<img loading="lazy" decoding="async" class="alignright size-full wp-image-6500" title="latino_faces" src="https://blog-api.23andme.com/wp-content/uploads/2010/05/latino_faces.jpg" alt="" width="400" height="265" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/05/latino_faces.jpg 400w, https://blogcms.23andme.com/wp-content/uploads/2010/05/latino_faces-300x199.jpg 300w" sizes="auto, (max-width: 400px) 100vw, 400px" />
Latin America is the home of dances as varied as the stately rumba and the racy salsa. It ranges over searing deserts, rocky heights, and sultry jungles. Perhaps it should not be a surprise, as a new study published this week in the <a href="https://dx.doi.org/10.1073/pnas.0914618107" target="_blank" rel="noopener noreferrer">Proceedings of the National Academy of Sciences</a> shows, that its people run the genetic gamut as well.
Researchers from NYU and Stanford gathered DNA from 100 people, each with ancestry from one of four Latin American populations: Colombian, Dominican, Ecuadorian, and Puerto Rican. History tells us to expect that these Latino populations should be a mixture of Native American, European, and African populations. By comparing the Latino DNA with reference individuals&#8217; DNA from these three source populations, using an analysis similar to that of 23andMe&#8217;s <a href="https://blog.23andme.com/articles/new-feature-ancestry-painting" target="_blank" rel="noopener noreferrer">Ancestry Painting</a> feature, the researchers found stark genetic differences between the Latino groups, and between individuals within each group.
The study found that Latino populations differ markedly in the contribution of the source populations. In Ecuador and Colombia, there is typically little African contribution to ancestry, and most individuals are genetic mixes of European and Native American. But in the Caribbean locations of Puerto Rico and the Dominican Republic, at the western reach of the African slave trade, people typically include substantial African ancestry.
Within each of these populations, individuals vary widely in their genetic ancestry composition. In the Colombian sample, for instance, there are individuals that are essentially fully European, people that are 50/50 European/Native American, and people that are 40/40/20 European/African/Native American.
Besides being a fascinating exploration of natural history, this study suggests that there may be practical consequences to Latin American genetic diversity. This is because medical genetic research can be more difficult in diverse populations. In the case of <a href="https://www.genome.gov/20019523" target="_blank" rel="noopener noreferrer">association studies</a>, the name of the game is to study two groups of people who differ only with respect to whether they have the disease of interest or not; people in the disease group should have the same mix of age, gender, ancestry, etc. as in the non-disease group. The genetic diversity of Latin American populations may hinder such studies because of the difficulty in building genetically-matched groups. The study&#8217;s authors suggest that new techniques may need to be developed to carry out genetic research in Latin America.

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The Widely Whirled New World: A Fresh Look at Latino Genetic Ancestry

<img loading="lazy" decoding="async" class="alignright size-full wp-image-6487" title="neanderthal_bones" src="https://blog-api.23andme.com/wp-content/uploads/2010/05/neanderthal_bones.jpg" alt="" width="309" height="371" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/05/neanderthal_bones.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2010/05/neanderthal_bones-249x300.jpg 249w" sizes="auto, (max-width: 309px) 100vw, 309px" />This picture shows three bones (Vi33.16, Vi33.25, Vi33.26) from Vindija cave, Croatia. Most of the Neandertal genome sequence was retrieved from these bones./ Image courtesy of Max-Planck-Institute EVA
A new study of the Neanderthal genome, published online today in the journal <a href="https://dx.doi.org/10.1126/science.1188021" target="_blank" rel="noopener noreferrer">Science</a>, presents strong evidence that humans and Neanderthals interbred.
There&#8217;s been a lot of debate about this subject in scientific circles (see this <a href="https://blog.23andme.com/2008/10/27/did-neanderthals-and-humans-mate-absence-of-evidence-is-not-evidence-of-absence/" target="_blank" rel="noopener noreferrer">Blog post</a> and the links within it) over the last few years. &nbsp; Even some of the researchers involved in the current study previously said they thought human-Neanderthal couplings were unlikely.
ScienceNews and <a href="http://arstechnica.com/science/news/2010/05/neanderthal-genome-draft-done-indicates-interbreeding-occurred.ars?utm_source=rss&amp;utm_medium=rss&amp;utm_campaign=rss" target="_blank" rel="noopener noreferrer">Ars Technica&#8217;s Nobel Intent </a>both have good overviews of the new study and what it means. &nbsp; Ars Technica&#8217;s John Timmer gives a great summary of why scientists now think that rather than replace Neanderthals, our human ancestors instead assimilated them:
<blockquote>At the same time, the genome sequence does provide evidence that humans and Neanderthals have interbred. This became apparent when the Neanderthal genome was paired against human genomes from different parts of the globe. The Neanderthal DNA consistently matched European and Asian samples better than it did African; the difference was small, but consistent. It suggested that the Neanderthals, which were restricted to Europe and Asia at the time modern humans originated in Africa, had interbred with humans once they began migrating out of Africa.
Because African human populations are older, they tend to have more divergent genomes. But the human-Neanderthal split is older still, so the authors figured that any areas of the genome where variation was larger in populations outside of Africa may have entered the human genome through interbreeding. If they did arise through interbreeding, then the non-African segments should match Neanderthals. Researchers found at least 10 regions that fit these predictions.
Although they can&#8217;t rule out the possibility that modern humans had already started diverging from Neanderthals before leaving Africa, the research team favors the idea of interbreeding in the Mid-East as the first modern humans left Africa. This would ensure that both the Asian and European populations picked up some Neanderthal DNA.</blockquote>
Be sure to check out the Science Magazine Neanderthal Genome Special Feature (free).

New Evidence Suggests Interbreeding Between Humans and Neanderthals

<img loading="lazy" decoding="async" class="alignright size-full wp-image-6465" title="Tummy Time!" src="https://blog-api.23andme.com/wp-content/uploads/2010/04/iStock_000001348449XSmall.jpg" alt="" width="355" height="235" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/04/iStock_000001348449XSmall.jpg 425w, https://blogcms.23andme.com/wp-content/uploads/2010/04/iStock_000001348449XSmall-300x199.jpg 300w" sizes="auto, (max-width: 355px) 100vw, 355px" />
Multiple sclerosis (MS) is an autoimmune disease that affects the central nervous system, causing unpredictable and varying symptoms that differ from person to person. About 1 in 700 people in the United States is affected by the disease. Because MS often runs in families, it&#8217;s thought that there is a substantial genetic component to the disease.
But genetics aren’t the whole story.   If one identical twin has MS, the chance that the other twin will also have the disease is increased by only 30%. Although this is more than the 5% increase in risk seen in non-identical twins, the fact that identical twins (who are theoretically completely the same at the DNA level) are not always concordant for MS has led researchers to assume that environmental factors of some sort must also play an important role.   Everything from viral infections to vitamin D deficiency due to low sun exposure has been suggested.
But the true identical-ness of identical twins has been called into question in recent years.   Research has shown that there may be subtle differences in their genomes.   To test whether tiny changes–either in DNA sequence, gene expression, or chemical modifications to the genome–might play a role in determining why one twin gets MS while the other is spared, researchers from the University of California, San Francisco and the National Center for Genome Resources used a variety of methods to go over the genomes of three sets of MS-discordant identical twins in unprecedented detail.
No matter how the scientists looked at the twins&#8217; genetics, nothing stood out to explain their differences in disease status.   These results, published online today in the journal <a href="https://dx.doi.org/10.1038/nature08990" target="_blank" rel="noopener">Nature</a>, are strong evidence that when it comes to MS, identical twins might enter the world with the same risk, but their individual experiences and exposures determine whether each one will get the disease.
The data from just these three twin pairs gives researchers important information about the relative contributions of genetic and environmental factors in MS.   But more work will be needed to replicate these results and to look even more closely at individual genomes.   The study&#8217;s lead author Sergio Baranzini said in a press release that his team will be able to broaden their study and look at even more twin pairs thanks to steady reductions in the cost of genome sequencing.
More on this story from <a href="https://www.nature.com/news/2010/100428/full/4641259a.html?s=news_rss" target="_blank" rel="noopener">Nature News</a>, <a href="https://www.wired.com/wiredscience/2010/04/multiple-sclerosis-twinmystery/" target="_blank" rel="noopener">Wired News</a> and TheScientist.com.
(23andMe customers can get an estimate of their genetic risk for MS based on analysis of two SNPs in the Multiple Sclerosis Research Report.)

Twin Study Points to Importance of Non-genetic Factors in Multiple Sclerosis

<img loading="lazy" decoding="async" class="alignright size-full wp-image-6445" title="elderly_1" src="https://blog-api.23andme.com/wp-content/uploads/2010/04/elderly_1.jpg" alt="" width="337" height="223" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/04/elderly_1.jpg 425w, https://blogcms.23andme.com/wp-content/uploads/2010/04/elderly_1-300x199.jpg 300w" sizes="auto, (max-width: 337px) 100vw, 337px" />
New research, published recently in the journal <a href="https://dx.doi.org/10.1212/WNL.0b013e3181d9edba " target="_blank" rel="noopener">Neurology</a>, has found the surprising result that a genetic variant previously associated with better cognitive function in young people appears to have the opposite effect as people get older.
Alexandra Fiocco and colleagues from the University of California, San Francisco, studied 2,858 men and women (1,679 white and 1,179 black) who were between the ages of 70 and 79 upon recruitment to the study in 1997.   All were in generally good health and had no difficulty with day-to-day activities.
Each person was given two tests at various points over an eight year follow up period: 1) the Modified Mini-Mental State Examination, a measure of global cognitive performance; and 2) the Digit Symbol Substitution Test, which measures response speed, sustained attention, visual spatial skills and set shifting, and has been reported to distinguish mild dementia from healthy aging.
The study participants&#8217; cognitive test results were then compared with their genotypes.   This genetic variant associated with cognitive decline is found in the COMT (catechol-O-methyltransferase) gene, which encodes an enzyme involved in a variety of chemical conversions in the body, including the degradation of the neurotransmitter dopamine.   The different versions of encode COMT proteins with either a valine (Val) or methionine (Met) at amino acid 158.   The Val version of COMT is associated with higher COMT enzyme activity, and therefore lower levels of dopamine in the brain, while the Met version is associated with lower enzyme activity and higher dopamine levels.
In experiments carried out mainly in younger people, the Met version of COMT has been shown to be associated with better cognitive function.
Fiocco, et al., however, found that it was the Val version of COMT that was associated with less cognitive decline over the course of eight years in the elders they studied.   In both white and black subjects, the Val version correlated with smaller reductions in Digit Symbol Substitution test scores.   In white subjects only, the Val version was also associated with smaller declines in Modified Mini-Mental State Examination scores.
Why might the Val version of COMT have a protective effect against cognitive decline?   The authors suggest that the higher levels of COMT activity, and thus lower levels of dopamine in the brain, associated with the Val version might be better for optimal cognitive function in older adults due to the fact that there is a reduction in dopamine receptors in the brain as people age.
In support of this, they point to data showing that the brains of people with dementia have decreased levels of COMT enzyme activity.
Results from a few other studies in older adults contradict the findings of the current report.   That, combined with the fact that the Val/Met variation in the gene appears to have opposite effects in younger people, means that much more research will be needed to truly understand the role of COMT in cognition.

Genetic Variant May Impact Rate of Cognitive Decline in the Elderly

<img loading="lazy" decoding="async" class="alignright size-full wp-image-6408" title="eggs flour and milk" src="https://blog-api.23andme.com/wp-content/uploads/2010/04/iStock_000008849940XSmall.jpg" alt="" width="360" height="240" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/04/iStock_000008849940XSmall.jpg 424w, https://blogcms.23andme.com/wp-content/uploads/2010/04/iStock_000008849940XSmall-300x200.jpg 300w" sizes="auto, (max-width: 360px) 100vw, 360px" />
For the millions of children and adults with severe food allergies, ingesting even tiny quantities of some of the most basic foods can result in a potentially deadly reaction.   Milk, eggs, nuts, fish, shellfish, soy and wheat are some of the most common offenders.
<h2>What is Eosinophilic esophagitis?</h2>
Some people with food sensitivities have something more than just a food allergy.   Eosinophilic esophagitis (EoE) is a condition in which exposure to certain foods causes the inappropriate migration of immune cells called eosinophils to the lining of the esophagus, where they release factors that lead to inflammation and swelling.
This can result in feeding difficulties and failure to thrive in young children, and difficulty in swallowing in adults.   Other symptoms include heartburn, vomiting and food impaction in the esophagus.   About one in 10,000 people is thought to have EoE, although some researchers think this may be an underestimate.
<h2>The Genetics of Eosinophilic esophagitis</h2>
Studies indicate that EoE has a strong genetic component, but previous research has linked only one gene to the condition.   However, in a recent issue of the journal <a href="https://dx.doi.org/10.1038/ng.547" target="_blank" rel="noopener noreferrer">Nature Genetics</a>, researchers from Cincinnati Children&#8217;s Hospital Medical Center and the Children&#8217;s Hospital of Philadelphia presented results of a genome-wide associations study of EoE that indicate that a gene known to play a role in asthma and <a href="https://blog.23andme.com/articles/snpwatch-genetic-variation-may-increase-risk-for-atopic-dermatitis">atopic dermatitis</a> (a type of <a href="https://blog.23andme.com/articles/new-23andme-eczema-report">eczema</a>) is also associated with the condition.
A total of 351 people with EoE and 3,140 unaffected controls, all children and young adults of European ancestry, were studied to find genetic variations associated with the condition.
<h2>The TSLP Protein</h2>
The strongest association with EoE revealed by the DNA analysis was with a SNP near the TSLP gene.  One variant in the gene is slightly protective, while the other increases the likelihood of developing the condition.
The researchers looked at esophagus tissue samples to learn more about TSLP.   They found that the gene is turned on at higher levels in people with EoE, and that there is a correlation between having the protective variant and levels of the TSLP protein.
The TSLP protein is known to regulate inflammatory responses.   It is a key initiator of allergic inflammatory diseases and has been shown to be overproduced in atopic dermatitis lesions and asthma-affected lungs.   People with EoE often also suffer from these other allergic conditions.
&#8220;Eosinophilic esophagitis is a highly allergic disease, and one that is rapidly expanding,&#8221; said Jonathan M. Spergel, director of the Center for Pediatric Eosinophilic Disorders at the Children&#8217;s Hospital of Philadelphia and a co-first author of the study, in a press release.
&#8220;This is the first genome-wide association study done of this disease, and now that we have elucidated a gene pathway, the hope is that physicians can eventually intervene in that pathway and discover a new treatment.&#8221;

Genetic Variant Associated with Food Allergy-related Disorder Eosinophilic Esophagitis

<img loading="lazy" decoding="async" class="alignright size-full wp-image-6398" title="sarcoma-large" src="https://blog-api.23andme.com/wp-content/uploads/2010/04/sarcoma-large1.jpg" alt="" width="315" height="257" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/04/sarcoma-large1.jpg 315w, https://blogcms.23andme.com/wp-content/uploads/2010/04/sarcoma-large1-300x245.jpg 300w" sizes="auto, (max-width: 315px) 100vw, 315px" />
Sarcomas are an extremely rare set of cancers that affect the bone and connective tissues such as muscle, bone, fat, cartilage, tendons, blood vessels, and the like. With the launch of the new Sarcoma Community, &nbsp;23andMe hopes to recruit a research cohort that will serve as a platform for research investigations into the causes and treatment of sarcomas.
Current and former sarcoma patients may participate by being genotyped and completing surveys about their disease and treatment response through the 23andMe web-based research platform. In return for their participation, they will receive access to the full 23andMe experience at no charge. &nbsp; For more information, please go to <a href="https://www.23andme.com/sarcoma" target="_blank" rel="noopener">https://www.23andme.com/sarcoma</a>.
Dr. Robert Maki, MD PhD, a sarcoma medical oncologist, has provided more information about sarcoma to help us raise awareness about this disease:
In 2010, some 13,000 cases of sarcoma will be seen in the United States. &nbsp; This is an extremely small number compared to the total of more than 1.4 million people who are diagnosed with cancer each year in this country. &nbsp; The small number of cases seen, the diversity in the biology of each type, and the variable anatomic site in which each tumor arises, have made understanding of sarcomas difficult. Research into the causes of and best treatments for each type of sarcoma is a high priority.
Diagnosed early, sarcomas are eminently curable. But when they are diagnosed at later stages when the tumors are large or have traveled beyond where they started (metastatic disease), there is a lower chance for a cure.
Treatment depends on the type of sarcoma involved, its site of origin, and whether the tumor has spread. For a “primary” sarcoma (an isolated tumor that has remained in the place it arose), surgery is nearly always a necessary part of treatment. Radiation is used when tumors are large, either before or after surgery, with the hopes of preventing recurrence. For certain types of sarcomas (Ewing sarcoma, osteosarcoma and rhabdomyosarcoma, for example) chemotherapy is also used to help prevent recurrence.
After initial treatment, if a sarcoma returns, the next steps taken depend on the specific clinical situation. In some cases, the tumor can once more be cut out surgically. For others, radiation can be used to control the tumor. If a sarcoma has spread, chemotherapy is the first choice treatment. &nbsp; These drugs, which are taken by mouth or through an I.V., can travel throughout the body to attack all sites of the disease at once.
Clinical trials are always in progress looking for new treatments for sarcomas. &nbsp; Medical oncologists often test new chemotherapy agents in people who have had recurrences of sarcoma that have proven unresponsive to other treatments. &nbsp; Some of these drugs then go on to be assessed for their ability to improve the cure rate among people suffering from their first bout with the disease.
There are almost surely genetic factors involved in sarcoma, but we researchers do not have a good handle on these yet. We expect the next few years to be important in helping oncologists determine genetic and non-genetic risk factors that predispose people to developing sarcomas.
Patients with questions regarding the genetics of their cancers are encouraged to ask their physicians about how best to address the risk to themselves and their family members.

23andMe Launches Sarcoma Community

<img loading="lazy" decoding="async" class="alignright size-full wp-image-1138" title="fundus" src="https://blog-api.23andme.com/wp-content/uploads/2008/08/fundus.jpg" alt="" width="350" height="260" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/08/fundus.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2008/08/fundus-300x223.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
Age-related macular degeneration (AMD) is the most common cause of irreversible vision loss in the western world among people over 60.
The two forms of the disease — wet and dry — both cause vision loss by destroying cells in the central portion of the retina.
<h6>Understanding AMD</h6>
In the last few years, progress in understanding AMD has been made thanks in part to the discovery of several common genetic variants, or SNPs, that together explain a large part of the risk for the disease.
Several of the AMD SNP associations have pointed to a role for the immune system in the disease. Now two new reports of genetic associations, published this week in the Proceedings of the National Academy of Sciences, point to a role for another biological pathway in AMD: HDL-cholesterol level regulation.
<h6>New Research</h6>
Two research groups, one led by scientists from <a href="https://dx.doi.org/10.1073/pnas.0912019107" target="_blank" rel="noopener noreferrer">Tufts University and the Massachusetts General Hospital (MGH)</a> and the other led by researchers from the <a href="https://dx.doi.org/10.1073/pnas.0912702107" target="_blank" rel="noopener noreferrer">University Michigan, the University of Pennsylvania and the Mayo Clinic</a>, each studied thousands of people with and without AMD.  All study subjects had European ancestry.
To increase their ability to find genetic variations associated with the disease, the researchers then shared their data and ran additional analyses.
Several variations previously associated with levels of high-density lipoprotein (HDL) cholesterol, the so-called &#8220;good&#8221; cholesterol, showed some association with AMD risk in the combined analysis.
<h6>The Strongest Genetic Association</h6>
The strongest signal was seen with a variant near the LIPC gene.   Each copy of the less common T version of this SNP was associated with 0.82 times odds of AMD compared to people with two copies of the C version.   The LIPC gene encodes the hepatic lipase enzyme, which is key to metabolism of HDL-cholesterol.
&#8220;This LIPC locus may greatly enhance our biologic understanding by opening up another pathway for consideration in the pathogenesis of AMD.   This finding could lead to insights regarding disease progression, ways to modify risk of AMD, and new treatments,&#8221; wrote the authors from Tufts/MGH.
<h6>The Role of Cholesterol</h6>
There has been previous speculation that cholesterol levels might play a role in AMD risk because cholesterol is a component of <a href="https://en.wikipedia.org/wiki/Drusen" target="_blank" rel="noopener noreferrer">drusen</a>, the deposits found in the retinas of people with the condition.
However, there has not been any clear scientific evidence of whether there is a connection.   Among studies in which a connection between cholesterol levels and AMD has been shown, there is disagreement about whether increased cholesterol levels increase or decrease AMD risk.
Adding to the confusion is the fact that among the cholesterol-related genetic variations, there is no clear-cut direction of effect.   Another version of this variant is associated with decreased AMD risk has been associated with increased blood HDL levels.
But for some of the other cholesterol-related SNPs with more modest associations that were identified in these studies, the association was in the opposite direction: the version associated with decreased AMD risk has been linked to lower HDL levels.
&#8220;We suspect these genetic variations found in the cholesterol pathway impact the retina differently from the circulatory system, so cholesterol levels in the blood may not provide meaningful information about AMD risk,&#8221; said Michigan/Penn/Mayo study lead author Anand Swaroop in a press release.
By combining their data, the two research groups also found evidence that a SNP near the TIMP3 and SYN3 genes is associated with AMD.
Each copy of the less common G version of was associated with 0.62 times odds of the condition compared to people with two copies of the A version.
Mutations in TIMP3 have been shown to induce abnormal blood vessel growth, and the gene has previously been linked to Sorsby&#8217;s fundus dystrophy, a condition with many features in common with AMD.
<h6>A Reevaluation</h6>
However, researchers had previously determined that TIMP3 was not linked to AMD.
The newly published results may lead to a reevaluation of this gene&#8217;s importance.
The authors of the Michigan/Penn/Mayo study acknowledge that because the effects of the SNPs identified in the two new studies are small, and the versions associated with decreased risk are rare, neither variant may be that important for prediction of AMD risk in the general population.
But they echo the sentiment of the authors of the Tufts/MGH study that this research may have identified a biological pathway–HDL cholesterol level regulation–that might be exploited for prevention or treatment.
They note that for psoriasis, an <a href="https://en.wikipedia.org/wiki/Ustekinumab" target="_blank" rel="noopener noreferrer">effective treatment</a> that targets the product of the IL23 gene has been developed, even though common variations in this gene have only a small effect on the overall risk for psoriasis.
Note: Effect sizes of the variants taken from Neale et al., authors of the Tufts/MGH study.

Genetic Associations with Brain Aneurysm

The tenth anniversary of the completion of the first draft of the human genome is approaching, apparently putting a lot of scientists in the mood for reflection on the past and speculation about the future of genetics.
The journal Nature has a series of opinion articles and two news articles on the subject. &nbsp; All are available online free of charge. &nbsp; There are also other human genome related materials available at <a href="https://www.nature.com/news/specials/humangenome/index.html#editorial" target="_blank" rel="noopener noreferrer">The Human Genome at Ten</a>.
<img loading="lazy" decoding="async" class="alignright size-full wp-image-6314" title="81-72" src="https://blog-api.23andme.com/wp-content/uploads/2010/04/81-72.jpg" alt="" width="377" height="282" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/04/81-72.jpg 500w, https://blogcms.23andme.com/wp-content/uploads/2010/04/81-72-300x225.jpg 300w" sizes="auto, (max-width: 377px) 100vw, 377px" />Researchers working at an NHGRI-supported large-scale sequencing center./The Broad Institute of MIT and Harvard/NHGRI multimedia gallery
<ul>
<li><a href="https://www.nature.com/nature/journal/v464/n7289/full/464674a.html" target="_blank" rel="noopener noreferrer">Has the revolution arrived? — Francis Collins</a></li>
<li><a href="https://www.nature.com/nature/journal/v464/n7289/full/464676a.html" target="_blank" rel="noopener noreferrer">Multiple personal genomes await — J. Craig Venter</a></li>
<li><a href="https://www.nature.com/nature/journal/v464/n7289/full/464678a.html" target="_blank" rel="noopener noreferrer">Point: Hypotheses First &#8211; Robert Weinberg</a></li>
<li><a href="https://www.nature.com/nature/journal/v464/n7289/full/464679a.html" target="_blank" rel="noopener noreferrer">Counterpoint: Data first &#8211; Todd Golub</a></li>
<li><a href="https://www.nature.com/news/2010/100331/full/464664a.html" target="_blank" rel="noopener noreferrer">Life is complicated — Erika Check Hayden</a></li>
<li><a href="https://www.nature.com/news/2010/100331/full/464668a.html" target="_blank" rel="noopener noreferrer">The human race — Alison Abbott</a></li>
</ul>
The British Medical Journal features a debate between two scientists over whether modern genetics is &#8220;blind alley.&#8221; &nbsp; These articles are also available free of charge.
<ul>
<li><a href="http://www.bmj.com/cgi/content/full/340/mar30_2/c1156?maxtoshow=&amp;hits=10&amp;RESULTFORMAT=&amp;fulltext=blind+alley&amp;searchid=1&amp;FIRSTINDEX=0&amp;sortspec=date&amp;resourcetype=HWCIT" target="_blank" rel="noopener noreferrer">Is modern genetics a blind alley? Yes — James Le Fanu</a></li>
<li><a href="http://www.bmj.com/cgi/content/full/340/mar30_2/c1088?maxtoshow=&amp;hits=10&amp;RESULTFORMAT=&amp;fulltext=blind+alley&amp;searchid=1&amp;FIRSTINDEX=0&amp;sortspec=date&amp;resourcetype=HWCIT" target="_blank" rel="noopener noreferrer">Is modern genetics a blind alley? No — D J Weatherall</a></li>
</ul>
It&#8217;s not just the anniversary of the draft sequence that looms. &nbsp; DNA Day, which was created in 2003 by a congressional resolution to celebrate the completion of the Human Genome Project and the 50th anniversary of the description of the double-helix structure of DNA by James D. Watson and Francis H.C. Crick, is coming up on April 25th. &nbsp; To accommodate classroom schedules, many events will be taking place on Friday, April 23rd.
We&#8217;ll be rounding up a listing of DNA Day activities in the coming week or so, but you can start your preparations by checking our listing of fun DNA activities.

Latest Posts — Page 176