Public release date: 6-Oct-2013 [ | E-mail | Share ]

Contact: Kara Gavin kegavin@umich.edu 734-764-2220 University of Michigan Health System

ANN ARBOR, Mich. A global hunt for genes that influence heart disease risk has uncovered 157 changes in human DNA that alter the levels of cholesterol and other blood fats a discovery that could lead to new medications.

Each of the changes points to genes that can modify levels of cholesterol and other blood fats and are potential drug targets. Many of the changes point to genes not previously linked to blood fats, also called lipids. A surprising number of the variations were also associated with coronary artery disease, type 2 diabetes, obesity, and high blood pressure.

The research also reveals that triglycerides another type of blood lipid play a larger role in heart disease risk than previously thought.

The results, published in two new papers appearing simultaneously in the journal Nature Genetics, come from the Global Lipids Genetics Consortium -- a worldwide team of scientists who pooled genetic and clinical information from more than 188,000 people from many countries and heritages.

The analysis of the combined data was led by a team from the University of Michigan Medical School and School of Public Health. They used sophisticated computing and statistical techniques to search for genetic variations that modify blood lipid levels.

The results increase by more than a third the total number of genetic variants linked to blood lipids. All but one of the variants associated with blood lipids are near stretches of DNA that encode proteins.

"These results give us 62 new clues about lipid biology, and more places to look than we had before," says Cristen Willer, Ph.D., the lead author of one paper and an assistant professor of Internal Medicine, Human Genetics and Computational Medicine & Bioinformatics at the U-M Medical School. "Once we take the time to truly understand these clues, we'll have a better understanding of lipid biology and cardiovascular disease -- and potentially new targets for treatment."

But, cautions senior author and U-M School of Public Health Professor Gonalo Abecasis, Ph.D., it will take much further work to study the implicated genes and to find and test potential drugs that could target them. The consortium's "open science" approach will include publishing further detail online for other researchers to use freely toward this goal.

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Massive DNA study points to new heart drug targets and a key role for triglycerides

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SALT LAKE CITY, Oct. 7, 2013 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (MYGN) today announced new clinical data from a study with myRisk Hereditary Cancer, a 25-gene hereditary cancer panel, that showed a 60 percent increase in mutations detected in cancer predisposition genes in patients with a prior history of colon cancer and/or polyps. Myriad is presenting this clinical study and data from four other studies this week at the Collaborative Group of the Americas on Inherited Colorectal Cancer (CGA) Annual Meeting in Anaheim, Calif.

Patients with a family history of colon cancer also are vulnerable to other cancers including breast, ovarian, endometrial and stomach cancer. The detection of individuals with mutations associated with hereditary colon cancer greatly increases the chances of successful medical management in those at-risk individuals, which will save lives and reduce the downstream healthcare costs. Also, once a patient has been identified as carrying a deleterious mutation that patient's family members can be tested to determine if they have an increased risk of cancer.

"The new data presented at this year's CGA meeting is ground breaking and underscores the importance of using multi-gene panels when testing patients for hereditary colon cancer," said Richard J. Wenstrup, MD, chief medical officer of Myriad. "Importantly, the data suggest that the use of a 25-gene hereditary cancer panel significantly improved the detection of mutations and is a more efficient way for patients to receive appropriate medical management."

Below is a summary of the key data being presented at the CGA annual meeting.

Abstract: Germline Mutations Identified by a 25-Gene Panel in Patients Undergoing Lynch Syndrome Testing

This study evaluated the mutation prevalence among cases referred for Lynch Syndrome (LS), the most common genetic cause of colon cancer, using the myRisk Hereditary Cancer test, a 25-gene hereditary cancer panel. The study presents data from two cohorts representing a total of 1,133 patients diagnosed with colon cancer or colorectal polyps. The results demonstrated that 10 percent of patients had deleterious mutations in the traditional hereditary colon cancer genes, but an additional 6 percent had deleterious mutations in other genes. This represents a 60 percent increase in the number of patients detected with deleterious mutations in cancer predisposing genes

Abstract: Overlap between Lynch Syndrome and Hereditary Breast and Ovarian Cancer Syndrome among Family Histories in Patients Tested for Hereditary Cancer Syndromes

This study investigated the overlap of personal and family histories in hereditary breast and ovarian cancer (HBOC) and hereditary colon cancer in 9,000 patients. Results showed that among patients tested for HBOC, 6.9 percent also had family histories that meet the National Comprehensive Cancer Network (NCCN) criteria for hereditary colon cancer. In addition, 30 percent of patients tested for hereditary colon cancer also met NCCN criteria for HBOC. This analysis demonstrates the overlap among patients with a family history of hereditary breast cancer and those with a family history of colon cancer, suggesting that patients may benefit from multi-gene panels to better improve the diagnosis of hereditary cancer syndromes.

Abstract: MSI-High Histology Is a Predictive Risk Factor for Lynch Syndrome

The objective of this study was to better understand the prevalence of hereditary colon cancer mutations in patients who have abnormal histology, regardless of family history. Approximately 13.9 percent (57/410) of patients with abnormal histology had a deleterious mutation. Importantly, among the patients who tested positive for a deleterious mutation, 77.2 percent (44/57) would not have met Amsterdam II criteria based on personal or family history for hereditary colon cancer testing if histology was not considered. These data support the use of histology to simplify patient selection for hereditary colon cancer testing.

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Myriad's myRisk Hereditary Cancer(TM) Test Improves Colon Cancer Testing by 60 Percent

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Washington, Oct. 7 (ANI): A global hunt for genes influencing heart disease risk has uncovered 157 changes in human DNA that alter levels of cholesterol and other blood fats - a finding that may lead to new medications.

Each of the changes points to genes that can modify levels of cholesterol and other blood fats and are potential drug targets. Many of the changes point to genes not previously linked to blood fats, also called lipids.

A surprising number of the variations were also associated with coronary artery disease, type 2 diabetes, obesity, and high blood pressure.

The research also reveals that triglycerides - another type of blood lipid - play a larger role in heart disease risk than previously thought.

The results increase by more than a third the total number of genetic variants linked to blood lipids. All but one of the variants associated with blood lipids are near stretches of DNA that encode proteins.

Lead author Cristen Willer, Ph.D., assistant professor of Internal Medicine, Human Genetics and Computational Medicine and Bioinformatics at the U-M Medical School, said that these results give us 62 new clues about lipid biology, and more places to look than we had before.

A further analysis of the massive dataset, published as a letter with lead authors Sekar Kathiresan and Ron Do from Harvard University and the Broad Institute, suggests that triglyceride levels have more impact on cardiovascular disease risk than previously thought.

This analysis found that genetic variations that increase triglyceride or LDL-cholesterol levels are also associated with higher incidence of heart disease. But the analysis also casts further doubt on the role of high density lipoprotein, known commonly as HDL or "good cholesterol", in heart disease risk. In recent years, many drugs that modify HDL cholesterol have failed to show a benefit in preventing heart disease.

The findings have been published in the journal Nature Genetics. (ANI)

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Gene therapy set to become future of heart disease treatment

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Marilynn Marchione, The Associated Press Published Saturday, October 5, 2013 5:20PM EDT

They were mystery diseases that had stumped doctors for years - adults with strange symptoms and children with neurological problems, mental slowness or muscles too weak to let them stand. Now scientists say they were able to crack a quarter of these cases by decoding the patients' genes.

Their study is the first large-scale effort to move gene sequencing out of the lab and into ordinary medical care, and it shows that high hopes for this technology are finally paying off.

"This is a direct benefit of the Human Genome Project," the big effort to decode our DNA, said Dr. Christine M. Eng of Baylor College of Medicine in Houston. "We're now able to directly benefit patients through more accurate diagnosis."

She led the study, which was published online Wednesday by the New England Journal of Medicine. It gives results on the first 250 patients referred to Baylor for a newer type of sequencing - just the DNA segments that hold the recipes for all the proteins the body needs. That's only about 1 percent of the whole genome.

Baylor has sequenced more patients beyond those in the study - 1,700 so far - and found gene flaws in 1 out of 4, Eng said.

That rate will improve as more genes are linked to diseases, but it's already much higher than the less comprehensive gene tests done now, said Rebecca Nagy, a scientist at Ohio State University and president of the National Society of Genetic Counselors.

"For some of these conditions there could be treatments that are lifesaving," she said.

Already, three people tested at Baylor were found to have a muscle disorder that can cause respiratory problems and even death. The condition is aggravated by infections and stress, and there are drugs to treat those and prevent serious episodes, Eng said.

In other cases, having a diagnosis helped parents like Lindsey and Brandon Collier decide whether to have more children. The Colliers, who live in Georgetown, Texas, about 30 miles north of Austin, searched for years for an answer to what was plaguing their son, Cannon, now 4.

Link:
Gene scans solve mystery illnesses in kids, adults

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Freeport, The Bahamas (PRWEB) October 03, 2013

Okyanos Heart Institute, whose mission is to bring a new standard of care and better quality of life to patients with coronary artery disease using cardiac stem cell therapy, has announced that they will be hosting a free educational seminar for the business community and all other interested individuals on Tuesday, October 22nd from 5:30 6:30 pm in the Coral Reef Room of the Pelican Bay Hotel in Lucaya, Grand Bahama Island. Registration is requested to attend as seating is limited.

Howard Walpole, M.D., M.B.A., F.A.C.C., F.S.C.A.I. and chief medical officer and interventional cardiologist for Okyanos Heart Institute will provide an overview of stem cell therapy for heart disease, the source of stem cells, how it is intended to work, and the protocol that will be used by the cath lab for patients once the facility is open in February, 2014. Erika Mangrum, SVP of Communications for the company, will provide an overview of what services will be needed by small businesses on the island, such as janitorial, hospital grade laundry, transportation, catering and more. A preliminary list of jobs that Okyanos Heart Institute will need to fill towards the end of the year will also be shared.

We welcome the local business community to learn about what we will be doing in treating patients with heart disease, said Walpole. Stem cell therapy is a growing field still with some confusion around where stem cells come from, what they do, and how they can potentially help someone with heart disease. We want to answer as many questions as we can.

President of The Grand Bahama Port Authority, Limited (GBPA) Ian Rolle, is pleased with how plans are progressing as the Institute prepares to open its doors locally in early 2014. Legislation has recently been enacted to support stem cell therapy, research and development in The Bahamas. This is of monumental proportions as Grand Bahama Island is now poised to become a leading centre for medical advancement, Rolle said. We heartily welcome the Okyanos Heart Institute and support their efforts towards public education. Additionally, the employment of skilled professionals and outsourcing of ancillary services, mean permanent engagement and greater business opportunities for many of our citizenry.

Okyanos Heart Institute will have a number of service needs from the local business community, said Mangrum. We hope to meet potential suppliers and servicers and share what our needs will be from service providers, and share employment needs once we are close to opening in February. We could not be more enthused about bringing patients to the beautiful island of Grand Bahama in the hopes of improving the quality of their lives by restoring flow to their hearts.

Registration for the seminar is requested as seating is limited. Call 242-688-2667 or email freeseminar(at)okyanos(dot)com by Oct 18.

ABOUT OKYANOS HEART INSTITUTE: (Oh key AH nos) Based in Freeport, The Bahamas, Okyanos Heart Institutes mission is to bring a new standard of care and a better quality of life to patients with coronary artery disease using cardiac stem cell therapy. Okyanos adheres to U.S. surgical center standards and is led by Chief Medical Officer Howard T. Walpole Jr., M.D., M.B.A., F.A.C.C., F.S.C.A.I. Okyanos Treatment utilizes a unique blend of stem and regenerative cells derived from ones own adipose (fat) tissue. The cells, when placed into the heart via a minimally-invasive catheterization, stimulate the growth of new blood vessels, a process known as angiogenesis. The treatment facilitates blood flow in the heart and supports intake and use of oxygen (as demonstrated in rigorous clinical trials such as the PRECISE trial). The literary name Okyanos (Oceanos) symbolizes flow. For more information, go to http://www.okyanos.com.

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Okyanos Heart Institute Offers Educational Seminar About Cardiac Stem Cell Therapy In Lucaya, Grand Bahama

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Oct. 3, 2013 When developing new drugs, monitoring cellular responses to candidate compounds is essential for assessing their efficacy and safety. Researchers from the RIKEN Center for Life Science Technologies report a new method to monitor and quantify the activity of gene promoters during the response to a drug, using the advanced gene expression analysis method CAGE followed by single-molecule sequencing. This research paves the way to a more precise analysis of cellular responses to drugs, at the level of individual promoters.

The study is published this week in the journal CPT: Pharmacometrics & Systems Pharmacology.

Microarray-based technologies are widely used to monitor cellular changes in response to drug administration at the level of genes. However, microarrays have several limitations due to the fact that they rely on pre-designed oligonucleotide probes and detection based on hybridization.

In order to circumvent the limitations imposed by the use of microarray-based technology for the development of new drugs, Dr Harukazu Suzuki and his team at CLST developed a new technique combining Cap Analysis of Gene Expression (CAGE) with 3rd generation, single-molecule sequencing. CAGE is a method developed at RIKEN to comprehensively map human transcription start sites and their promoters, and quantify the set of mRNAs in a cell, also called the transcriptome.

During CAGE the 5'-end of mRNAs is sequenced in order to produce a series of 20-30 nucleotide sequences that can then be mapped onto the genome and provide information about the level of expression of genes. Dr Suzuki and his team used CAGE, combined with a single-molecule sequencer, to monitor the effect of three drugs, U0126, wortmannin and gefitinib on human breast cancer cells.

U0126 and wortmannin are known to inhibit the Ras-ERK and phosphatidylinositol-3-kinase (PI3K)-Akt signalling pathways within cells. Gefinitib is a potent inhibitor of the epidermal growth factor receptor kinase (EGFR kinase) and mainly inhibits the Ras-ERK and PI3K-Akt pathways downstream of EGFR.

The researchers identified a distinct set of promoters that were affected by low doses of the drugs, and therefore showed sensitivity to a weak inhibition of the Ras-ERK and PI3K-Akt signal-transduction pathways. This level of precision would would have been very difficult to achieve using microarray-based profiling.

Furthermore, a quantitative analysis showed that the inhibitory profiles of both U0126 and wortmannin are constitutive components of the transcriptome profile obtained by inhibition of the EGFR kinase. Using a regression model, the researchers were able to quantitatively predict the promoter activity profile of gefitinib, based on the U0126 and wortmannin profiles.

These results demonstrate the potential utility of highly quantitative promoter activity profiling in drug research.

"Quantitative transcriptome analysis is potentially widely applicable to determine the target proteins and action mechanisms of uncharacterized compounds," concludes Dr Suzuki. "Our study paves the way for quantitative analysis of drug responses at the promoter level, and moreover, is potentially applicable for the evaluation of combinatorial or serial drug treatment in a clinical setting," he adds.

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Advanced technology for gene expression analysis can facilitate drug development

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