Sharma, M.D., and Katherine Smentkowski, M.D., continues to expand Chesapeake Urology's reach into specialties such as prostate cancer, men's sexual and reproductive medicine, reconstructive surgery, as well as general urology.

David A. Levy, M.D. is a recognized expert in prostate cryosurgery, an outpatient curative prostate cancer procedure that he has been performing for the past 15 years. He has published numerous peer-reviewed manuscripts on prostate cryosurgery detailing patient selection criteria, procedure-related side effects and outcomes analyses, as well as the definition of treatment success for the procedure for patients with newly diagnosed prostate cancer and those treated for recurrence following failed radiation therapy.

Dr. Levy also has substantial experience in prostate cancer nutrition and directed a Prostate Cancer Nutrition Genetics Clinic in Cleveland where he treated more than 450 prostate cancer patients in a non-operative manner over the past six years.

He graduated from Washington University in St. Louis in 1985. He received his Doctorate of Medicine degree from the Chicago Medical School and completed his General Surgery Internship and Urology Residency at University Hospitals of Cleveland, Case Western Reserve University. Following his residency, Dr. Levy completed a fellowship in Urologic Oncology at the MD Anderson Cancer Center in Houston, Texas.

Dr. Levy sees patients at Chesapeake Urology's Hanover and Saint Agnes Hospital/Angelos Medical Pavilion offices.

Devang Sharma, M.D. is a comprehensive men's health specialist with fellowship training in male infertility, sexual dysfunction, and reconstructive surgery. In addition to general urology, his practice is focused on men with urinary complaints related to the bladder, prostate, or urethra, erectile dysfunction, Peyronie's disease, low testosterone, fertility concerns, and prostate cancer survivorship. He brings advanced training and expertise in contemporary treatments including no-scalpel vasectomy, Greenlight photovaporization of the prostate, UroLift, penile injection and shockwave therapy, penile implants, artificial urinary sphincters and slings, urethral reconstruction, and microsurgical techniques including vasectomy reversal, varicocele repair, sperm extraction, and spermatic cord denervation.

Dr. Sharma graduated summa cum laude from the University of Maryland with a degree in Bioengineering. He graduated with honors from the Geisel School of Medicine at Dartmouth, then completed Urology Residency and Andrology Fellowship at the University of Virginia.

Dr. Sharma sees patients at Chesapeake Urology's office at Holy Cross Germantown Hospital.

Katherine Smentkowski, M.D.focuses on general urology as well as bladder and kidney cancer, kidney stones and minimally invasive and robotic surgery for upper urinary tract reconstruction. Her fellowship training at Thomas Jefferson University focused on robotic management of both benign and malignant urological conditions. This included prostate, bladder, kidney and ureteral cancers as well as reconstructive techniques for ureteropelvic junction obstruction and ureteral strictures.

Dr. Smentkowski earned her Bachelor of Science degree in Physiology and Neurobiology from the University of Maryland, College Park, MD. She received her Medical Doctorate at Eastern Virginia Medical School (EVMS) in Norfolk, VA where she was involved in community outreach and elected into the Alpha Omega Alpha Honor Society. She went on to complete Urological Residency at EVMS as well as a Fellowship in Minimally Invasive and Robotic Surgery at the Thomas Jefferson University in Philadelphia, PA.

Dr. Smentkowski sees patients in Chesapeake Urology's Columbia office.

About Chesapeake Urology

Chesapeake Urology, an affiliate of United Urology Group, is a fully-integrated urology practice providing a comprehensive array of urologic services to its patients. The Company operates 24 medical offices and 17 AAAHC-certified ambulatory surgery centers in Anne Arundel, Baltimore, Harford, Howard, Carroll, Montgomery, Prince George's, Wicomico, Worchester counties in Maryland, Baltimore City, and Sussex County, Delaware, and has a staff of more than 900 including 90 physicians, 84 who are urologists. Chesapeake Urology has been named one of the top places to work in healthcare nationally by Modern Healthcare magazine and Becker's ASC Review, and locally by the Baltimore Sun, Baltimore magazine and the Baltimore Business Journal. For additional information, please visit ChesapeakeUrology.com.

Media Contact: Patricia Schnably, Senior Vice President, Marketing & CommunicationsUnited Urology Group25 Crossroads Drive, Suite 306, Owings Mills, MD 21117443-738-8107[emailprotected]

SOURCE Chesapeake Urology

Read more:
Chesapeake Urology Welcomes Three New Physicians, Expanding Specialty Services in Anne Arundel, Howard, and Montgomery Counties and Baltimore City -...

Hair loss can be the result of complex environmental and genetic processes. In the former camp lies responses to stressful situations and certain cancer treatments. In the genetic camp is androgenetic alopecia - commonly known as pattern baldness. It usually runs in the family, which, on the face of it, seems dispiriting.

Fighting genetics may seem like a losing battle but evidence does suggest you can reverse this form of hair loss.

One strategy that has yielded surprising results is applying a melatonin solution to the scalp.

Most people will associate melatonin with sleep - the hormone plays a central role in the bodys sleep-wake cycle.

As the National Sleep Foundation explains, its production increases with evening darkness, promoting healthy sleep and helping to orient our circadian rhythm.

READ MORE:Hair loss treatment - Dr Sara explains the best type of shampoo to stimulate hair growth

Circadian rhythms are 24-hour cycles that are part of the bodys internal clock, governing important processes such as the sleep-wake cycle.

Theres evidence that the benefits of melatonin extend to treating hair loss.

This is because melatonin also affects hair growth, as the hair growth cycle in mammals is under circadian control, according to The Lifespan Research Institute, a research body that focuses on anti-ageing compounds.

"As with other circadian cycles, the hair growth cycle becomes dysregulated and lower in amplitude with age," explains the research body.

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In a randomised double-blind study of 40 women with hair loss, melatonin solution applied to the scalp increased hair growth significantly relative to placebo.

What's more, in a study published in the International journal of trichology, 1891 male and female patients with androgenic alopecia applied a topical melatonin solution for three months.

At three months 61 percent of patients had no hair loss, compared to 12.2 percent at the start; 22 percent had new hair growth at three months compared to four percent at baseline.

The incidence of seborrheic dermatitis also declined, from 34.5 percent at baseline to 9.9 percent at three months.

Seborrheic (seb-o-REE-ik) dermatitis is a common skin condition that mainly affects your scalp.

The skin condition can cause an itchy, flaky rash, which may lead to hair loss due to excessive itching.

According to the NHS, finasteride and minoxidil are the main treatments for male pattern baldness.

"Minoxidil can also be used to treat female pattern baldness. Women shouldn't use finasteride," explains the NHS.

There are a number of drawbacks to consider before taking these treatments.

According to the NHS, these treatments:

These treatments:

Alternatively, some wigs are available on the NHS, but you may have to pay unless you qualify for financial help.

While considering your options, you may benefit from some psychological support.

Your GP may be able to help you get some counselling or you can join a support group, adds the NHS.

The rest is here:
Losing hair fast? Applying this natural solution to the scalp resulted in new hair growth - Express

IRVINE, Calif.--(BUSINESS WIRE)--While studying the genetics of the androgen receptor, a team of scientists discovered a possible breakthrough treatment for COVID-19.

The team led by Andy Goren, MD from Applied Biology, Flavio A. Cadegiani, MD, MSc, PhD from Corpometria Institute in Brazil, along with other collaborators, have published their discovery in several medical journals. The manuscript, What Does Androgenetic Alopecia have to do with COVID-19? An Insight into a Potential New Therapy (doi: 10.1111/dth.13365), elucidates the possible role of androgens in controlling the infectivity of SARS-CoV-2 in human lung cells.

According to Dr. Goren, Our earlier discovery potentially links SARS-CoV-2 infectivity to androgens, the same hormones implicated in male pattern baldness and prostate cancer; thus, anti-androgens originally developed for prostate cancer may prove a breakthrough therapy for COVID-19. One of the most promising anti-androgens is proxalutamide, a next generation anti-androgen.

The study on the effects of proxalutamide on COVID-19 has received national IRB approval and will be conducted in Brasilia, Brazil, in non-hospitalized patients with mild-to-moderate COVID-19 disease. Recruitment of volunteers should start this week.

According to Dr. Cadegiani, We are excited to commence this study that could potentially benefit millions of patients and change the course of COVID-19.

More information about the study (ClinicalTrials.gov Identifier: NCT04446429) is available at clinicaltrials.gov (https://clinicaltrials.gov/ct2/show/NCT04446429?term=NCT04446429&draw=2&rank=1).

The approval was received on September 17th, 2020 from the IRB of the National Board of Ethics Committee (CONEP), from the Brazilian Ministry of Health, under the name The Proxa-AndroCoV Trial, number (CAAE) 36700320.8.0000.0023.

ABOUT APPLIED BIOLOGY

Founded in 2002, Applied Biology, Inc. (www.appliedbiology.com), headquartered in Irvine, California, is a biotechnology company specializing in hair and skin science. Applied Biology develops breakthrough drugs and medical devices for the treatment of androgen mediated dermatological conditions. Applied Biology's R&D pipeline includes a topically applied prophylactic treatment for chemotherapy induced alopecia; a novel diagnostic device that can aid dermatologists in identifying non-responders to topical minoxidil; an adjuvant therapy for non-responders to topical minoxidil; and a novel therapy for female pattern hair loss.

ABOUT CORPOMETIRA INSTITUTE

Corpometria institute was founded in 2013, and is focused on treating, researching and optimizing healthcare of the major unsolved endocrine-related conditions, including patients with obesity, sarcopenia, menopause and andropause, chronic fatigue and burnout, undertrained athletes, and rare metabolic and endocrine diseases.

Corpometria R&D pipeline includes three major clusters: amplifying genetic testing, epigenetic influences and metabolomic analyses of patients with not-fully clarified metabolic and endocrine-related illnesses; development of machine learning and AI-based algorithm for personalized metabolic responses and changes to specific eating, exercising and sleeping characteristics; and full elucidation of endocrine physiology of the sport, including specific hormonal and metabolic responses and adaptations to sports according to intensity, volume, frequency and type of physical activity, and in combination with a variety of nutritional, psychological, social, and sleeping characteristics.

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Applied Biology and Corpometria Institute Receive National IRB Approval to Study a Potential Breakthrough Therapy for COVID-19 - Business Wire

Castrating male piglets has always been quite a controversial topic for farmers and consumers alike, but more pressure is being applied these days by the latter to ban the practice.

It is common knowledge that the meat from uncastrated males can have a rather unpleasant smell or taste when it is cooked: this is known as boar taint. During a recent webinar facilitated by the group Innovative Approaches for Pork Production with Entire Males (IPEMA), a body supported by the EU to look at various methods to producing entire male pigs, a number of alternatives to the surgical castration of piglets were discussed.

Preparations for castration. Will the practice continue as it is? - Photo: Mark Pasveer

Castrated male pigs convert feed to meat less efficiently than entire males but the process of surgical castration without pain relief is painful to the animal. There is a growing consensus within Europe that this process should be discontinued favouring a different approach. In total, 3 different alternatives are available including surgical castration with pain relief, immunocastration and simply leaving the animals as entire males.

IPEMA classifies surgical castration with pain relief as an intermediate short term solution that is inefficient and adds costs. Focusing on the other 2 alternatives, IPEMA found that leaving the pigs uncastrated as entire males increased the aggressive behaviour of the animals and that they mounted their pen mates.

Also, there were issues with boar taint on the meat and other meat quality problems such as lower fat amounts, and being less tender.

During immunocastration, a vaccine is injected that inhibits steroid production by the testes. It is only when a second vaccination is administered, that there is any difference to the animals behaviour and a gradual improvement to meat quality.

There is a number of issues associated with immunocastration including stress during vaccination, and some concerns over meat quality depending on the timing of the second vaccination to the time of slaughter. The biggest challenge though, is that most markets in the European Union are reluctant to accept this as a husbandry process as they assume consumers are against it.

There was discussion as well about how breeding and genetics can be used as tools to reduce boar taint, improve the meat quality and reduce aggressive behaviour of entire male pigs. At the end of the day, whatever method is used going forward will be heavily influenced by consumer and market demands.

During the past 20 years, surgical castration of piglets has been strongly contested by animal welfare organisations. The discussions acknowledged that each of the alternatives has pros and cons but the biggest road blocks to consumer acceptance were boar taint for entire male production and consumer acceptance of immunocastration.

Dutch pig farmer Annechien ten Have-Mellema closed the webinar by recognising there is a lot of work to do on the topic of pig castration. She said: A lot of scientists are working on the alternatives for pig castration. It is a complex issue and it is very nice that there is a collaboration in this network between scientists and stakeholders in the supply chain.

She continued to say, We can see that Europe is moving to pig castration with anaesthesia, immuno vaccination, or towards entire males. We are all on a different stage but the process is irreversible. The work is not ready and has only started. Awareness and knowledge sharing is very important. The European Union also has a responsibility to facilitate this work.

Read the rest here:
Examining the alternatives to piglet castration - Pig Progress

by Nabaa Muhammad and Michael Z. Muhammad | The Final Call | @TheFinalCall

Emphatically no, Walt Boarderly, an entrepreneur and Philadelphia business owner, replied when asked if he would take the Covid-19 vaccine. Mr. Boaderly isnt anti-vaccine, saying he will take the flu shot. There is just too much uncertainty when it comes to this new vaccine, he said.

Blacks do not trust President Trumps Covid-19 vaccine push, and there is plenty of reason to be distrustful. Black people have been the victims of medical experiment, exploitation and abuses by their White enslavers and White doctors from the time the good ship Jesus hit Americas shores. These medical researchers have been like a pack of crazed dogs chasing their helpless prey.

In her comprehensive book Medical Apartheid, Harriett Washington details abuses committed against Blacks and how throughout the 19th century medical schools used Blacks in live surgical demonstrations.

In more recent times, she wrote, Blacks have been disproportionately enrolled in risky, nonbeneficial research in gynecology, oncology, surgery, pediatrics, infectious diseases, and genetics.

Medical Apartheid tells the story of slaves and Black freedmen used in hospitals for experiments without their knowledge or consent. Blacks have historically been victims of grave-robbing, unauthorized autopsies and dissections, Frankenstein-like behavior by White medical researchers.

The American Medical Womens Association sponsored a Sept. 19 Zoom conversation on Medical Apartheid as part of its Racism in Medicine Monthly Discussion.

Primary participants in the discussion were medical students and pre-med students.

The session opened with some basic questions, like whether doctors during slavery focused on the health of enslaved persons. Surprisingly many participants believed those doctors were concerned about slaves healththey werent. The doctors had a pact to inspect slaves to make sure they were fit for work, to determine their value given their ability to work and performed examinations for insurance companies before policies on slaves were issued to slave owners.

Dr. P. Oneeka Williams, a urologist based in Brighton, Mass., was one of two main presenters. She saluted Ms. Washington for her work and talked about the pervasive practice of using enslaved people for experiments.

She focused on Dr. James Marion Sims as the father of gynecology, lionized for his treatments for women. But, said Dr. Williams, These advances along with so many other physicians, really came on the backs of the violations and the atrocities and the disgusting treatment of Black bodies.

Born in 1813 in South Carolina, Dr. Simms underwent one and a half years of medical training, which he considered inadequate and started practicing on Alabama plantations. He experimented on enslaved Black children stricken by tetanus and enslaved Black women. In 1845, he used forceps, despite limited experience, to deliver a child from a slave girl. The baby died and the mother developed a vesicorectal fistula, a devastating condition involving the bladder and the rectum. It was a condition that women, Black and White, often suffered from. He acquired 11 slave women with the condition, housed them and started experimenting with surgical repair. The woman had no consent, no anesthesia and were put on display. The surgeries were painful, frequently broke down and required multiple surgeries with physicians coming to observe his procedures, said Dr. Williams, a Black woman. The enslaved womens piercing screams could be heard, she said.

Dr. Simms developed a procedure to treat the condition, practicing for three years on enslaved Black women. He started publishing articles about his dubious success in 1852 and began operating on White women. As abolitionists objected to using Blacks for medical experimentation, he started to hide the race of his test subjects. He later became president of the American Medical Association and opened the first hospital for women in New York City in 1875. His name is enshrined on buildings, hospitals and statues were erected in his honor.

In 2018, protests led to the removal of his statue in New Yorks Central Park. Officials relocated it to his gravesite in Brooklyn.

Biases and racism would not impact on the medical profession any differently than it impacts on any other categories in life, said Dr. Williams.

Race-based beliefs became seen as real science and are still perpetuated, she added.

Dr. Williams believes educating and raising awareness of medical students and professionals alongside elementary, high school and college students are important to help resolve the problem. She has seen instances today in which physicians have not valued Black lives, though it may not be conscious.

Medical Apartheid chronicles how in the 17th and 18th century enslaved Blacks were used for vaccine trials, smallpox in particular, without their consent and once the vaccines were effective, the cures were released into the general population, said Dr. Williams.

We have to look at history so that when people try to diminish the concerns of Black people about being potentially the unwitting participants of some type of trial that is about using us as guinea pigs that its not a kind of hearsay. Its not oh I think, Im guessing, she continued.

Here its factual information that supports why the skepticism exists and why there has to be a clear set of strategies about how do you really help Blacks to feel confident and reassured that they are not going to be used in a kind of experimentation process that has been done even in our contemporary times. This is not centuries ago, this is within recent history, 10, 20, 30 years, were still seeing situations where Blacks have been used as part of unconsenting experimental protocols to their detriment.

Even the infamous Tuskegee Experiment has aspects that are not generally talked about. In Medical Apartheid, the author reveals how the syphilis study, started in 1932, was based on the belief that racial differences and irresponsible Black behavior accounted for syphilis infections among poor Blacks. Most cases were actually due to disease transmission from mothers to children.

There was a profit motive in the study as the federal government hoped to come out with a lucrative vaccine and wanted to follow the 600 male patients until they died.

When the federal governments wickedness was uncovered, some documents were hidden from a panel that was supposed to look into the genocidal activity and the victims were eventually paid a pittance. In 1943, penicillin, a treatment for syphilis, was discovered but never given to study victims. In addition to the deaths of the men, at least 40 wives and almost 20 children were infected.

In 1965, the study was discovered and a leftist, social activist group tried to stop it, but was ignored. By 1969, 100 men had died from direct and indirect complications from syphilis. Peter Buxton, a Polish immigrant, working within the study called for ending it. In 1972, he shared the nefarious experiment with a friend, who was an AP reporter. Ted Kennedy held hearings, an investigation was opened, but a historian was never involved and a panel was formed to look into the study. The panel was given less than one year to do its work, some documents were deliberately hidden, the panel chair forced a softening of the language of the initial report and submitted it with a cover letter abstaining from agreement with the report.

Tapes of interviews with every victim were kept but destroyed, and in 1995 a doctor determined the studys chief purpose was to create a reliable vaccine and the results of the study were used to create advanced tests for syphilis and vaccines that were marketed globally.

The original U.S. contract with the Alabama Dept. of Health stipulated that the U.S. government owns any invention arising from the Tuskegee Syphilis Study, and so, the U.S. government profited tremendously off the backs of these men and their families and continued to do so, said the moderator for the online session. The CDC also soft pedals the Tuskegee Syphilis Study, though President Clinton apologized for it, she added.

If you look at themes throughout the book, this is all economically driven, commented Dr. Williams. The very agencies that are supposed to be committed to protect the population, to protect the people, the American government, when you look at what was really the motivation for this study.

Even today we are seeing what we are seeing with covid and misinformation, deception, parties that are changing the narrative, changing information, changing things that impact our peoples lives, she said. Things like not testing asymptomatic people have far-reaching effects into the health of the nation, Dr. Williams observed.

Youre exposing people to a potential deadly pathogen, she continued. But who are the people who are disproportionately suffering from that virus? All of these threads when you look at how interwoven the government agencies have been in the deception, in the abuse of Black and Brown bodies, its really very, very disconcerting, said Dr. Williams.

Black only medicine?

Dr. Vanessa Al Rashida, who practices medicine in New Mexico, presented information about the continued use of race as a basis for research based on a chapter in Medical Apartheid.

The public health field has contributed to misinformation going back to slavery, said Dr. Al Rashida. Early U.S. Census studies found free Blacks suffered more from alcoholism and died because of recklessness, she said. The theory was Whites needed to shepherd Black people, the physician added.

In 2005, a drug that the Food and Drug Administration initially denied for wide use was approved for use only in Black Americans with heart failure, she said. The drug was Bidil.

In the 1980s, surveys had found heart failure was twice as common in older Blacks than Caucasians, which is not the case today, she said.

But Blacks dying more often led the company NitroMed to postulate a genetic cause of the disease disparity. FDA approved research for the drug. Clyde Yancey, a Black cardiologist, and others objected to the premise of race-based differences as opposed to differences based on environment and lifestyle. The NitroMed approach ignored these things but a Black cardiologists group approved the study.

Most diseases Blacks suffer are driven by environment, not any inherent difference based on genetics and race, said Dr. Al Rashida.

The African American Heart Failure Trials in 2003 was composed of Blacks only, one group with approved heart medications put against another group of Black Americans using heart medications and Bidil, she explained.

She questioned the methodology of the study, which showed some Bidil benefit in curbing deaths, and FDA approved the drug which is still used today.

The study made me sick for a while, said Dr. Al Rashida.

A non-genetic disease of heart failure, which other studies have shown is often due to high blood pressure caused by environmental factors in Black Americans, is being treated with genetic treatments, she said. That concerns her. Research has shown little genetic difference between people based on race, said Dr. Al Rashida, who read Medical Apartheid in medical school. It was given to her as a gift from a family friend.

The Nitro-Med study would have had more weight if it compared Black Americans to Caucasians, she said. But, it only compared Black Americans and the reason for that was money, she said.

It was not economically feasible for the company to add in Caucasians with African Americans to be compared in the study, said Dr. Al Rashida.

Its also kind of scary to me that future studies are being based on this whole precipice that race is playing a part in diseases that we are seeing in the country. Whereas thats not the case at all. Its environment and its also lifestyle behaviors too that have been rooted back into slavery.

That includes how Black people eat, added Dr. Al Rashida.

I try to be very optimistic and I want to see better for our country, but at the same time, its very scaryespecially with the current leadership that we have in certain institutions. Its going to be a very difficult hill to climb essentially, she said.

If research determines that illness or disorders are based on racial differences, not environment, it is easier to dismiss the need to make changes in society and argue the conditions or illnesses are inevitable.

Prisons, hospitals and the devils playground for reckless research

There are other concerns about vaccines and negative impacts on Blacks. Since 2014, controversy has brewed over a Centers for Disease researcher who charged the agency with hiding research results linking an experimental measles vaccines with increased Black male children developing autism. Dr. William Thompson, who made the charges, has called for an opportunity to testify before Congress. Though CDC denies his charge, there has been no congressional hearing.

Ms. Washington has written about a 1970 Johns Hopkins Free Child Care program for more than 7,000 young boys, 95 percent from underprivileged Negro familieswho used as guinea pigs in a three-year experiment that could have branded them as latent criminals for life. Funded by the National Institutes of Health, the project extracted blood samples, ostensibly to test for anemia and other medical problems. She wrote that testing was done without parental knowledge or consent.

In a piece published in the Baltimore Sun, Ms. Washington wrote, In 1962, Dr. Chester M. Southam of the Sloan-Kettering Institute injected at least 396 inmates at Ohio State Prisonalmost half of them blackwith live humancancercells.

According to Allan Hornblum, author of Acres of Skin: Human Experiments at Holmesburg Prison, Holmesburg Prison became one of Americas largest, nontherapeutic, human research factories. The Pennsylvania prison was about 85 percent Black, and there were very few high school graduates, he wrote.

Dr. Albert Kligman, Ph.D. and M.D., University of Pennsylvania, began dermatology research before 1951 when he visited the prison, said the book author.

Dr. Klingman envisioned using the skin of inmates his dermatology drug trials, trials for anti-obesity drugs, viral infections, and bacterial infections, wrote Mr. Hornblum.

All kinds of tests, foot powder, eye drops, face creams, underarm deodorant, toothpaste, liquid diets, were used, leaving inmates scarred and often suffering. Dr. Klingman reportedly declared, All I saw before me were acres of skin It was like a farmer seeing a fertile field for the first time, according to the book.

In 1979, the Philadelphia Inquirer disclosed that Holmesburg inmates had been used as guinea pigs to test whether mind-altering drugs were useful as Army weapons. In 1981 the paper reported that inmates had been dosed with dioxin to test the herbicides effects on humans.

In American Mengele: Human Radiation Experiments, Ryan Grimm detailed what he called experiments more horrible than Tuskegee. He wrote about experiments conducted by Dr. Eugene L. Saenger at Cincinnati General Hospital from 1960 to 1972. The Department of Defense paid him, and several government agencies used his findings.

What makes radiation experiments like Saengers more horrible than those at Tuskegee is that, in these cases, doctors were not merely watching an already existing disease take its course. Instead, Saenger deliberately injected hundreds of people with potentially lethal doses of radiation, knowing that most of them would die rather quickly, wrote Mr. Grimm.

At least 89 people are acknowledged to have died due to Saengers treatment, although the number is likely well above 200. Dr. Saenger even copped to the crime and openly defended his actions as necessary preparation for nuclear war.He was never charged with a crime.

His average patient had five years of formal education, an average I.Q. of 89 and 62 percent were Black.

A study conducted in part by researchers from the Maryland Center for Health Equity at the University of Maryland-College Park, found many Blacks dont get flu shots because they dont trust the vaccine.

Blackdoctors.org reported 58 percent of respondents to their survey would not take a Covid-19 vaccination as soon as it is available. Fifty-eight percent said no to the vaccine, 22 percent reported they would take the vaccine but had concerns. Eighty percent respondents either said no or had concerns about taking a Covid-19 vaccine, citing mistrust of the health care system.

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We Can't Trust You: Experimentation, Exploitation and the Hidden History of American Medical Abuses - Final Call News - FinalCall.com News

Researchers say your biological sex affects gene expression in nearly every type of tissue influencing body fat, cancer and birth weight.

Gene expression is the amount of product created by a gene for cell function, the international team of researchers explained.

They said their findings could prove important for personalised medicine, creating new drugs and predicting patient outcomes.

"These discoveries suggest the importance of considering sex as a biological variable in human genetics and genomics studies," said project leader Barbara Stranger, an associate professor of pharmacology at Northwestern University Feinberg School of Medicine in Chicago.

Unreported links

The researchers analysed 44 types of healthy human tissue from 838 people to find out if there were differences between women and men in the average amount of gene expression.

They discovered that 37% of all human genes were expressed at different levels in women and men in at least one type of tissue.

They also identified 369 instances where a genetic variant present in males and females affected gene expression to a different degree in each sex. This led to the discovery of 58 previously unreported links between genes and blood pressure, cholesterol levels, breast cancer and body fat percentage.

Gender differences in gene expression were also found for genes involved in how the body responds to medications, how women control blood sugar levels in pregnancy, how the immune system functions and how cancer develops.

Critical component of personalised medicine

"If specific genes or genetic variants contribute differentially to a given trait in males and females, it could suggest sex-specific biomarkers, therapeutics and drug dosing," Stranger said in a Northwestern news release.

"In the future, such knowledge may form a critical component of personalised medicine or may reveal disease biology that remains obscured when considering males and females as a single group," she said.

The study was published in the journal Science.

Image credit: iStock

Excerpt from:
Your sex affects your genes for body fat, cancer and birth weight - Health24

KENILWORTH, N.J.--(BUSINESS WIRE)--AstraZeneca and Merck (NYSE: MRK), known as MSD outside the United States and Canada, today announced final results from the Phase 3 PROfound trial which showed LYNPARZA demonstrated a statistically significant and clinically meaningful improvement in overall survival (OS) versus enzalutamide or abiraterone in men with metastatic castration-resistant prostate cancer (mCRPC) who have BRCA1/2 or ATM gene mutations. Patients had progressed on prior treatment with enzalutamide and/or abiraterone.

Prostate cancer is the second most common type of cancer in men, with an estimated 1.3 million new patients diagnosed worldwide in 2018. Approximately 20-30% of men with mCRPC have an homologous recombination repair (HRR) gene mutation, of which BRCA1/2 and ATM mutations are a subpopulation. Approximately 10-20% of early stage hormone-sensitive prostate cancer cases will develop into CRPC within approximately five years.

In the key secondary endpoint of OS in men with BRCA1/2 or ATM gene mutations, LYNPARZA reduced the risk of death by 31% vs. retreatment with enzalutamide or abiraterone (HR 0.69 [95% CI, 0.50, 0.97], p=0.0175). Median OS was 19.1 months for LYNPARZA vs. 14.7 months for enzalutamide or abiraterone, despite 66% of men on these treatments having crossed over to receive treatment with LYNPARZA following disease progression.

An exploratory analysis also showed a non-statistically significant improvement in OS in the overall trial population of men with HRR gene mutations (BRCA1/2, ATM, CDK12 and 11 other HRR-mutated [HRRm] genes), reducing the risk of death by 21% with LYNPARZA vs. enzalutamide or abiraterone (HR 0.79 [95% CI, 0.61, 1.03]. Median OS was 17.3 months vs. 14 months for enzalutamide or abiraterone.

The most common adverse reactions (ARs) 15% were anemia (50%), nausea (43%), fatigue/asthenia (42%), decreased appetite (31%), diarrhea (21%), vomiting (20%) and constipation (19%). Grade 3 or above ARs were anemia (23%), nausea (2%), fatigue or asthenia (3%), decreased appetite (2%) and diarrhea (1%). Twenty percent of patients on LYNPARZA discontinued treatment due to ARs and 23% had their dose reduced due to an AR.

Dr. Johann de Bono, one of the principal investigators of the PROfound trial and head of drug development at the Institute for Cancer Research and the Royal Marsden Hospital, said, LYNPARZA has demonstrated significant clinical benefit across key endpoints in PROfound and the final overall survival results for men with BRCA1/2 or ATM mutations reinforce its potential to change the standard of care for men with metastatic castration-resistant prostate cancer. The PROfound trial shows that LYNPARZA can play an important role in this new era of precision medicine in prostate cancer, bringing targeted therapy at a molecular level to patients with a historically poor prognosis and few treatment options.

Dr. Jos Baselga, executive vice president, Oncology R&D, AstraZeneca said, These results help to transform the treatment landscape in certain men with metastatic castration-resistant prostate cancer, where overall survival has been very difficult to achieve. LYNPARZA is the only PARP inhibitor to demonstrate overall survival versus enzalutamide or abiraterone for men with BRCA or ATM mutations. We look forward to continuing to bring LYNPARZA to these patients around the world.

Dr. Roy Baynes, senior vice president and head of global clinical development, chief medical officer, Merck Research Laboratories, said, The PROfound trial is the first positive Phase 3 trial using molecular biomarker testing to help identify treatment options for certain men with metastatic castration resistant prostate cancer. These results further underpin the importance of genomic testing for HRR gene mutations to help identify this at-risk patient population and help physicians make treatment decisions. These results demonstrate the potential of LYNPARZA for mCRPC patients with certain HRR mutations.

Final OS results from the PROfound trial were presented on Sunday, Sept. 20, 2020, during the Presidential Symposium at the European Society for Medical Oncology (ESMO) Virtual Congress 2020 and published simultaneously in The New England Journal of Medicine.

Summary of OS results

OS data cut-off date was March 20, 2020.

Men with BRCA1/2 and ATM mutations (Cohort A)Secondary Endpoint

Overall populationof men with HRR mutations(Cohorts A+B)Exploratory Endpoint

LYNPARZA n=162

Control

n=83

LYNPARZA n=256

Control

n=131

Median, months

19.1

14.7

17.3

14.0

Hazard ratio (95% CI)

0.69 (0.50, 0.97)

0.79 (0.61, 1.03)

P-value

0.0175

N/A

The Phase 3 PROfound trial had met its primary endpoint in August 2019, showing significantly improved radiographic progression-free survival (rPFS) in men with mutations in BRCA1/2 or ATM genes, and had met a key secondary endpoint of rPFS in the overall HRRm population, which formed the basis of the U.S. Food and Drug Administration approval in May 2020. Regulatory reviews are ongoing in the EU and other regions.

AstraZeneca and Merck are exploring additional trials in metastatic prostate cancer including the ongoing Phase 3 PROpel trial, with first data expected in 2021, evaluating LYNPARZA as a first-line medicine for patients with mCRPC in combination with abiraterone acetate versus abiraterone acetate alone.

About PROfound

PROfound is a prospective, multi-center, randomized, open-label, Phase 3 trial evaluating the efficacy and safety of LYNPARZA versus enzalutamide or abiraterone in patients with mCRPC who have progressed on prior treatment with abiraterone or enzalutamide and have a qualifying HRR tumor mutation (BRCA1/2, ATM, CDK12, BARD1, BRIP2, CHEK1, CHEK2, PALB2, PPP2R2A, RAD51B, RAD51D, RAD54L).

The trial was designed to analyze patients with HRRm genes in two cohorts: the primary endpoint was rPFS in those with mutations in BRCA1/2 or ATM genes and then, if LYNPARZA showed clinical benefit, a formal analysis was performed of the overall trial population of patients with HRRm genes (BRCA1/2, ATM, CDK12 and 11 other HRR mutated genes; a key secondary endpoint).

In the U.S., patients are selected for treatment with LYNPARZA based on the following FDA-approved companion diagnostics:

IMPORTANT SAFETY INFORMATION

CONTRAINDICATIONS

There are no contraindications for LYNPARZA.

WARNINGS AND PRECAUTIONS

Myelodysplastic Syndrome/Acute Myeloid Leukemia (MDS/AML): Occurred in <1.5% of patients exposed to LYNPARZA monotherapy, and the majority of events had a fatal outcome. The duration of therapy in patients who developed secondary MDS/AML varied from <6 months to >2 years. All of these patients had previous chemotherapy with platinum agents and/or other DNA-damaging agents, including radiotherapy, and some also had a history of more than one primary malignancy or of bone marrow dysplasia.

Do not start LYNPARZA until patients have recovered from hematological toxicity caused by previous chemotherapy (Grade 1). Monitor complete blood count for cytopenia at baseline and monthly thereafter for clinically significant changes during treatment. For prolonged hematological toxicities, interrupt LYNPARZA and monitor blood count weekly until recovery.

If the levels have not recovered to Grade 1 or less after 4 weeks, refer the patient to a hematologist for further investigations, including bone marrow analysis and blood sample for cytogenetics. Discontinue LYNPARZA if MDS/AML is confirmed.

Pneumonitis: Occurred in <1% of patients exposed to LYNPARZA, and some cases were fatal. If patients present with new or worsening respiratory symptoms such as dyspnea, cough, and fever, or a radiological abnormality occurs, interrupt LYNPARZA treatment and initiate prompt investigation. Discontinue LYNPARZA if pneumonitis is confirmed and treat patient appropriately.

Embryo-Fetal Toxicity: Based on its mechanism of action and findings in animals, LYNPARZA can cause fetal harm. A pregnancy test is recommended for females of reproductive potential prior to initiating treatment.

Females

Advise females of reproductive potential of the potential risk to a fetus and to use effective contraception during treatment and for 6 months following the last dose.

Males

Advise male patients with female partners of reproductive potential or who are pregnant to use effective contraception during treatment and for 3 months following the last dose of LYNPARZA and to not donate sperm during this time.

Venous Thromboembolic Events: Including pulmonary embolism, occurred in 7% of patients with metastatic castration-resistant prostate cancer who received LYNPARZA plus androgen deprivation therapy (ADT) compared to 3.1% of patients receiving enzalutamide or abiraterone plus ADT in the PROfound study. Patients receiving LYNPARZA and ADT had a 6% incidence of pulmonary embolism compared to 0.8% of patients treated with ADT plus either enzalutamide or abiraterone. Monitor patients for signs and symptoms of venous thrombosis and pulmonary embolism, and treat as medically appropriate, which may include long-term anticoagulation as clinically indicated.

ADVERSE REACTIONSFirst-Line Maintenance BRCAm Advanced Ovarian Cancer

Most common adverse reactions (Grades 1-4) in 10% of patients in clinical trials of LYNPARZA in the first-line maintenance setting for SOLO-1 were: nausea (77%), fatigue (67%), abdominal pain (45%), vomiting (40%), anemia (38%), diarrhea (37%), constipation (28%), upper respiratory tract infection/influenza/ nasopharyngitis/bronchitis (28%), dysgeusia (26%), decreased appetite (20%), dizziness (20%), neutropenia (17%), dyspepsia (17%), dyspnea (15%), leukopenia (13%), UTI (13%), thrombocytopenia (11%), and stomatitis (11%).

Most common laboratory abnormalities (Grades 1-4) in 25% of patients in clinical trials of LYNPARZA in the first-line maintenance setting for SOLO-1 were: decrease in hemoglobin (87%), increase in mean corpuscular volume (87%), decrease in leukocytes (70%), decrease in lymphocytes (67%), decrease in absolute neutrophil count (51%), decrease in platelets (35%), and increase in serum creatinine (34%).

ADVERSE REACTIONSFirst-Line Maintenance Advanced Ovarian Cancer in Combination with Bevacizumab

Most common adverse reactions (Grades 1-4) in 10% of patients treated with LYNPARZA/bevacizumab compared to a 5% frequency for placebo/bevacizumab in the first-line maintenance setting for PAOLA-1 were: nausea (53%), fatigue (including asthenia) (53%), anemia (41%), lymphopenia (24%), vomiting (22%) and leukopenia (18%). In addition, the most common adverse reactions (10%) for patients receiving LYNPARZA/bevacizumab irrespective of the frequency compared with the placebo/bevacizumab arm were: diarrhea (18%), neutropenia (18%), urinary tract infection (15%), and headache (14%).

In addition, venous thromboembolic events occurred more commonly in patients receiving LYNPARZA/bevacizumab (5%) than in those receiving placebo/bevacizumab (1.9%).

Most common laboratory abnormalities (Grades 1-4) in 25% of patients for LYNPARZA in combination with bevacizumab in the first-line maintenance setting for PAOLA-1 were: decrease in hemoglobin (79%), decrease in lymphocytes (63%), increase in serum creatinine (61%), decrease in leukocytes (59%), decrease in absolute neutrophil count (35%), and decrease in platelets (35%).

ADVERSE REACTIONSMaintenance Recurrent Ovarian Cancer

Most common adverse reactions (Grades 1-4) in 20% of patients in clinical trials of LYNPARZA in the maintenance setting for SOLO-2 were: nausea (76%), fatigue (including asthenia) (66%), anemia (44%), vomiting (37%), nasopharyngitis/upper respiratory tract infection (URI)/influenza (36%), diarrhea (33%), arthralgia/myalgia (30%), dysgeusia (27%), headache (26%), decreased appetite (22%), and stomatitis (20%).

Study 19: nausea (71%), fatigue (including asthenia) (63%), vomiting (35%), diarrhea (28%), anemia (23%), respiratory tract infection (22%), constipation (22%), headache (21%), decreased appetite (21%), and dyspepsia (20%).

Most common laboratory abnormalities (Grades 1-4) in 25% of patients in clinical trials of LYNPARZA in the maintenance setting (SOLO-2/Study 19) were: increase in mean corpuscular volume (89%/82%), decrease in hemoglobin (83%/82%), decrease in leukocytes (69%/58%), decrease in lymphocytes (67%/52%), decrease in absolute neutrophil count (51%/47%), increase in serum creatinine (44%/45%), and decrease in platelets (42%/36%).

ADVERSE REACTIONSAdvanced gBRCAm Ovarian Cancer

Most common adverse reactions (Grades 1-4) in 20% of patients in clinical trials of LYNPARZA for advanced gBRCAm ovarian cancer after 3 or more lines of chemotherapy (pooled from 6 studies) were: fatigue/asthenia (66%), nausea (64%), vomiting (43%), anemia (34%), diarrhea (31%), nasopharyngitis/upper respiratory tract infection (URI) (26%), dyspepsia (25%), myalgia (22%), decreased appetite (22%), and arthralgia/musculoskeletal pain (21%).

Most common laboratory abnormalities (Grades 1-4) in 25% of patients in clinical trials of LYNPARZA for advanced gBRCAm ovarian cancer (pooled from 6 studies) were: decrease in hemoglobin (90%), mean corpuscular volume elevation (57%), decrease in lymphocytes (56%), increase in serum creatinine (30%), decrease in platelets (30%), and decrease in absolute neutrophil count (25%).

ADVERSE REACTIONSgBRCAm, HER2-negative Metastatic Breast Cancer

Most common adverse reactions (Grades 1-4) in 20% of patients in OlympiAD were: nausea (58%), anemia (40%), fatigue (including asthenia) (37%), vomiting (30%), neutropenia (27%), respiratory tract infection (27%), leukopenia (25%), diarrhea (21%), and headache (20%).

Most common laboratory abnormalities (Grades 1-4) in >25% of patients in OlympiAD were: decrease in hemoglobin (82%), decrease in lymphocytes (73%), decrease in leukocytes (71%), increase in mean corpuscular volume (71%), decrease in absolute neutrophil count (46%), and decrease in platelets (33%).

ADVERSE REACTIONSFirst-Line Maintenance gBRCAm Metastatic Pancreatic Adenocarcinoma

Most common adverse reactions (Grades 1-4) in 10% of patients in clinical trials of LYNPARZA in the first-line maintenance setting for POLO were: fatigue (60%), nausea (45%), abdominal pain (34%), diarrhea (29%), anemia (27%), decreased appetite (25%), constipation (23%), vomiting (20%), back pain (19%), arthralgia (15%), rash (15%), thrombocytopenia (14%), dyspnea (13%), neutropenia (12%), nasopharyngitis (12%), dysgeusia (11%), and stomatitis (10%).

Most common laboratory abnormalities (Grades 1-4) in 25% of patients in clinical trials of LYNPARZA in the first-line maintenance setting for POLO were: increase in serum creatinine (99%), decrease in hemoglobin (86%), increase in mean corpuscular volume (71%), decrease in lymphocytes (61%), decrease in platelets (56%), decrease in leukocytes (50%), and decrease in absolute neutrophil count (25%).

ADVERSE REACTIONSHRR Gene-mutated Metastatic Castration Resistant Prostate Cancer

Most common adverse reactions (Grades 1-4) in 10% of patients in clinical trials of LYNPARZA for PROfound were: anemia (46%), fatigue (including asthenia) (41%), nausea (41%), decreased appetite (30%), diarrhea (21%), vomiting (18%), thrombocytopenia (12%), cough (11%), and dyspnea (10%).

Most common laboratory abnormalities (Grades 1-4) in 25% of patients in clinical trials of LYNPARZA for PROfound were: decrease in hemoglobin (98%), decrease in lymphocytes (62%), decrease in leukocytes (53%), and decrease in absolute neutrophil count (34%).

DRUG INTERACTIONS

Anticancer Agents: Clinical studies of LYNPARZA with other myelosuppressive anticancer agents, including DNA-damaging agents, indicate a potentiation and prolongation of myelosuppressive toxicity.

CYP3A Inhibitors: Avoid coadministration of strong or moderate CYP3A inhibitors when using LYNPARZA. If a strong or moderate CYP3A inhibitor must be coadministered, reduce the dose of LYNPARZA. Advise patients to avoid grapefruit, grapefruit juice, Seville oranges, and Seville orange juice during LYNPARZA treatment.

CYP3A Inducers: Avoid coadministration of strong or moderate CYP3A inducers when using LYNPARZA.

USE IN SPECIFIC POPULATIONS

Lactation: No data are available regarding the presence of olaparib in human milk, its effects on the breastfed infant or on milk production. Because of the potential for serious adverse reactions in the breastfed infant, advise a lactating woman not to breastfeed during treatment with LYNPARZA and for 1 month after receiving the final dose.

Pediatric Use: The safety and efficacy of LYNPARZA have not been established in pediatric patients.

Hepatic Impairment: No adjustment to the starting dose is required in patients with mild or moderate hepatic impairment (Child-Pugh classification A and B). There are no data in patients with severe hepatic impairment (Child-Pugh classification C).

Renal Impairment: No dosage modification is recommended in patients with mild renal impairment (CLcr 51-80 mL/min estimated by Cockcroft-Gault). In patients with moderate renal impairment (CLcr 31-50 mL/min), reduce the dose of LYNPARZA to 200 mg twice daily. There are no data in patients with severe renal impairment or end-stage renal disease (CLcr 30 mL/min).

INDICATIONS

LYNPARZA is a poly (ADP-ribose) polymerase (PARP) inhibitor indicated:

First-Line Maintenance BRCAm Advanced Ovarian Cancer

For the maintenance treatment of adult patients with deleterious or suspected deleterious germline or somatic BRCA-mutated (gBRCAm or sBRCAm) advanced epithelial ovarian, fallopian tube or primary peritoneal cancer who are in complete or partial response to first-line platinum-based chemotherapy. Select patients for therapy based on an FDA-approved companion diagnostic for LYNPARZA.

First-Line Maintenance HRD Positive Advanced Ovarian Cancer in Combination with Bevacizumab

In combination with bevacizumab for the maintenance treatment of adult patients with advanced epithelial ovarian, fallopian tube or primary peritoneal cancer who are in complete or partial response to first-line platinum-based chemotherapy and whose cancer is associated with homologous recombination deficiency (HRD) positive status defined by either:

Select patients for therapy based on an FDA-approved companion diagnostic for LYNPARZA.

Maintenance Recurrent Ovarian Cancer

For the maintenance treatment of adult patients with recurrent epithelial ovarian, fallopian tube or primary peritoneal cancer, who are in complete or partial response to platinum-based chemotherapy.

Advanced gBRCAm Ovarian Cancer

For the treatment of adult patients with deleterious or suspected deleterious germline BRCA-mutated (gBRCAm) advanced ovarian cancer who have been treated with 3 or more prior lines of chemotherapy. Select patients for therapy based on an FDA-approved companion diagnostic for LYNPARZA.

gBRCAm HER2-negative Metastatic Breast Cancer

Original post:
LYNPARZA Reduced Risk of Death by 31% vs. Enzalutamide or Abiraterone for Men with BRCA1/2 or ATM-Mutated Metastatic Castration Resistant Prostate...

Male Breast Cancer Treatment Market forecast to 2026

The Global Male Breast Cancer Treatment Market report provides information about the Global industry, including valuable facts and figures. This research study explores the Global Market in detail such as industry chain structures, raw material suppliers, with manufacturing The Male Breast Cancer Treatment Sales market examines the primary segments of the scale of the market. This intelligent study provides historical data from 2015 alongside a forecast from 2020 to 2026.

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Male Breast Cancer Treatment Market size, development, key opportunity, application and forecast to 2026 | Pfizer, Roche, GlaxoSmithKline, Sanofi,...

Its been quite a tough year for our wildlife population.

At least 30,000 koalas across the country lost their lives in last summers devastating bushfires - and in New South Wales alone, up to 71 per cent of the population was wiped out.

Watch the full story above

Now, legislation aimed to protect the species has received backlash from some landowners.

But amongst the bad news, the country has banded together for our furry friends.

State and Federal governments have pledged millions of dollars to the cause, and people all over the country have knitted mittens to aid those affected by the fires.

But theres still a long way to go to save our koalas.

Its not good, to put it very bluntly, said Chad Staples, a zookeeper from Mogo and Featherdale Wildlife Parks.

The fires were devastating for so many species but a tree-dwelling species is going to be affected far worse.

They were already under intense pressure prior to the fires, so its not good.

A tree-dwelling species is going to be affected far worse.

Australian forests need fire to regenerate, and its very natural - but that was a big-scale, high-intensity fire, and that wiped out a lot.

If koala populations were already in big numbers, you would have that flow come back in as the forest comes back.

But because wed already isolated so many of those pockets, for them to breed back to those numbers will take decades.

As part of the rehabilitation process, its important that we keep as much of their habitat as possible.

They will come back if we can allow them to, Staples said.

With the help of zoos, we can always breed koalas to go back - but if theres nowhere for them to go back to, its pretty dire.

Koala corridors are also important so one group of koalas will not get cut off from others.

Koalas need to be able to breed with different groups within their species - and without corridors, they also cant get to new food sources or escape fires.

If you have a pocket of good habitat, that is great for that area, but you need genetic drift, Staples said.

If you have any sort of island population, theres nothing coming in or going out, so youre essentially bottlenecking - and its a very short-term solution.

The corridor allows for males to move between changing genetics and strengthening the whole genome of the population.

In some more uplifting news, Archer, a koala at Featherdale Wildlife Park, has become a dad for the first time.

And the names of Archers two baby joeys have been chosen with a little help from royalty.

The female joey is being named after Princess Eugenie, and the male is being named Jack, after her husband, Staples said.

Theyve been massive supporters and theyre dying to come back out when everyone can travel again.

Go here to read the rest:
Australia's 2020 bushfires wiped out 71 per cent of NSW's koala population - and restoring the numbers will take 'decades' - 7NEWS.com.au

BOTHELL, Wash. & KENILWORTH, N.J.--(BUSINESS WIRE)--Seattle Genetics, Inc. (Nasdaq: SGEN) and Merck (NYSE: MRK), known as MSD outside the United States and Canada, today announced two new strategic oncology collaborations.

The companies will globally develop and commercialize Seattle Genetics ladiratuzumab vedotin, an investigational antibody-drug conjugate (ADC) targeting LIV-1, which is currently in phase 2 clinical trials for breast cancer and other solid tumors. The collaboration will pursue a broad joint development program evaluating ladiratuzumab vedotin as monotherapy and in combination with Mercks anti-PD-1 therapy KEYTRUDA (pembrolizumab) in triple-negative breast cancer, hormone receptor-positive breast cancer and other LIV-1-expressing solid tumors. Under the terms of the agreement, Seattle Genetics will receive a $600 million upfront payment and Merck will make a $1.0 billion equity investment in 5.0 million shares of Seattle Genetics common stock at a price of $200 per share. In addition, Seattle Genetics is eligible for progress-dependent milestone payments of up to $2.6 billion.

Separately, Seattle Genetics has granted Merck an exclusive license to commercialize TUKYSA (tucatinib), a small molecule tyrosine kinase inhibitor, for the treatment of HER2-positive cancers, in Asia, the Middle East and Latin America and other regions outside of the U.S., Canada and Europe. Seattle Genetics will receive $125 million from Merck as an upfront payment and is eligible for progress-dependent milestones of up to $65 million.

Collaborating with Merck on ladiratuzumab vedotin will allow us to accelerate and broaden its development program in breast cancer and other solid tumors, including in combination with Mercks KEYTRUDA, while also positioning us to leverage our U.S. and European commercial operations, said Clay Siegall, Ph.D., President and Chief Executive Officer of Seattle Genetics. The strategic collaboration for TUKYSA will help us reach more patients globally and benefit from the established commercial strength of one of the worlds premier pharmaceutical companies.

These two strategic collaborations will enable us to further diversify Mercks broad oncology portfolio and pipeline, and to continue our efforts to extend and improve the lives of as many patients with cancer as possible, said Dr. Roger M. Perlmutter, President, Merck Research Laboratories. We look forward to working with the team at Seattle Genetics to advance the clinical program for ladiratuzumab vedotin, which has shown compelling signals of efficacy in early studies, and to bring TUKYSA to even more patients with cancer around the world.

Ladiratuzumab Vedotin Collaboration Details

Under the terms of the agreement, Seattle Genetics and Merck will collaborate and equally share costs on the global development of ladiratuzumab vedotin and other LIV-1-targeting ADCs. The companies have agreed to jointly develop and share future costs and profits for ladiratuzumab vedotin on a 50:50 basis worldwide. Merck will pay Seattle Genetics $600 million upfront and make a $1.0 billion equity investment in 5.0 million shares of Seattle Genetics common stock at a price of $200 per share. In addition, Seattle Genetics will be eligible to receive up to $2.6 billion in milestone payments, including $850 million in development milestones and $1.75 billion in sales milestones.

The companies will jointly develop and commercialize ladiratuzumab vedotin and equally share profits worldwide. The companies will co-commercialize in the U.S. and Europe. Seattle Genetics will be responsible for marketing applications for approval in the U.S. and Canada, and will record sales in the U.S., Canada and Europe. Merck will be responsible for marketing applications for approval in Europe and in countries outside the U.S. and Canada, and will record sales in countries outside the U.S., Europe and Canada. Including the upfront payment, equity investment proceeds and potential milestone payments, Seattle Genetics is eligible to receive up to $4.2 billion.

The closing of the equity investment is contingent on completion of review under the Hart-Scott-Rodino Antitrust Improvements Act of 1976 (HSR Act).

TUKYSA Collaboration Details

Under the terms of the agreement, Merck has been granted exclusive rights to commercialize TUKYSA in Asia, the Middle East and Latin America and other regions outside of the U.S., Canada and Europe. Seattle Genetics retains commercial rights and will record sales in the U.S., Canada and Europe. Merck will be responsible for marketing applications for approval in its territory, supported by the positive results from the HER2CLIMB clinical trial.

Merck will also co-fund a portion of the TUKYSA global development plan, which encompasses several ongoing and planned trials across HER2-positive cancers, including breast, colorectal, gastric and other cancers set forth in a global product development plan. Seattle Genetics will continue to lead ongoing TUKYSA global development planning and operational execution. Merck will solely fund and conduct country-specific clinical trials necessary to support anticipated regulatory applications in its territory.

Seattle Genetics will receive from Merck $125 million as an upfront payment and is eligible to receive progress-dependent milestones of up to $65 million. Seattle Genetics will also receive $85 million in prepaid research and development payments to be applied to Mercks global development funding obligations. In addition, Seattle Genetics would receive tiered royalties on sales of TUKYSA in Mercks territory.

The financial impact of these collaborations is not included in Seattle Genetics 2020 guidance.

Seattle Genetics Conference Call Details

Seattle Genetics management will host a conference call to discuss these collaborations today at 6:00 a.m. Pacific Time (PT); 9:00 a.m. Eastern Time (ET). The event will be simultaneously webcast and available for replay from the Seattle Genetics website at http://www.seattlegenetics.com, under the Investors section. Investors may also participate in the conference call by calling 844-763-8274 (domestic) or +1 412-717-9224 (international). The conference ID is 10147850.

About Ladiratuzumab Vedotin

Ladiratuzumab vedotin is a novel investigational ADC targeted to LIV-1. Most metastatic breast cancers express LIV-1, which also has been detected in several other cancers, including lung, head and neck, esophageal and gastric. Ladiratuzumab vedotin utilizes Seattle Genetics proprietary ADC technology and consists of a LIV-1-targeted monoclonal antibody linked to a potent microtubule-disrupting agent, monomethyl auristatin E (MMAE) by a protease-cleavable linker. This novel ADC is designed to bind to LIV-1 on cancer cells and release the cell-killing agent into target cells upon internalization. Ladiratuzumab vedotin may also cause antitumor activity through other mechanisms, including activation of an immune response by induction of immunogenic cell death.

About TUKYSA (tucatinib)

TUKYSA is an oral, small molecule tyrosine kinase inhibitor (TKI) of HER2, a protein that contributes to cancer cell growth. TUKYSA in combination with trastuzumab and capecitabine was approved by the U.S. Food and Drug Administration (FDA) in April 2020 for adult patients with advanced unresectable or metastatic HER2-positive breast cancer, including patients with brain metastases, who have received one or more prior anti-HER2-based regimens in the metastatic setting. In addition, TUKYSA received approval in Canada, Singapore, Australia and Switzerland under the Project Orbis initiative of the FDA Oncology Center of Excellence that provides a framework for concurrent submission and review of oncology products among international partners. A marketing application is under review in the European Union.

TUKYSA is being evaluated in several ongoing clinical trials and additional studies are planned. Current trials include the following:

For additional information, visit http://www.clinicaltrials.gov.

TUKYSA Important Safety Information

Warnings and Precautions

If diarrhea occurs, administer antidiarrheal treatment as clinically indicated. Perform diagnostic tests as clinically indicated to exclude other causes of diarrhea. Based on the severity of the diarrhea, interrupt dose, then dose reduce or permanently discontinue TUKYSA.

Monitor ALT, AST, and bilirubin prior to starting TUKYSA, every 3 weeks during treatment, and as clinically indicated. Based on the severity of hepatoxicity, interrupt dose, then dose reduce or permanently discontinue TUKYSA.

Adverse Reactions

Serious adverse reactions occurred in 26% of patients who received TUKYSA. Serious adverse reactions in 2% of patients who received TUKYSA were diarrhea (4%), vomiting (2.5%), nausea (2%), abdominal pain (2%), and seizure (2%). Fatal adverse reactions occurred in 2% of patients who received TUKYSA including sudden death, sepsis, dehydration, and cardiogenic shock.

Adverse reactions led to treatment discontinuation in 6% of patients who received TUKYSA; those occurring in 1% of patients were hepatotoxicity (1.5%) and diarrhea (1%). Adverse reactions led to dose reduction in 21% of patients who received TUKYSA; those occurring in 2% of patients were hepatotoxicity (8%) and diarrhea (6%).

The most common adverse reactions in patients who received TUKYSA (20%) were diarrhea, palmar-plantar erythrodysesthesia, nausea, fatigue, hepatotoxicity, vomiting, stomatitis, decreased appetite, abdominal pain, headache, anemia, and rash.

Lab Abnormalities

In HER2CLIMB, Grade 3 laboratory abnormalities reported in 5% of patients who received TUKYSA were: decreased phosphate, increased ALT, decreased potassium, and increased AST. The mean increase in serum creatinine was 32% within the first 21 days of treatment with TUKYSA. The serum creatinine increases persisted throughout treatment and were reversible upon treatment completion. Consider alternative markers of renal function if persistent elevations in serum creatinine are observed.

Drug Interactions

Use in Specific Populations

For more information, please see the full Prescribing Information for TUKYSA here.

About KEYTRUDA (pembrolizumab) Injection, 100 mg

KEYTRUDA is an anti-PD-1 therapy that works by increasing the ability of the bodys immune system to help detect and fight tumor cells. KEYTRUDA is a humanized monoclonal antibody that blocks the interaction between PD-1 and its ligands, PD-L1 and PD-L2, thereby activating T lymphocytes which may affect both tumor cells and healthy cells.

Merck has the industrys largest immuno-oncology clinical research program. There are currently more than 1,200 trials studying KEYTRUDA across a wide variety of cancers and treatment settings. The KEYTRUDA clinical program seeks to understand the role of KEYTRUDA across cancers and the factors that may predict a patient's likelihood of benefitting from treatment with KEYTRUDA, including exploring several different biomarkers.

Selected KEYTRUDA (pembrolizumab) Indications

Melanoma

KEYTRUDA is indicated for the treatment of patients with unresectable or metastatic melanoma.

KEYTRUDA is indicated for the adjuvant treatment of patients with melanoma with involvement of lymph node(s) following complete resection.

Non-Small Cell Lung Cancer

KEYTRUDA, in combination with pemetrexed and platinum chemotherapy, is indicated for the first-line treatment of patients with metastatic nonsquamous non-small cell lung cancer (NSCLC), with no EGFR or ALK genomic tumor aberrations.

KEYTRUDA, in combination with carboplatin and either paclitaxel or paclitaxel protein-bound, is indicated for the first-line treatment of patients with metastatic squamous NSCLC.

KEYTRUDA, as a single agent, is indicated for the first-line treatment of patients with NSCLC expressing PD-L1 [tumor proportion score (TPS) 1%] as determined by an FDA-approved test, with no EGFR or ALK genomic tumor aberrations, and is stage III where patients are not candidates for surgical resection or definitive chemoradiation, or metastatic.

KEYTRUDA, as a single agent, is indicated for the treatment of patients with metastatic NSCLC whose tumors express PD-L1 (TPS 1%) as determined by an FDA-approved test, with disease progression on or after platinum-containing chemotherapy. Patients with EGFR or ALK genomic tumor aberrations should have disease progression on FDA-approved therapy for these aberrations prior to receiving KEYTRUDA.

Small Cell Lung Cancer

KEYTRUDA is indicated for the treatment of patients with metastatic small cell lung cancer (SCLC) with disease progression on or after platinum-based chemotherapy and at least 1 other prior line of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials.

Head and Neck Squamous Cell Cancer

KEYTRUDA, in combination with platinum and fluorouracil (FU), is indicated for the first-line treatment of patients with metastatic or with unresectable, recurrent head and neck squamous cell carcinoma (HNSCC).

KEYTRUDA, as a single agent, is indicated for the first-line treatment of patients with metastatic or with unresectable, recurrent HNSCC whose tumors express PD-L1 [combined positive score (CPS) 1] as determined by an FDA-approved test.

KEYTRUDA, as a single agent, is indicated for the treatment of patients with recurrent or metastatic head and neck squamous cell carcinoma (HNSCC) with disease progression on or after platinum-containing chemotherapy.

Classical Hodgkin Lymphoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with refractory classical Hodgkin lymphoma (cHL), or who have relapsed after 3 or more prior lines of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Primary Mediastinal Large B-Cell Lymphoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with refractory primary mediastinal large B-cell lymphoma (PMBCL), or who have relapsed after 2 or more prior lines of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials. KEYTRUDA is not recommended for treatment of patients with PMBCL who require urgent cytoreductive therapy.

Urothelial Carcinoma

KEYTRUDA is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma (mUC) who are not eligible for cisplatin-containing chemotherapy and whose tumors express PD-L1 [combined positive score (CPS) 10], as determined by an FDA-approved test, or in patients who are not eligible for any platinum-containing chemotherapy regardless of PD-L1 status. This indication is approved under accelerated approval based on tumor response rate and duration of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials.

KEYTRUDA is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma (mUC) who have disease progression during or following platinum-containing chemotherapy or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.

KEYTRUDA is indicated for the treatment of patients with Bacillus Calmette-Guerin (BCG)-unresponsive, high-risk, non-muscle invasive bladder cancer (NMIBC) with carcinoma in situ (CIS) with or without papillary tumors who are ineligible for or have elected not to undergo cystectomy.

Microsatellite Instability-High or Mismatch Repair Deficient Cancer

KEYTRUDA is indicated for the treatment of adult and pediatric patients with unresectable or metastatic microsatellite instability-high (MSI-H) or mismatch repair deficient (dMMR)

This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials. The safety and effectiveness of KEYTRUDA in pediatric patients with MSI-H central nervous system cancers have not been established.

Microsatellite Instability-High or Mismatch Repair Deficient Colorectal Cancer

KEYTRUDA is indicated for the first-line treatment of patients with unresectable or metastatic MSI-H or dMMR colorectal cancer (CRC).

Gastric Cancer

KEYTRUDA is indicated for the treatment of patients with recurrent locally advanced or metastatic gastric or gastroesophageal junction (GEJ) adenocarcinoma whose tumors express PD-L1 (CPS 1) as determined by an FDA-approved test, with disease progression on or after two or more prior lines of therapy including fluoropyrimidine- and platinum-containing chemotherapy and if appropriate, HER2/neu-targeted therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Esophageal Cancer

KEYTRUDA is indicated for the treatment of patients with recurrent locally advanced or metastatic squamous cell carcinoma of the esophagus whose tumors express PD-L1 (CPS 10) as determined by an FDA-approved test, with disease progression after one or more prior lines of systemic therapy.

Cervical Cancer

KEYTRUDA is indicated for the treatment of patients with recurrent or metastatic cervical cancer with disease progression on or after chemotherapy whose tumors express PD-L1 (CPS 1) as determined by an FDA-approved test. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Hepatocellular Carcinoma

KEYTRUDA is indicated for the treatment of patients with hepatocellular carcinoma (HCC) who have been previously treated with sorafenib. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Merkel Cell Carcinoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with recurrent locally advanced or metastatic Merkel cell carcinoma (MCC). This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Renal Cell Carcinoma

KEYTRUDA, in combination with axitinib, is indicated for the first-line treatment of patients with advanced renal cell carcinoma (RCC).

Tumor Mutational Burden-High

KEYTRUDA is indicated for the treatment of adult and pediatric patients with unresectable or metastatic tumor mutational burden-high (TMB-H) [10 mutations/megabase (mut/Mb)] solid tumors, as determined by an FDA-approved test, that have progressed following prior treatment and who have no satisfactory alternative treatment options. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials. The safety and effectiveness of KEYTRUDA in pediatric patients with TMB-H central nervous system cancers have not been established.

Cutaneous Squamous Cell Carcinoma

KEYTRUDA is indicated for the treatment of patients with recurrent or metastatic cutaneous squamous cell carcinoma (cSCC) that is not curable by surgery or radiation.

Selected Important Safety Information for KEYTRUDA

Immune-Mediated Pneumonitis

KEYTRUDA can cause immune-mediated pneumonitis, including fatal cases. Pneumonitis occurred in 3.4% (94/2799) of patients with various cancers receiving KEYTRUDA, including Grade 1 (0.8%), 2 (1.3%), 3 (0.9%), 4 (0.3%), and 5 (0.1%). Pneumonitis occurred in 8.2% (65/790) of NSCLC patients receiving KEYTRUDA as a single agent, including Grades 3-4 in 3.2% of patients, and occurred more frequently in patients with a history of prior thoracic radiation (17%) compared to those without (7.7%). Pneumonitis occurred in 6% (18/300) of HNSCC patients receiving KEYTRUDA as a single agent, including Grades 3-5 in 1.6% of patients, and occurred in 5.4% (15/276) of patients receiving KEYTRUDA in combination with platinum and FU as first-line therapy for advanced disease, including Grades 3-5 in 1.5% of patients.

Monitor patients for signs and symptoms of pneumonitis. Evaluate suspected pneumonitis with radiographic imaging. Administer corticosteroids for Grade 2 or greater pneumonitis. Withhold KEYTRUDA for Grade 2; permanently discontinue KEYTRUDA for Grade 3 or 4 or recurrent Grade 2 pneumonitis.

Immune-Mediated Colitis

KEYTRUDA can cause immune-mediated colitis. Colitis occurred in 1.7% (48/2799) of patients receiving KEYTRUDA, including Grade 2 (0.4%), 3 (1.1%), and 4 (<0.1%). Monitor patients for signs and symptoms of colitis. Administer corticosteroids for Grade 2 or greater colitis. Withhold KEYTRUDA for Grade 2 or 3; permanently discontinue KEYTRUDA for Grade 4 colitis.

Immune-Mediated Hepatitis (KEYTRUDA) and Hepatotoxicity (KEYTRUDA in Combination With Axitinib)

Immune-Mediated Hepatitis

KEYTRUDA can cause immune-mediated hepatitis. Hepatitis occurred in 0.7% (19/2799) of patients receiving KEYTRUDA, including Grade 2 (0.1%), 3 (0.4%), and 4 (<0.1%). Monitor patients for changes in liver function. Administer corticosteroids for Grade 2 or greater hepatitis and, based on severity of liver enzyme elevations, withhold or discontinue KEYTRUDA.

Hepatotoxicity in Combination With Axitinib

KEYTRUDA in combination with axitinib can cause hepatic toxicity with higher than expected frequencies of Grades 3 and 4 ALT and AST elevations compared to KEYTRUDA alone. With the combination of KEYTRUDA and axitinib, Grades 3 and 4 increased ALT (20%) and increased AST (13%) were seen. Monitor liver enzymes before initiation of and periodically throughout treatment. Consider more frequent monitoring of liver enzymes as compared to when the drugs are administered as single agents. For elevated liver enzymes, interrupt KEYTRUDA and axitinib, and consider administering corticosteroids as needed.

Immune-Mediated Endocrinopathies

KEYTRUDA can cause adrenal insufficiency (primary and secondary), hypophysitis, thyroid disorders, and type 1 diabetes mellitus. Adrenal insufficiency occurred in 0.8% (22/2799) of patients, including Grade 2 (0.3%), 3 (0.3%), and 4 (<0.1%). Hypophysitis occurred in 0.6% (17/2799) of patients, including Grade 2 (0.2%), 3 (0.3%), and 4 (<0.1%). Hypothyroidism occurred in 8.5% (237/2799) of patients, including Grade 2 (6.2%) and 3 (0.1%). The incidence of new or worsening hypothyroidism was higher in 1185 patients with HNSCC (16%) receiving KEYTRUDA, as a single agent or in combination with platinum and FU, including Grade 3 (0.3%) hypothyroidism. Hyperthyroidism occurred in 3.4% (96/2799) of patients, including Grade 2 (0.8%) and 3 (0.1%), and thyroiditis occurred in 0.6% (16/2799) of patients, including Grade 2 (0.3%). Type 1 diabetes mellitus, including diabetic ketoacidosis, occurred in 0.2% (6/2799) of patients.

Monitor patients for signs and symptoms of adrenal insufficiency, hypophysitis (including hypopituitarism), thyroid function (prior to and periodically during treatment), and hyperglycemia. For adrenal insufficiency or hypophysitis, administer corticosteroids and hormone replacement as clinically indicated. Withhold KEYTRUDA for Grade 2 adrenal insufficiency or hypophysitis and withhold or discontinue KEYTRUDA for Grade 3 or Grade 4 adrenal insufficiency or hypophysitis. Administer hormone replacement for hypothyroidism and manage hyperthyroidism with thionamides and beta-blockers as appropriate. Withhold or discontinue KEYTRUDA for Grade 3 or 4 hyperthyroidism. Administer insulin for type 1 diabetes, and withhold KEYTRUDA and administer antihyperglycemics in patients with severe hyperglycemia.

Immune-Mediated Nephritis and Renal Dysfunction

KEYTRUDA can cause immune-mediated nephritis. Nephritis occurred in 0.3% (9/2799) of patients receiving KEYTRUDA, including Grade 2 (0.1%), 3 (0.1%), and 4 (<0.1%) nephritis. Nephritis occurred in 1.7% (7/405) of patients receiving KEYTRUDA in combination with pemetrexed and platinum chemotherapy. Monitor patients for changes in renal function. Administer corticosteroids for Grade 2 or greater nephritis. Withhold KEYTRUDA for Grade 2; permanently discontinue for Grade 3 or 4 nephritis.

Immune-Mediated Skin Reactions

Immune-mediated rashes, including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN) (some cases with fatal outcome), exfoliative dermatitis, and bullous pemphigoid, can occur. Monitor patients for suspected severe skin reactions and based on the severity of the adverse reaction, withhold or permanently discontinue KEYTRUDA and administer corticosteroids. For signs or symptoms of SJS or TEN, withhold KEYTRUDA and refer the patient for specialized care for assessment and treatment. If SJS or TEN is confirmed, permanently discontinue KEYTRUDA.

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