<img loading="lazy" decoding="async" class="alignright size-full wp-image-3194" title="bloodtravel1" src="https://blog-api.23andme.com/wp-content/uploads/2009/03/bloodtravel1.jpg" alt="" width="350" height="260" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/03/bloodtravel1.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2009/03/bloodtravel1-300x223.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
The U.S. Food and Drug Administration (FDA) has <a href="https://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm203888.htm" target="_blank" rel="noopener noreferrer">updated the label information</a> for the commonly used anti-clotting medication Plavix ® (clopidogrel) to stress to physicians that patients carrying certain genetic variations may not receive the full benefit from the drug.
Plavix reduces the chance a harmful clot will develop by preventing blood cells called platelets from sticking together. Usually prescribed in combination with aspirin, Plavix has been shown to help reduce the risk of subsequent heart attacks or strokes in people who have already suffered from a cardiovascular event. Plavix also reduces the risk of heart attack and stroke in people diagnosed with peripheral artery disease.   The drug is also is used to lower the risk of blood clots in people with unstable angina (chest pain) caused by partially blocked arteries and in those who have had a stent implanted to help keep their arteries open.
Once inside the body, Plavix is absorbed in the intestines and then converted into its active form by enzymes in the liver. But some people have genetic variations that reduce the activity of one of the most critical enzymes – CYP2C19. This, in turn, reduces the amount of active drug in the bloodstream and its effectiveness in preventing clots.
The FDA first added information about poor metabolizers of Plavix to the drug label in May 2009. Additional data has prompted them to add the boxed warning to further caution physicians that some of their patients may be at risk, inform them that testing for CYP2C19 variations is available (although no test is FDA-approved specifically for determining Plavix efficacy), and recommend that other medications or increased dosages of Plavix be used in patients identified as poor metabolizers.
“We want to highlight this warning to make sure health care professionals use the best information possible to treat their patients,” said Mary Ross Southworth, Pharm.D., a clinical analyst in the Division of Cardiovascular and Renal Products in the FDA’s Center for Drug Evaluation and Research, in a press release.
A recently approved drug, Effient ® (prasugrel), may be an alternative for some patients identified as poor metabolizers. Like Plavix, Effient prevents platelets from forming blood clots. The advantage is that the conversion of Effient to its active form can take place in the presence of the genetic variations that affect Plavix. Studies have shown that Effient is effective at preventing heart attacks, strokes and stent-blocking clots.   The risk of dangerous bleeding, however, is higher with this drug.
23andMe Health Edition and Complete Edition customers can view their data for genetic variations in CYP2C19 in the Clopidogrel (Plavix) Efficacy Drug Response Report.
A downloadable PDF version of the Clopidogrel (Plavix) Efficacy report is available to help customers share their results with their doctors.
Only a physician can determine whether Plavix is the right medication for a particular patient and at what dosage it should be given.   The information contained in 23andMe Drug Response reports should not be used to independently establish a drug regimen or abolish or adjust an existing course of treatment.   If you are concerned about Plavix, talk to a health professional.
<ul>
<li>Read more about the Plavix label update<a href="http://www.genomeweb.com/blog/fdas-new-plavix-black-box-warning-could-trigger-surge-cyp2c9-testing" target="_blank" rel="noopener noreferrer"> here </a>and here.</li>
<li>Just last month the FDA updated the label on another anti-clotting medication, warfarin, to include more information on the effects of genetic variations.   Read more<a href="https://blog.23andme.com/articles/fda-updates-label-on-commonly-used-blood-thinner-to-include-dosing-recommendations-based-on-genetics" target="_blank" rel="noopener noreferrer"> here </a>in the Blog.</li>
</ul>

23andMe Blog

23andMe Blog Team

FDA Adds Boxed Warning to Plavix Label to Highlight Reduced Effectiveness of the Drug In Poor Metabolizers

<img loading="lazy" decoding="async" class="alignright size-full wp-image-3242" title="colon" src="https://blog-api.23andme.com/wp-content/uploads/2009/04/colon.jpg" alt="" width="360" height="240" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/04/colon.jpg 360w, https://blogcms.23andme.com/wp-content/uploads/2009/04/colon-300x200.jpg 300w" sizes="auto, (max-width: 360px) 100vw, 360px" />

<a href="http://www.nlm.nih.gov/medlineplus/colorectalcancer.html" target="_blank" rel="noopener">Colorectal cancer</a> is the third most common cancer (excluding skin cancers) and the second leading cause of cancer-related deaths in the United States.
Each year about 150,000 people are diagnosed with the disease.
Risk factors for colorectal cancer include age (most cases occur in people over 50), ethnicity (African Americans and Ashkenazi Jews have particularly high rates of the disease), a personal history of colon polyps or colorectal cancer, and the presence of inflammatory bowel disease (Crohn&#8217;s disease or ulcerative colitis).  
Obesity, physical inactivity, smoking and heavy drinking have also all been associated with increased risk for colorectal cancer.
Genetics contribute to a person&#8217;s colorectal cancer risk, although non-genetic factors seem to play a larger role.  
About 5% of people with colorectal cancer, however, develop the disease as a result of either <a href="http://www.clevelandclinic.org/registries/inherited/fap.htm" target="_blank" rel="noopener">familial adenomatous polyposis</a> (FAP) or <a href="http://www.mayoclinic.com/health/lynch-syndrome/DS00669" target="_blank" rel="noopener">Lynch syndrome</a>, two cancer syndromes caused by serious genetic mutations.
Anyone with a family history of colorectal cancer should talk to their health care professional about what screening procedures, and possibly what genetic tests, are right for them.
Research to find common genetic variants associated with colorectal cancer risk has yielded several good associations, but together they explain only a small part of the genetic contribution to the disease.
There are probably many more variants with small effects left to be found, as well as rare variants with larger effects.   
Learn More About Your Risk
Several online tools are available to help you get a better idea of your risk for colorectal cancer.

<ul>
<li>National Cancer Institute </li>
<li><a href="http://www.siteman.wustl.edu/crc.aspx?id=459" target="_blank" rel="noopener">Washington University School of Medicine Siteman Cancer Center </a></li>
<li>My Family Health Portrait &#8211; a free online tool provided by the Surgeon General that can help you assemble your family&#8217;s health history</li>
</ul>
Get Involved
You can contact the following organizations to learn more about colorectal cancer and find out how to get involved in Colorectal Cancer Awareness Month.
<ul>
<li><a href="http://www.ccalliance.org/" target="_blank" rel="noopener">Colon Cancer Alliance</a></li>
<li><a href="http://www.cancer.org/docroot/home/index.asp" target="_blank" rel="noopener">American Cancer Society</a></li>
</ul>
And for those who want an up-close lesson about colorectal cancer, click <a href="http://www.preventcancer.org/education2c.aspx?id=3794" target="_blank" rel="noopener">here</a> to see if the Prevent Cancer Super Colon is coming to a town near you.

March is Colorectal Cancer Awareness Month

<img loading="lazy" decoding="async" class="alignright size-full wp-image-6082" title="iStock_000004774463XSmall" src="https://blog-api.23andme.com/wp-content/uploads/2010/03/iStock_000004774463XSmall.jpg" alt="" width="332" height="220" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/03/iStock_000004774463XSmall.jpg 425w, https://blogcms.23andme.com/wp-content/uploads/2010/03/iStock_000004774463XSmall-300x199.jpg 300w" sizes="auto, (max-width: 332px) 100vw, 332px" />
Researchers have identified several genetic variations associated with the timing of a baby&#8217;s first tooth and the number of teeth at age one. The results, published recently in the journal <a href="http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1000856" target="_blank" rel="noopener">PLoS Genetics</a>, could be important for understanding more about human health than just this rite of passage all babies must go through.
Nascent teeth form in the womb, but for most babies the first one doesn&#8217;t poke through the gums until sometime<a href="http://www.babycenter.com/0_developmental-milestones-teething_6574.bc" target="_blank" rel="noopener"> between four and seven months</a> of age. Some little ones, however, begin teething as early as three months, while others may take a year or more to sprout their first pearly whites. Although the genetic bases for many syndromes involving serious problems with tooth formation have been discovered, until now not much work has been done to understand how our DNA impacts the normal variation in teething seen in the population.
British and Finnish researchers analyzed the DNA of about 6,000 people (approximately 1,500 from the U.K. and 4,500 from Finland) who had been followed by epidemiologists since early in their mothers&#8217; pregnancies. Genetic variants in 10 different regions of the genome had at least a suggestive link to age at first tooth eruption and/or number of teeth at one year. Those SNPs with statistically significant associations with at least one of the traits are shown in the table below.
<img loading="lazy" decoding="async" class="alignright size-full wp-image-6079" title="plos_figure" src="https://blog-api.23andme.com/wp-content/uploads/2010/03/plos_figure.jpg" alt="" width="333" height="238" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/03/plos_figure.jpg 450w, https://blogcms.23andme.com/wp-content/uploads/2010/03/plos_figure-300x215.jpg 300w" sizes="auto, (max-width: 333px) 100vw, 333px" />Subjects are classified by the number of delayed tooth eruption alleles. SNPs are chosen so that they had the strongest signal for number of teeth at each locus. Mean time of first tooth eruption is plotted in red and number of teeth by the age of one year in black. The bars represent the number of individuals for each count of ‘delayed tooth eruption’ alleles. The line through points is a linear regression fit. doi:10.1371/journal.pgen.1000856.g002 

Much as has been the case for genetic associations with <a href="https://blog.23andme.com/2008/04/07/snpwatch-large-studies-find-snps-with-small-effects-on-height/" target="_blank" rel="noopener">height</a>, another highly heritable and complex human trait, the variations the researchers linked with teething characteristics explain only a tiny fraction–about 3-4%–of the total variance seen in the population. More studies, with larger samples, will be needed in order to identify more SNPs, including those with smaller effect sizes and rare variants.
Based on the significant SNPs found in the study, the authors defined a summary statistic called the &#8220;delayed tooth eruption measure,&#8221; which is calculated by adding up how many copies of the &#8220;delayed&#8221; version of each SNP a person carries. For women the total possible is 10 (two copies of each of five SNPs). Because one of the SNPs is on the X chromosome, for men the total possible is nine.
Based on the Finnish sample, the researchers calculated that individuals with a delayed tooth eruption measure of eight or more have an average of 1.5 fewer teeth at 12 months of age, and later tooth eruption by 1.1 months, compared to individuals with a score of three or less.
The researchers also evaluated whether or not any of the SNPs found in their study of infant teething were associated with the need for orthodontic treatment by age 31 in their Finnish sample. The only significant finding was a SNP that showed only suggestive evidence for an association with timing of first tooth eruption and number of teeth at age one (i.e., it is not in the table above). Each G at increased the odds of requiring orthodontic treatment by 1.35 times.
All of the SNPs identified in this study are in or around genes known to have roles in organ formation, growth and development, or cancer. The authors suggest that studies of teething and other aspects of infant development may have far reaching implications.
&#8220;The discoveries of genetic and environmental determinants of human development will help us to understand the development of many disorders which appear later in life. We hope also that these discoveries will increase knowledge about why fetal growth seems to be such an important factor in the development of many chronic diseases, &#8221; said Professor Marjo-Riitta Jarvelin, the study&#8217;s senior author, in a press release.

SNPwatch: Researchers Identify Variations Associated with When Junior Gets His First Chompers

The Final Episode of Faces of America

<img loading="lazy" decoding="async" class="alignright size-medium wp-image-6064" title="heartrhythm" src="https://blog-api.23andme.com/wp-content/uploads/2010/02/heartrhythm-300x209.jpg" alt="" width="300" height="209" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/02/heartrhythm-300x209.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2010/02/heartrhythm.jpg 350w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Atrial fibrillation (AF) is the most common irregular heart rhythm, affecting one in four people over the age of 40. While not usually life-threatening on its own, individuals with the condition are at increased risk of stroke and heart failure. AF appears most frequently in older, male individuals with a history of obesity or cardiovascular problems, but some people develop it at a young age and with no obvious heart disease. This type of AF, known as “lone” AF, tends to run in families but is otherwise difficult to diagnose.
<a href="https://blog.23andme.com/articles/snpwatch-genetic-variation-may-increase-risk-of-atrial-fibrillation-and-stroke/">Previous studies</a> covered by The Blog have linked common genetic variants to AF, but these studies have focused mainly on the typical, later-onset type of AF. Led by Patrick Ellinor and Stefan Kaab, a group of researchers from the United States and Europe investigated the genetic basis for lone AF in a group of about 1,300 people of European ancestry with the condition and more than 12,000 people without AF. Their study, published this week in <a href="https://dx.doi.org/10.1038/ng.537">Nature Genetics</a>, connected the genetic variant with increased risk of lone AF.
The variant is located near KCNN3, a gene that codes for an ion channel responsible for controlling the movement of potassium in and out of cells. KCNN3 ion channels in particular are found in “excitable” tissues such as the brain and heart. In mice, abnormalities in the behavior of the KCNN3 gene have been associated with increased blood pressure, but the exact role of KCNN3 in the human heart is unclear. Further research is needed to explore whether KCNN3 may have therapeutic applications for treatment of AF.

Genetic Variant Associated With Lone Atrial Fibrillation

<img loading="lazy" decoding="async" class="alignright size-full wp-image-3461" title="africaglobe" src="https://blog-api.23andme.com/wp-content/uploads/2009/04/africaglobe.jpg" alt="" width="261" height="260" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/04/africaglobe.jpg 347w, https://blogcms.23andme.com/wp-content/uploads/2009/04/africaglobe-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2009/04/africaglobe-300x300.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2009/04/africaglobe-271x271.jpg 271w" sizes="auto, (max-width: 261px) 100vw, 261px" />
The journal Current Biology has a special review issue on the global genetic history of Homo sapiens.   The articles are written for a fairly technical audience, but if it&#8217;s a topic you&#8217;re interested in, you might want to check it out.   All of the articles are available online for free.
<ul>
<li><a href="http://www.cell.com/current-biology/fulltext/S0960-9822%2809%2902071-5" target="_blank" rel="noopener">Archaeogenetics – Towards a ‘New Synthesis’?</a></li>
<li><a href="http://www.cell.com/current-biology/fulltext/S0960-9822%2809%2902065-X" target="_blank" rel="noopener">The Evolution of Human Genetic and Phenotypic Variation in Africa</a></li>
<li><a href="http://www.cell.com/current-biology/fulltext/S0960-9822%2809%2902069-7" target="_blank" rel="noopener">The Archaeogenetics of Europe</a></li>
<li><a href="http://www.cell.com/current-biology/fulltext/S0960-9822%2809%2902068-5" target="_blank" rel="noopener">The Human Genetic History of South Asia</a></li>
<li><a href="http://www.cell.com/current-biology/fulltext/S0960-9822%2809%2902067-3" target="_blank" rel="noopener">The Human Genetic History of East Asia: Weaving a Complex Tapestry</a></li>
<li><a href="http://www.cell.com/current-biology/fulltext/S0960-9822%2809%2902120-4" target="_blank" rel="noopener">The Human Genetic History of Oceania: Near and Remote Views of Dispersal</a></li>
<li><a href="http://www.cell.com/current-biology/fulltext/S0960-9822%2809%2902066-1" target="_blank" rel="noopener">The Human Genetic History of the Americas: The Final Frontier</a></li>
<li><a href="http://www.cell.com/current-biology/fulltext/S0960-9822%2809%2902070-3" target="_blank" rel="noopener">The Genetics of Human Adaptation: Hard Sweeps, Soft Sweeps, and Polygenic Adaptation</a></li>
</ul>

Attention Human Genetic History Buffs

<img loading="lazy" decoding="async" class="alignright wp-image-6020 size-full" title="itpa" src="http://35.88.189.111/wp-content/uploads/2010/02/itpa.jpg" alt="Illustration of ITPA protein structure" width="350" height="238" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/02/itpa.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2010/02/itpa-300x204.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
People chronically infected with the hepatitis C virus currently have only one treatment option. The treatment combines polyethylene glycol (PEG)-related interferon-alpha and ribavirin (RBV).
This drug regimen fails to eradicate the virus in about half of all patients who receive it, but even when it does work. Not only that, but the side effects can be so harmful that treatment has to be scaled back or abandoned altogether.
<h2>New Research</h2>
In up to two-thirds of all hepatitis C patients, RBV treatment leads to the destruction of red blood cells. In addition, it decreases the amount of oxygen that can be transported throughout the body, a condition called hemolytic anemia.
New research, published online yesterday in the journal <a href="https://dx.doi.org/10.1038/nature08825" target="_blank" rel="noopener noreferrer">Nature</a>, shows that genetic variants that cause a usually benign enzyme deficiency actually offer some protection against this condition.
The study was conducted by researchers Jacques Fellay, Alexander Thompson, and Dongliang Ge at Duke, along with colleagues from the Schering-Plough Research Institute and the Johns Hopkins School of Medicine. Together, they studied about 1300 European Americans, 200 African Americans, and 100 Hispanics receiving hepatitis C treatment.
The patients had their hemoglobin (the oxygen-carrying protein in red blood cells) levels measured at the beginning of their treatment. Then, measured again at the four-week mark. This is when many patients must begin treatment to stimulate red blood cell production due to RBV-induced anemia.
The researchers also analyzed the patient&#8217;s DNA. They looked for genetic variants associated with hemoglobin level changes.
<h2>Genetic Variants of Interest</h2>
The researchers found several variants on chromosome 20 had a significant association with maintaining good hemoglobin levels after RBV treatment.   A deeper analysis of this DNA region revealed that the effect could be traced to two variations in the ITPA gene.
The ITPA gene encodes an enzyme that helps break down a substance called inosine triphosphate in cells.
The less common versions of the two variants the researchers identified reduce the ITPA enzyme&#8217;s function.
In most people this isn&#8217;t a problem.   For people taking drugs called thiopurines, which are used to prevent organ rejection in transplant patients and to treat leukemias and autoimmune disease, reduced ITPA activity may lead to<a href="https://www.ncbi.nlm.nih.gov/pubmed/19151640?ordinalpos=1&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&amp;linkpos=5&amp;log$=relatedreviews&amp;logdbfrom=pubmed" target="_blank" rel="noopener noreferrer"> toxicity</a>.   What the new study found is that for people receiving treatment for hepatitis C, less ITPA enzyme function is actually a good thing.
Of the people in the current study predicted to have less than one-third of the normal ITPA activity due to their genetics, none ended up with hemoglobin levels below the level traditionally set as a threshold for RBV dose reduction.   Of those with normal ITPA levels, 11.7% had their hemoglobin levels dip into the danger zone.
<h2>Looking Ahead</h2>
More research into the genetics of RBV-induced anemia will be needed.   The exact effect varied among the different populations studied, the researchers estimate that about 20-30% of the variability in hemoglobin level reduction in response to RBV treatment was explained two variants.   There was no significant association between these SNPs and the efficacy of hepatitis C treatment.
Because having low levels of ITPA enzyme activity do not seem to cause problems for most people.
The authors suggest that drugs that inhibit this enzyme could be developed so that people receiving RBV treatment for hepatitis C could be protected against anemia. Even if they do not carry the protective genetic variations.
Illustration of ITPA protein structure: <a href="https://en.wikipedia.org/wiki/File:Protein_ITPA_PDB_2car.png" target="_blank" rel="noopener noreferrer">Emw</a>

Enzyme Deficiency May Protect Against Serious Hepatitis C Treatment Side Effect

<img loading="lazy" decoding="async" class="alignright size-full wp-image-6003" title="bushmen" src="https://blog-api.23andme.com/wp-content/uploads/2010/02/bushmen.jpg" alt="" width="350" height="232" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/02/bushmen.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2010/02/bushmen-300x199.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />Group of hunters from the Ju/’hoansi tribe in the Namibian Bush/ Stephan C. Schuster
Researchers from Penn State University, the University of New South Wales in Australia, and the Baylor College of Medicine have sequenced the genomes of four individuals from different groups of the click-speaking San of southern Africa, as well as of Bishop Desmond Tutu of South Africa.   Their results, published online yesterday in the journal <a href="https://dx.doi.org/10.1038/nature08795" target="_blank" rel="noopener">Nature</a>, are providing striking new insights into human genetic diversity.
Joanna Mountain, 23andMe&#8217;s Senior Director of Research, has been studying the genetics of click-speaking peoples of Africa for over ten years.   Dr. Mountain said the new study &#8220;has demonstrated that any two San individuals are as genetically different from one another as a European and a Chinese individual. Clearly the linguistic diversity of the San is matched or even exceeded by their genetic diversity. Furthermore, even though the San Bushmen are often described, even by this study&#8217;s authors, as the &#8216;oldest known lineage of modern humans,&#8217; the new genetic data reveal that the San have evolved genetically as much as any group, partly through the random mutations that occur over time, but also through changes that enabled them to handle their often challenging, exceedingly dry environment.&#8221;
Read more about this study:
<ul>
<li><a href="https://www.nytimes.com/2010/02/18/science/18genome.html" target="_blank" rel="noopener">New York Times</a></li>
<li>Technology Review</li>
<li>Not Exactly Rocket Science</li>
</ul>

Southern African Genomes Sequenced

<img loading="lazy" decoding="async" class="alignright size-full wp-image-5986" title="iStock_000000081817XSmall" src="https://blog-api.23andme.com/wp-content/uploads/2010/02/iStock_000000081817XSmall.jpg" alt="" width="364" height="273" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/02/iStock_000000081817XSmall.jpg 400w, https://blogcms.23andme.com/wp-content/uploads/2010/02/iStock_000000081817XSmall-300x225.jpg 300w" sizes="auto, (max-width: 364px) 100vw, 364px" />
The candles on your birthday cake tell you how many years you&#8217;ve lived through, but they might not be a reflection of your biological age.
Little bits of DNA called telomeres protect the ends of chromosomes.   Over time, through repeated rounds of cell division, telomeres get shorter and shorter.   Thus, telomere length is a marker of biological aging. Research recently published in the journal <a href="https://dx.doi.org/10.1038/ng.532" target="_blank" rel="noopener noreferrer">Nature Genetics</a> that found a common DNA variation associated with telomere length suggests that some people are genetically programmed to age at a faster rate.
Researchers from the University of Leicester and King&#8217;s College London analyzed the DNA of more than 12,000 Europeans.   They found that each copy of the less common G version of the SNP was associated with about a 75 base pair reduction in average telomere length.   This is equivalent to about 3.6 years of biological aging as measured by telomere length loss.
This finding could have important implications because biological aging isn&#8217;t just a matter of wrinkles and aching joints.   Shorter telomeres have been linked with age-associated conditions such as heart disease and certain types of cancer.   But that&#8217;s not to say that people with variants that predict shorter telomeres should give up on doing all they can to keep young.
&#8220;Genetically susceptible people may age even faster when exposed to proven &#8216;bad&#8217; environments for telomeres like smoking, obesity or lack of exercise–and end up several years biologically older and succumbing to more age-related disease,&#8221; said one of the study&#8217;s senior authors, Tim Spector of King&#8217;s College London, in a<a href="http://www.eurekalert.org/pub_releases/2010-02/uol-sif020410.php" target="_blank" rel="noopener noreferrer"> press release</a>.
<ul>
<li>A previous Blog post about telomeres can be found <a href="https://blog.23andme.com/2008/08/26/snpwatch-too-short-too-fast-%E2%80%93-a-genetic-variation-associated-with-telomere-length/" target="_blank" rel="noopener noreferrer">here</a>.</li>
<li>You may have heard about telomeres in the news recently: The <a href="http://nobelprize.org/nobel_prizes/medicine/laureates/2009/illpres.html" target="_blank" rel="noopener noreferrer">Nobel Prize in Physiology or Medicine 2009 </a>was awarded jointly to Elizabeth Blackburn, Carol Greider and Jack Szostak &#8220;for the discovery of how chromosomes are protected by telomeres and the enzyme telomerase.&#8221;</li>
</ul>

Latest Posts — Page 178