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DNA defect linked to ovarian cancer
Posted on August 3rd, 2009 No comments03 Aug 2009 – 2:00 PDT – medicalnewstoday.com
By searching millions of DNA variations in the genomes of thousands of women with and without ovarian cancer, scientists have discovered a previously undetected region of DNA which when altered, can increase a woman’s risk of developing ovarian cancer by 40 per cent. The hope is that this will one day lead to a reliable screening test for a disease that currently has a high mortality rate because it is difficult to detect early.
The study was conducted by an international research team that included UK scientists from University College London (UCL), the Cancer Research UK Genetic Epidemiology Unit, and the University of Cambridge, and is published in the 2 August online issue of Nature Genetics.
Ovarian cancer is the fifth most common cancer in women in the UK, where around 6,800 new cases are diagnosed every year, which is a rate of about 130 women a week finding out they have the disease.
However, ovarian cancer is the most common cause of cancer death in women in the UK, where it kills around 4,300 women every year.
The human genome, the DNA-coded blueprint of how to make a human being, has more than 10 million genetic variants, of which just a small number will increase a woman’s chance of getting ovarian cancer.
Scientists already know that variants in the BRCA1 and BRCA2 breast cancer genes significantly increase a woman’s chances of getting ovarian cancer, but these are rare and account for less than 5 per cent of ovarian cancers.
Senior author Dr Simon Gayther of UCL said this study identified a significant new variant and there is real hope that as more are found:
“We can start to identify the women at greatest risk and this could help doctors to diagnose the disease earlier when treatment has a better chance of being successful.”
Gayther and his gynaecological cancer research team’s work is supported by funds from Cancer Research UK and The Eve Appeal charity.
For the study the scientists analysed 2.5 million variations in DNA base pairs from the genomes of 1,810 women with, and 2,535 women without ovarian cancer in the UK.
DNA base pairs are like letters of the words that spell out the genetic code. Strips of DNA base pairs (the “words” if you like) are called single nucleotide polymorphisms (SNPs). Small alterations in the coding of particular SNPs, akin to “spelling errors” in words, link to ovarian cancer risk.
After eight years of searching, Gayther and colleagues found an SNP on chromosome 9 that was uniquely linked to ovarian cancer. Each of us has 23 pairs of chromosomes, each “copy” in the pair comes from one biological parent.
In collaboration with the international Ovarian Cancer Association Consortium (OCAC) they confirmed the finding in another group of 7,000 women with ovarian cancer and 10,000 women without the disease. The samples came from women all over the world.
The scientists estimated that:
- Women carrying that particular version of the SNP on both copies of chromosome 9 have a 40 per cent higher lifetime risk of developing ovarian cancer than women who do not carry it on either copy of chromosome 9.
- The risk for women carrying both copies is 14 in 1,000 compared to 10 in 1,000.
- About 15 per cent of women in the UK have both copies of the variant.
- Women with only one copy of the variant have a 20 per cent higher lifetime risk of developing ovarian cancer than women who have none.
- The risk for women carrying only one copy is 12 in 1,000 compared to 10 in 1,000.
- About 40 per cent of women in the UK have one copy.
David Lammy, the Member of Parliament for Tottenham and Minister for Higher Education and Intellectual Property, had particular reason to be interested in this research because it included a DNA sample from his mother, Rose Lammy, who died of ovarian cancer last year. She carried both copies of the DNA variant that Gayther and colleagues identified.
Lammy said the study brings us a step closer toward earlier diagnosis of ovarian cancer, when treatment is more likely to succeed. He told the media:
“I am pleased that Mum’s sample was included in this study.”
“We now know the fact that she had this altered DNA meant that her lifetime risk had risen from 10 in 1,000 to 14 in 1,000, an increase of 40 per cent compared to those women who don’t carry this DNA variation,” he added.
“A genome-wide association study identifies a new ovarian cancer susceptibility locus on 9p22.2.”
Honglin Song, Susan J Ramus, Jonathan Tyrer, Kelly L Bolton, Aleksandra Gentry-Maharaj et al.
Nature Genetics, Published online: 2 August 2009.
DOI:10.1038/ng.424Source: UCL News.
Written by: Catharine Paddock, PhD
Copyright: Medical News TodayDNAWellnessinfo.com Resource: http://www.medicalnewstoday.com/articles/159620.php
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Role of genes in weight management
Posted on July 11th, 2009 No commentsweightlossnutrition.com
Science is constantly trying to get behind the main factors for the obesity epidemic. From our hurried, fast food lifestyle to our laziness and penchant for T.V. watching rather than exercise, it seems relatively clear that, in most cases, the obesity epidemic is a result of our lifestyle choices. But for some, their genetics play a role that may be hard to fight against.
Family reunions let everyone in the family come together and see the role that genetics has played in their life; maybe you have Aunt Bertha’s red hair or Cousin Vinny’s brown eyes. Unfortunately, you can also inherit Uncle Roger’s pot belly and Grandpa Joe’s wide tush. This is because genetics plays a role in your fat cells and where they are stored.
Because of your DNA, you have a genetic predisposition to carry fat cells in the same areas as your family. Since families blend the DNA of many different people, you may take after one side of your family more than another. This could mean that you and your brother have the genetic predisposition to having love handles while your older sister doesn’t.
In addition to your propensity to carry fat in certain places, you’ll find that your body’s response to exercise mimics others in your family as well. If you have the right genes, you may find that you build muscle very quickly when weight training or, if you’re on the unfortunate end, you don’t.
But, what is the role of genes in weight management? Can you manipulate your genes to work for you rather than against you? For some with genetically linked health issues like thyroid problems, medications can be a solution. Medications can help your body run as it should and can pick up the slack for any glands that are impaired due to genetic lineage.
For most people, medication is not the answer. Instead, learning how your body responds to food and exercise if key to fighting your genes and managing your weight. If your family is filled with overweight people, and you see the signs in your own body that this is probably your destiny too, follow these steps to head genetics off at the pass.
- Eat right. Cut out sugars, simple carbohydrates (like white rice and white bread), and stay away from fast food. For some, learned eating habits play a bigger role in weight gain than genetics. Be sure to reevaluate the food lessons you’ve learned from your family and try to make the right decisions regarding what goes in your mouth.
- Exercise regularly. Ideally, you should exercise for one hour a day, five to six days per week. Unfortunately, real life often gets in the way of this. If you can exercise four times per week for one half hour per work out, you’ll find you can stave off the effects of genetics.
- Stick with it. Fighting your genes is not easy and you may find that you have to work harder than others to receive fewer results. Just remember the alternative facing you and stick with it.
Before embarking on any new physical fitness routine or new and improved eating plan, you should consult a physician. In addition to letting you know if the routine you want to try is healthy for you, they may have some other helpful tips to give you. Speaking with a nutritionist about your eating plan will also help you get ideas for variety and make sure that you haven’t included any foods that will hurt your weight management goals rather than help them.
DNAWellnessinfo.com Resource: http://www.weightlossnutrition.org/genes-weight-management/
DNA Guided Nutrition Breakthrough: http://www.dnaguidedwellnessproducts.com
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Dad’s Genes May Play Greater Role Than Thought
Posted on June 15th, 2009 No comments06.15.09, 12:00 PM EDT forbes.com
Data on ‘packaging’ in sperm cells may also help assess infertility
MONDAY, June 15 (HealthDay News) — Biologists say they have discovered a clever packaging scheme that allows the genetic material in sperm to have far more influence over development of a fertilized egg than had been imagined.The discovery has potential applications in helping infertile men, said Brad Cairns, a professor of oncological sciences at the University of Utah and a leader of the team reporting the finding in the June 14 online edition of Nature.
The vast majority of the DNA molecules that carry genetic information are tightly packaged in sperm cells, Cairns said. That tight packaging enables a win in what is literally a race for life because the first sperm to reach an egg fertilizes it, and the tightest packages are the most streamlined.
“But when it comes to development, the sperm is at a real disadvantage,” Cairns said. “The vast majority of their genes are tightly packed in material that is not helpful in giving them full expression.”
In every cell other than sperm, DNA molecules are wrapped around structures called histones, an arrangement that allows for easy transmission of their genetic instructions. But only 4 percent of sperm DNA is arranged around histones. The other 96 percent is in a dense, impenetrable material called protamine.
“The hypothesis has been that this 4 percent of DNA in histones is randomly distributed,” Cairns said. “We challenged the hypothesis and found that the DNA that is in histones is not randomly distributed but is located at important genes for embryonic development.”
The discovery was made by using DNA from sperm at the University of Utah’s in vitro fertilization clinic. “We isolated the DNA attached to histones and sequenced it,” Cairns said. “We found genes that are important in guiding the development of the embryo.”
The discovery raises “obvious questions” about the importance of DNA packaging in sperm on human fertility, he said.
“Do infertile men have problems in packaging, and is that the basis of their problem?” Cairns asked. “We already have preliminary evidence that the majority of infertile men have problems in gene packaging. There is an incorrect ratio of histones to protamine.”
Cairns said that the gene packaging issue is related to another biological aspect of DNA expression — DNA methylation. Some subunits of the DNA molecules ordinarily have molecules called methyl groups attached to them. Lack of methylation can also contribute to infertility, he said.
The Utah group is working on a test that could define the root issues in men with fertility problems, Cairns said. “We are working toward a clinical diagnostic test for infertile men that would assess their packaging and DNA methylation status so that we could counsel them on whether they can have success in achieving fertility,” he said.
The concept of possible intervention to improve fertility is much more distant, he said.
From the basic science point of view, one major lesson of the discovery is that DNA is not the only molecule that can carry genetic information from generation to generation, said William G. Kelly, an associate professor of biology at Emory University, whose review article will appear in the same issue of the journal.
What the study shows “is that the histones still sitting there have really important information that actually guides the genes that regulate early events in the development of the next generation,” Kelly said.
That idea has been proposed, but “it was not clear that this information could survive the packaging in sperm,” he said.
“This firmly shows that information that’s there can be information that is passed across generations and that is not encoded in DNA,” Kelly said.
More information
The Yale Fertility Center has more on the causes and treatment of infertility.
DNAWellnessinfo.com Resource: http://www.forbes.com/feeds/hscout/2009/06/15/hscout628024.html
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New era of gene-based personalized medicine’ dawning
Posted on June 14th, 2009 No commentsPosted on Sunday, 06.14.09 on miamiherald.com
By ROBERT S. BOYD
McClatchy Newspapers
WASHINGTON — Six years ago, scientists announced the completion of the Human Genome Project, a historic effort to decipher each of the 3 billion letters in the genetic instruction book for our species. A single anonymous male from Buffalo, N.Y. – code name RP11 – provided the bulk of the DNA used for the project.
Now, many thousands more people are contributing DNA samples for a wide array of follow-on studies designed to turn the project’s findings to practical use in health care, genetics and biological research.
Researchers and doctors have opened a new era of “personalized medicine” that seeks to tailor therapies to patients based on their unique genetic makeups and medical histories.
According to the National Cancer Institute, the days are passing when most cancer tumors were thought to be essentially the same and patients got the same drugs.
“We’re not very good at selecting therapies for individual patients,” Dr. Rick Hockett, the chief medical officer of Affymetrix, a genetics firm in Santa Clara, Calif., told a conference on personalized medicine this month in Washington. “Targeted therapy,” he said, can “improve the benefit-risk ratio for patients.”
For example, Hockett said that heart patients who took the popular anti-clotting drug Plavix had a greatly increased risk of serious problems, including death, if they had two tiny mutations in their genes.
Massachusetts General Hospital in Boston and the Memorial Sloan-Kettering Cancer Center in New York have begun to screen lung tumors for genetic abnormalities that could reveal whether a particular treatment is likely to work or should be avoided.
Last year, Dr. Richard Wilson, the director of the Genome Sequencing Center at Washington University in St. Louis, compared 20,000 genes in cancer cells from a woman who died of leukemia with healthy cells also taken from her body. Wilson identified 10 mutations – or genetic mistakes – related to her cancer, including one that blocks chemotherapy drugs from getting inside the cancerous cell.
Other developments in the approaching world of personalized medicine include:
-A “Personal Genome Project” led by George Church, a geneticist at Harvard Medical School in Boston, aims to recruit 100,000 people of diverse backgrounds to analyze their genomes and medical histories.
The first 10 participants already have published their personal data – including their pictures, weights and smoking and drinking habits, as well as their DNA – on the Internet for anyone to see at www.personalgenomes.org/pgp10.html.
To take part, volunteers donate hair and saliva samples for DNA analysis. So far, 13,000 people have asked to be enrolled. For privacy, their data will be encoded by number, not by individual names.
The goal is to discover which genetic variations are related to which diseases, so that targeted therapies can be designed. According to Church, at least 1,449 genes have been linked to potential illnesses. For instance, a gene called ApoE is associated with a higher risk of Alzheimer’s.
-The National Human Genome Research Institute in Bethesda, Md., has launched a “1000 Genomes Project,” which has started to collect DNA from 1,000 individuals from Africa, Asia and Europe. The goal is to provide much broader and deeper information than the original, limited Human Genome Project could.
Researchers are seeking clues to individual differences in susceptibility to disease, response to drugs and sensitivity to the environment.
Just as astronomers see farther and more clearly into the universe with bigger telescopes, the results of the 1000 Genomes Project will give us greater resolution as we view our own genetic blueprint,” Francis Collins, the former director of the National Human Genome Research Institute, said in a statement explaining the plan. “We’ll be able to see more things more clearly than before, and that will be important for understanding the genetic contributions to health and illness.”
-The National Geographic Society is collecting DNA from about 300,000 people for a “Genographic Project” that traces their distant ancestries from continent to continent all the way back to their African roots.
Researchers at 10 centers around the world collect DNA samples from local populations. A team led by Spencer Wells, a genetic anthropologist and the magazine’s “explorer in residence” in Washington, will analyze the samples.
In addition, anyone who wishes to can buy a $100 self-testing kit and provide a saliva sample to the Genographic project. Participants will get back reports that describe in general terms the migration of their ancestors from their original roots in Africa some 60,000 years ago.
-A booming, but controversial, genetic testing industry also has sprouted, offering to analyze a person’s DNA – at a price – for possible susceptibility to cancer, Alzheimer’s and dozens of other diseases.
More than 1,000 such tests are on the market, Kathy Hudson, the director of the Genetics and Public Policy Center at Johns Hopkins University in Washington, told a congressional committee.
According to the Human Genome Project’s Web site, some genetic tests have “greatly improved or even saved lives,” but there are concerns that they might be used by insurance companies to deny coverage or by employers deciding whom to hire or promote.
To meet these concerns, Congress passed a “Genetic Information Non-Discrimination Act” last year, which is just starting to have an impact.
“The portions of it relating to health insurance just went into effect on May 21, and so will apply to next year’s (health) plan for most people,” said Susannah Baruch, of the Genetics and Public Policy Center. The parts of the new law that relate to the use of genetic information on the job won’t take effect until Nov. 21, but the Equal Employment Opportunity Commission already has drafted regulations.
ON THE WEB
More on personalized medicine: www.personalizedmedicinecoalition.org
Personal Genome Project: http://www.personalgenomes.org
1000 Genomes Project: http://www.1000genomes.org/page.php
National Geographic’s Genographic Project: https://genographic.nationalgeographic.com
DNAWellnessinfo.com Resource: http://www.miamiherald.com/news/politics/AP/story/1096679.html
DNA Guided Nutrition Breakthrough: http://www.dnaguidedwellnessproducts.com
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Genes Play a Role in Glycemic Control in People With Type 1 Diabetes
Posted on June 6th, 2009 3 commentsearthtimes.com – Sat, 06 Jun 2009 13:15:23 GMT
NEW ORLEANS, LA — 06/06/09 — Researchers have proven that glycemic control in type 1 diabetes is not fully dependent on the individual’s behavior, but is in part subject to genetic influence, according to a presentation here today at the American Diabetes Association’s 69th Scientific Sessions. “We identified four genes related to glycemic control in type 1 diabetes,” said Andrew D. Paterson, MBChB, Senior Scientist in the Program for Genetics and Genome Biology, Hospital for Sick Children in Toronto, and lead author of the study. “Two of these genes also affect risk for complications — kidney, eye, and cardiovascular disease — and one gene has a strong effect on the rate of hypoglycemia.”
“This finding does not give people with diabetes the freedom to slack off on their careful nutrition, exercise, and medication regimens because behavior clearly plays the major role in glycemic control,” cautioned Dr. Paterson. “Eventually, the genetic variations we found may be used to identify individuals at risk for poor glycemic control and for diabetic complications, so that steps could be taken to intensify control or implement other measures. But in the interim, this knowledge may influence the design and analysis of genetic studies attempting to identify risk factors for long-term diabetic complications and lead us in new research directions to better understand the mechanisms of glycemic control.”
Nearly 24 million Americans have diabetes, a group of serious diseases characterized by high blood glucose levels that result from defects in the body’s ability to produce and/or use insulin. Diabetes can lead to severely debilitating or fatal complications, such as heart disease, blindness, kidney disease, and amputation. It is a leading cause of death by disease in the United States.
Type 1 is an immune-mediated form of diabetes involving destruction of the insulin-producing beta cells in the pancreas that typically leads to absolute insulin deficiency. Type 1 diabetes accounts for 5% to 10% of all diagnosed cases of diabetes and usually strikes children or young adults, although disease onset can occur at any age.
The first data suggesting that A1C, a measure of average glucose control over the prior two to three months, might be influenced by genetics came in 2001 in a British study looking at identical twins, where one twin had type 1 and the other did not, called discordance. “It was found that when the twin without diabetes had an A1C in the high normal range, the twin with diabetes would have an A1C in the high range for someone with diabetes,” said Dr. Paterson. “Essentially, they were playing to the same drummer but in a different key.”
In the current study, the researchers mined the extensive data available from one of the world’s most well-documented studies of people with type 1 diabetes: the Diabetes Control and Complications Trial (DCCT) — an NIH-sponsored study. It was initiated over 25 years ago and enrolled 1,441 people in a comparison of intensive versus conventional control of blood glucose. Conventional control during the DCCT required only one or two insulin injections and blood checks daily, with the aim of preventing overt diabetes symptoms, and typically yields A1C levels of 9% or more. Intensive control to bring A1C levels as close to normal as possible (6% or less) required at least three insulin injections a day or treatment with an insulin pump, guided by at least four glucose self-monitoring checks a day. The initial results, reported in 1993, demonstrated dramatic reductions in the development of eye, nerve, and kidney damage. Intensive control also lowered the risk of heart disease according to data published in 2005 as part of the follow-up study of DCCT participants, called the Epidemiology of Diabetes Interventions and Complications (EDIC) observation study, which is still continuing.
The researchers in this genetic study had access to every quarterly A1C test performed on people in the original DCCT over the course of an average of 6 1/2 years. To identify important genetic loci (the positions that genes occupy on a chromosome) influencing glycemic control in type 1, they performed high resolution genome-wide studies using the mean A1C values and capillary glucose of people in the conventional treatment group and compared loci of interest to people in the intensive treatment group.
They determined the genotypes of a million SNPs across the genome for over 1,300 participants in the DCCT. (SNPs are single-nucleotide polymorphisms, pronounced “snips” — DNA sequence variations in the genome.) Each of these SNPs was tested for association with the participants’ average A1Cs over the course of the trial.
They identified four major gene loci related to A1C levels. One in both treatment groups reached genome-wide significance — SORCS1 gene 10q25.1. Three achieved close to genome-wide significance: 14q32.13 (GSC) and 9p22 (BNC2) in the combined treatment groups; and 15q21.3 (WDR72) in the intensive group. Further, evidence indicated that SORCS1 was associated with hypoglycemia (low blood glucose), and BNC2 was associated with kidney and eye complications.
“While this information gives us insight into the mechanisms influencing glycemic control in people with type 1, it is important to remember that the overall influence of genes is small and may vary from person to person and, perhaps, in response to behavior,” Dr. Paterson explained. “For example, while the SORCS1 gene accounted for about 5% of the variability in glycemic control in the conventional treatment arm of the DCCT, A1C levels in people with type 1 diabetes have improved since those days as diabetes care teams and patients have learned about the value of more intensive control,” he said. “So we don’t know whether that number would be the same in a contemporary treatment setting.” For example, in the EDIC study, A1C levels of the former conventional control group dropped from 9% to 8.1% after they were taught intensive control at the end of the DCCT.
The American Diabetes Association is leading the fight against the deadly consequences of diabetes and fighting for those affected by diabetes. The Association funds research to prevent, cure and manage diabetes; delivers services to hundreds of communities; provides objective and credible information; and gives voice to those denied their rights because of diabetes. Founded in 1940, our mission is to prevent and cure diabetes and to improve the lives of all people affected by diabetes. For more information please call the American Diabetes Association at 1-800-DIABETES (1-800-342-2383) or visit www.diabetes.org. Information from both these sources is available in English and Spanish.
Abstract 58-OR
Contact:
Diane Tuncer
(703) 299-5510Colleen Fogarty
(703) 549-1500 ext. 2146DNAWellnessinfo.com Resource: http://www.earthtimes.org/articles/show/genes-play-a-role-in,851904.shtml
DNA Nutrition Breakthrough: http://www.dnaguidedwellnessproducts.com
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