<img loading="lazy" decoding="async" class="alignright size-full wp-image-2857" title="bloodclot" src="https://blog-api.23andme.com/wp-content/uploads/2009/02/bloodclot.jpg" alt="bloodclot" width="324" height="240" />
A new report in the <a href="http://jama.ama-assn.org/cgi/content/full/302/8/849?home" target="_blank" rel="noopener noreferrer">Journal of the American Medical Association</a> adds to the mounting evidence that genetic variations impact the efficacy of clopidogrel (Plavix ®), a drug used to prevent blood clots in people who have had a heart attack or stroke and also those with peripheral artery disease and unstable angina.
<h6>Drug Response</h6>
Previous research has shown that certain variations in the CYP2C19 gene prevent the body from converting clopidogrel into its active form. That reduces the amount of anti-clotting effect people get from the medication, increasing their risk for heart attacks, strokes and death from cardiovascular causes.
(23ndMe customers can learn how their data fits in with this research in a previous <a href="https://blog.23andme.com/2008/12/23/snpwatch-genetic-variants-may-reduce-ability-of-anti-clotting-drug-clopidogrel-to-prevent-a-second-heart-attack/" target="_blank" rel="noopener noreferrer">Blog</a> post or in the Clopidogrel Efficacy Drug Response Report.)
The researchers, led by Alan Shuldiner of the University of Maryland School of Medicine, determined that BMI, lipid levels and age account for about 10% of the variation in clopidogrel&#8217;s ability to prevent blood clotting. Variation in the CYP2C19 gene accounted for another 12%, meaning that other factors, probably both genetic and non-genetic, are also at work.
<h6>CYP2C19</h6>
For patients whose genetics may reduce the benefits of clopidogrel treatment, there are other options. Prasugrel (Effient ®) was recently approved by the FDA and appears not to be affected by the same variations that impact clopidogrel efficacy, although there are some concerns about bleeding caused by this drug.   Several other drugs (ticagrelor, cangrelor, elinogrel) that could be used for clotting reduction in place of clopidogrel are currently in clinical trials.
Clinical trials have not yet been conducted to show if identifying people with variants of the CYP2C19 before prescribing clopidogrel actually improves health outcomes.   If such studies do show a benefit and this type of testing becomes routine, people with these variants might be steered away from clopidogrel by their doctors, which would seem to be a boon for the makers of newer medications.
<h6>Genetic and Non-Genetic Factors</h6>
But in an editorial accompanying the study in JAMA, <a href="http://jama.ama-assn.org/cgi/content/extract/302/8/896" target="_blank" rel="noopener noreferrer">Deepak Bhatt</a> suggests that testing for these variations would also allow physicians to know for whom clopidogrel will work (probably). This would be an important piece of information considering that the patent on clopidogrel is set to expire in <a href="https://www.reuters.com/article/rbssHealthcareNews/idUSN1843632020090818" target="_blank" rel="noopener noreferrer">2011</a>, so cheaper generic forms of the drug will be available then.
&#8220;Although such testing currently is expensive, the cost will decrease and hopefully will coincide with supportive data.   Furthermore, if such testing allowed use of a less expensive generic anitplatelet drug,&#8221; he writes. &#8220;The test might essentially pay for itself.&#8221;

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More Evidence that Genetics Can Reduce the Efficacy of Anti-Clotting Medication Clopidogrel

<img loading="lazy" decoding="async" class="alignright size-medium wp-image-2057" title="DNA Strand" src="https://blog-api.23andme.com/wp-content/uploads/2008/11/istock_000000628100xsmall-300x225.jpg" alt="DNA Strand" width="300" height="225" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/11/istock_000000628100xsmall-300x225.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2008/11/istock_000000628100xsmall.jpg 400w" sizes="auto, (max-width: 300px) 100vw, 300px" />
A new genetic screening process has helped researchers understand the genetic causes of cancer, such as how mutations accumulated in a person&#8217;s life can cause leukemia.
The study compared a person&#8217;s own DNA to that of their cancerous cells. Using this technique researchers found DNA mutations that may have led to abnormal cell growth, or cancer.
Researchers at Washington University School of Medicine in St. Louis sequenced a single leukemia patient&#8217;s healthy and cancerous DNA. They were able to pinpoint several mutations out of hundreds that appeared likely to have contributed to his cancer&#8217;s development. He is the second patient with acute myeloid leukemia (AML) to have his entire genome and that of his cancerous tissue fully sequenced. Typically only the portions of the genome that are known to be prone to cancer-causing mutations are sequenced.

“If we only look at genes with known or suspected links to cancer, we’ll miss many mutations that are potentially relevant,” co-author Richard Wilson said in statement.
The study by Mardis et al., published in The New England Journal of Medicine,  identified a total of 750 mutations in the patient’s AML genome. Most of them proved irrelevant. However, 64 were likely to be cancer-related. Two previously known mutations were newly linked to leukemia.
<h6>Personalized Sequencing</h6>
Timothy Lay, the senior author of the study, explained that most patients with this type of leukemia are treated similarly, at least in the beginning. This study&#8217;s patient, for example, received various chemotherapy drugs. Defining cancer mutations could help determine which patients need aggressive treatment. So, for example, a stem cell transplant, which could be effectively treated with less intense therapies.
Personalized sequencing of entire cancer genomes is possible now because the accuracy and cost of genome sequencing technology has dramatically improved. This study took only a few months at one-third the cost of the first AML patient, who was sequenced only one year ago.
To date 350 cancer mutations are known, but thousands of cancer genomes will need to be screened to truly explain the genetic basis for cancer. This information could be used not just to guide physicians to the most effective treatment, but also to inform patients about their prognosis.
<h6>Living in the Know</h6>
But do patients even want to know?
A recent study published in the  Journal of Genetic Counseling suggests they do. Researchers found that 98 of 99 patients with ocular melanoma, a rare, untreatable eye cancer, wanted to know. Even if their cancer had a genetic marker that gave them a 50 percent chance of dying within five years. Patients were relieved when the risk was low. However, even when the risk was high they were enabled to plan financially and make the most of their time alive.
This very personalized medicine will continue to be driven by improved diagnostic testing, according to James Downing in a recent editorial in The New England Journal of Medicine. This will identify more predictive disease markers, and lead to new therapies directed at cancer-specific mutations. He believes this technology will likely be used clinically long before we have a complete knowledge of cancer genes.

Revelations from Sequencing of Second Cancer Patient

<img loading="lazy" decoding="async" class="alignright size-full wp-image-4470" title="ManinCrowd" src="https://blog-api.23andme.com/wp-content/uploads/2009/08/ManinCrowd.jpg" alt="ManinCrowd" width="347" height="346" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/08/ManinCrowd.jpg 347w, https://blogcms.23andme.com/wp-content/uploads/2009/08/ManinCrowd-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2009/08/ManinCrowd-300x300.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2009/08/ManinCrowd-271x271.jpg 271w" sizes="auto, (max-width: 347px) 100vw, 347px" />
Nearly a year ago today, the Blog <a title="Blog post of 28 Aug 2008" href="https://blog.23andme.com/2008/08/28/faces-in-a-crowd-new-dna-technique-can-pick-one-persons-dna-signature-out-of-hundreds/">reported</a> that researchers had figured out how to pick a known person&#8217;s DNA out of a database containing genetic information for up to 200 unidentified individuals.
The feat made it possible to determine, for example, if a particular suspect&#8217;s DNA was present in a mix of several peoples&#8217; collected at a crime scene. It also raised the possibility, at least theoretically, that somebody could figure out if a particular person&#8217;s DNA was part of a research database or some other pool of anonymous data.
Now another team of researchers has calculated the limits of this needle-in-a-haystack technique. It turns out that if the number of data points revealed is small enough, an individual&#8217;s DNA can remain undetectable.

Before UCLA geneticist Stan Nelson and his colleagues published their paper last year, it had been a common practice to publish summary data from research DNA collections so members of the genetics community could build on each others&#8217; research. (Note: 23andMe does not share individual-level data without explicit consent, and is working on ways of distributing summary data without compromising privacy.) It was assumed that aggregation would make it impossible to tell whether a particular individual had contributed to that collection. But in the wake of the announcement of the new detection method, major genome centers swiftly <a title="Blog post of 29 Aug 2008" href="https://blog.23andme.com/2008/08/29/labs-remove-genetic-data-from-public-databases-after-forensic-breakthrough/">removed</a> summary data from public view to avoid the possibility of compromising the identity of any research participants.
In a paper published today in <a href="https://www.nature.com/ng/journal/vaop/ncurrent/abs/ng.436.html" target="_blank" rel="noopener">Nature Genetics</a>, researchers from UC Berkeley take the first step towards a less extreme route to protecting individuals&#8217; identities than simply withholding all information. The researchers developed methods to calculate precisely how much genetic information from a research DNA collection may be revealed without risk of exposing the identities of the study participants.
At the heart of the <a href="http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1000167" target="_blank" rel="noopener">PLoS Genetics</a> paper that started the hubbub was a statistical test that the authors used to show that they could reliably tell whether someone was present in a DNA mixture. The new study not only provides an improved version of this test, but proves that the new approach is the best of all possible detection methods. Since no better test could be devised, if theirs is unable to detect whether an individual was part of a mixture of DNA, they can be confident that no test would be able to do it.
Armed with this certainty, the authors explore just how much information from a research DNA collection may be reported without risk of divulging who was in the study. It turns out that for a collection of 1,000 individuals, up to 10,000 individual data points can be revealed with little risk of exposing anyone to identification.
This makes it somewhat easier for geneticists to share their data. But these days an individual&#8217;s genetic data typically consists of a genome-wide panel of 500,000 to a million single-letter DNA variations known as SNPs – so the problem still isn&#8217;t solved completely.

On Finding Needles in Genetic Haystacks

<img loading="lazy" decoding="async" class="alignright size-full wp-image-4436" title="Acute_leukemia-ALL" src="https://blog-api.23andme.com/wp-content/uploads/2009/08/Acute_leukemia-ALL.jpg" alt="Acute_leukemia-ALL" width="330" height="375" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/08/Acute_leukemia-ALL.jpg 347w, https://blogcms.23andme.com/wp-content/uploads/2009/08/Acute_leukemia-ALL-264x300.jpg 264w" sizes="auto, (max-width: 330px) 100vw, 330px" />
Acute lymphoblastic leukemia (ALL) is the most common childhood cancer in developed nations, affecting between 30 and 45 out of every one million kids.   But not much is known about the genetics of the disease.
Two research groups set out to learn more by looking for common genetic variations associated with the disease.   Their results, published online this week in Nature Genetics, provide new insight into the development of ALL.
British researchers led by <a href="https://dx.doi.org/10.1038/ng.430" target="_blank" rel="noopener noreferrer">Elli Papaemmanuil</a> studied a total of 907 ALL cases and 2,398 controls with European ancestry.   They identified three genetic variants associated with increased risk for the disease.
The strongest of these, , is near the IKZF1 gene, which encodes a protein involved in the development of white blood cells.   Deletions of the region of DNA containing this gene are common in forms of ALL that have a poor prognosis.   Each copy of a G at increases the odds of ALL by 1.69 times.
The second most strongly associated SNP was in ARID5B, a gene previously linked to a different form of blood cancer called acute promyelocytic leukemia.   Each copy of a G at was associated with 1.65 times increased odds of ALL.
Finally, Papaemmanuil et al. found that each copy of a G at was associated with 1.34 times increased odds of ALL.
All three SNPs were even more strongly associated with ALL when the researchers restricted their analysis to a subtype of the disease called B-cell ALL.   Within this form of the disease, in ARID5B seems to be highly associated with a further subtype called hyperdiploid ALL.   This form of the disease has a better response to methotrexate chemotherapy than other subtypes of ALL.
The authors conclude that the variations they identified underlie approximately 64% of all cases of ALL.
&#8220;Our findings provide the first unambiguous evidence that common genetic variation influences the risk of developing pediatric ALL and strong rationale for searching for additional risk variants through further GWA [genomewide association] scans,&#8221; the authors write.
In a separate study of 441 ALL cases and 16,912 controls, <a href="https://dx.doi.org/10.1038/ng.432" target="_blank" rel="noopener noreferrer">Lisa Trevino</a> and colleagues from the United States also found evidence for the involvement of variants in and around the ARID5B gene in B-hyperdiploid ALL.   The riskier versions of SNPs closely related to were not only correlated with disease risk, but also with a response to methotrexate that at least partially underlies its greater efficacy in B-hyperdiploid ALL.
&#8220;The data…suggest that the same genetic variation that predisposes to B-hyperdiploid ALL may underlie the superior response of this subtype to chemotherapy.   Thus, genomic variation may affect not only disease risk but treatment outcome as well,&#8221; they write.
Photo: <a href="https://en.wikipedia.org/wiki/File:Acute_leukemia-ALL.jpg" target="_blank" rel="noopener noreferrer">VashiDonsk</a>

Genetic Variants Associated With Risk Of Childhood Acute Lymphoblastic Leukemia Identified

<img loading="lazy" decoding="async" class="alignright wp-image-1965 size-medium" src="http://35.88.189.111/wp-content/uploads/2008/11/hivvirus-300x223.jpg" alt="" width="300" height="223" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/11/hivvirus-300x223.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2008/11/hivvirus.jpg 350w" sizes="auto, (max-width: 300px) 100vw, 300px" />
AIDS used to be considered a male-specific health problem – &nbsp;but now, the majority of its victims are female.
Those numbers aside, <a href="http://aje.oxfordjournals.org/cgi/content/abstract/168/5/532" target="_blank" rel="noopener">some studies</a> have shown that certain females take much longer than males to progress to AIDS after being infected with HIV. Now, researchers have now found a mechanism that might explain this difference.
A two-stage study by Siddiqui et al. identified a genetic variant on the X chromosome that may slow progression from HIV-1 to AIDS in women. The study analyzed both primates and humans, demonstrating that genetic association findings can successfully translate across species, even over an evolutionary distance of 25 million years.

The researchers first analyzed 136 rhesus monkeys infected with SIV (simian immunodeficiency virus). They found a common genetic marker on the X chromosome among those monkeys that progressed slowly to AIDS-related disease. Researchers then studied 303 HIV-infected humans and found an analogous marker on the X chromosome –the SNP &nbsp; – &nbsp;that may affect progression to AIDS in human females.
The results, published in the online version of <a href="http://www.cell.com/AJHG/abstract/S0002-9297(09)00304-8" target="_blank" rel="noopener">The American Journal of Human Genetics</a>, indicate that in humans, females with one copy of the C version of progressed to AIDS more slowly than either females with TT or males with a C or T. (Note that females have two X chromosomes, while males only have one.)
Females with one copy of the C version of the SNP took an average of eight years to progress from HIV infection to AIDS, nearly four times less than females with no copies or males. Women with two copies of C are so rare that none were found in the study.
Previous research has linked some degree of HIV resistance to a mutation in SNP i3003626, which is in a gene that encodes the CCR5 receptor.
The CT genotype of is more frequent among Asians than Europeans or Africans, suggesting that future research may find that HIV-1 positive Asian females have a slower progression to AIDS. Future studies may also be able to use this X chromosomal variant as a clue toward new drug development for both genders.

Genetic Variation in X Chromosome May Slow Progression of AIDS

<img loading="lazy" decoding="async" class="alignright size-full wp-image-4361" title="Two young girls bullying other young girl outdoors" src="https://blog-api.23andme.com/wp-content/uploads/2009/08/iStock_000008979485XSmall.jpg" alt="Two young girls bullying other young girl outdoors" width="346" height="229" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/08/iStock_000008979485XSmall.jpg 425w, https://blogcms.23andme.com/wp-content/uploads/2009/08/iStock_000008979485XSmall-300x199.jpg 300w" sizes="auto, (max-width: 346px) 100vw, 346px" />
It&#8217;s no accident that we often refer to rejection or insult as a slap in the face – research shows the same brain signaling pathways are involved in both physical and emotional pain.
And morphine, a drug well known for its ability to dull physical pain, also reduces separation-induced emotional distress in monkeys, dogs, guinea pigs, rats and chickens.   This is thought to depend on changes in signaling through a morphine receptor called MOR (mu-opioid receptor) that is also implicated in emotional pain in humans. Studies have shown that signaling through MOR is reduced when women recall upsetting events like the death of a loved one or the breakup of a romantic relationship.
Given that MOR seems to be at the center of the overlap between physical and emotional pain, researchers from the UCLA Department of Psychology wondered whether a genetic variation in the gene that encodes MOR that is already known to impact sensitivity to physical pain might also affect how thick-skinned a person is.
Baldwin M. Way and colleagues surveyed 122 healthy young adults about their sensitivity to social rejection.   The assessment measured the tendency of study subjects to be fearful that social interactions will result in hurt feelings, criticism and being a burden to others.   The results, published online this week in the <a href="https://dx.doi.org/10.1073/pnas.0812612106" target="_blank" rel="noopener">Proceedings of the National Academy of Sciences</a>, show that people with one or two of the variants had significantly higher levels of self-reported sensitivity to social rejection. The variants are also associated with needing more morphine for pain relief after surgery.
A subset of the study participants also had their brains scanned in an fMRI machine while playing an online ball-tossing game.   The subjects thought they were playing with two people, but in reality they were interacting with a pre-set computer program.   The game simulated social rejection by having the subjects&#8217; virtual playmates leave them out of the fun.
Just as in the survey, the variant was associated with heightened responses to social rejection.   Higher brain activity was recorded in the anterior cingulate cortex and the anterior insula brain regions associated with the processing of both physical and emotional pain, in people with one or two of the variants.
As is usually the case, the results of this study should be considered preliminary until other researchers replicate them. But based on their results, along with previous research, the authors conclude that, &#8220;… at multiple biological levels, including the neurochemical, neuroanatomical, and now genetic, feeling hurt physically shares more than just linguistic commonality with feeling hurt socially.&#8221;

Genetic Variation In Morphine Receptor May Play A Part In Coping With Social Rejection

<img loading="lazy" decoding="async" class="alignright size-medium wp-image-4345" src="https://blog-api.23andme.com/wp-content/uploads/2009/08/african-dog-300x242.jpg" alt="african dog" width="300" height="242" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/08/african-dog-300x242.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2009/08/african-dog.jpg 400w" sizes="auto, (max-width: 300px) 100vw, 300px" />
The Rexes and Spots of the world have been man&#8217;s best friend for 15,000 years. But when and where did humans begin domesticating these furry companions?
Previous theories suggested that the domesticated dog originated in East Asia and then spread to Africa, Oceania and the Americas. But a recent study by Cornell University researchers has found Mr. Chompers may not have originated in East Asia after all.
Boyko et al. analyzed more than 300 SNPs throughout the genome, as well as a chunk of the maternally inherited mitochondrial DNA and an assortment of other genetic markers in hundreds of village dogs from seven different regions of Egypt, Uganda and Namibia, along with African dog breeds, Puerto Rican street dogs, and mixed-breeds from the United States.

The results, published online ahead of print this month in the <a href="https://www.pnas.org/content/early/2009/07/31/0902129106" target="_blank" rel="noopener">Proceedings of the National Academy of Sciences</a>, showed that African village dogs were the most genetically diverse of all the dogs screened. This diversity was comparable to that in East Asian village dog populations.
Mixed-breed dogs and even African breeds, such as Pharaoh hounds and Salukis, lack such genetic diversity since they have been artificially selected and bred.
African village dogs consistently showed this diverse, indigenous ancestry, with the exception of dogs from central Namibia and Giza who showed genetic signs of some mixing with other non-native dogs. This mixing could be due to earlier mating with human-bred dogs or the relative proximity of Giza to Eurasia, which is home to most known breeds.
<a href="https://blog.23andme.com/2009/04/30/scientists-publish-largest-ever-study-on-the-genetics-of-modern-africans/" target="_blank" rel="noopener">&#8220;Like ancient human populations, these ancient dog populations developed genetic signatures characteristic of their geographic locale,&#8221;</a> the authors wrote.
Africa has the highest amount of <a href="http://www.sciencemag.org/cgi/content/abstract/1172257" target="_blank" rel="noopener">genetic diversity in humans</a> because humans originated and have been living there longer than on any other continent. Similarly, the high genetic diversity of African village dogs suggests that our canine friends may have also originated in Africa. But the similar level of diversity among East Asian village dogs means that region can&#8217;t be ruled out as the birthplace of Canis lupus familiaris. So, more research will be needed to determine exactly when and where canines diverted from baring fangs to chasing boomerangs.
Photo credit: Corin Boyko

Genetic Study Suggests Dogs Domesticated in Africa

<img loading="lazy" decoding="async" class="alignright size-full wp-image-4325" title="RedHairDentalPain" src="https://blog-api.23andme.com/wp-content/uploads/2009/08/RedHairDentalPain.jpg" alt="RedHairDentalPain" width="350" height="233" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/08/RedHairDentalPain.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2009/08/RedHairDentalPain-300x200.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
Redheads might have a better excuse than the rest of us for avoiding the dentist.
For several years now scientists have known that the same genetic variations that give redheads their fiery manes can increase the amount of general or local anesthetic a person needs in order to be properly put out or numbed up.
<h2>Dental Pain</h2>
New research suggests that the effect of these variations is strong enough, and hasn&#8217;t been addressed by dentists well enough, that the people who carry them are more than twice as likely as those who don&#8217;t to avoid going to the dentist altogether.Researchers at the University of Kentucky surveyed 67 redheads and 77 dark haired people about their general anxiety levels, their dental treatment-related anxiety and their fear of dental pain.
The results, published in the July issue of the Journal of the American Dental Association, reveal that while hair color has no effect on general anxiety, redheads are more likely to be apprehensive about sliding into the dentist&#8217;s chair.
A closer look at the data showed that increased dental-treatment anxiety and fear of dental pain is found in all people with the variants in the MC1R gene associated with red hair, even those people who carry these variations despite having dark hair.
<h2>The MC1R Gene</h2>
The protein encoded by the MC1R gene is found in melanocytes, the cells that give hair and skin their color.
The variants associated with <a href="https://www.23andme.com/topics/traits/red-hair">red hair</a> alter the protein&#8217;s function, tipping the balance of pigment production in melanocytes from black-brown eumelanin to red-yellow pheomelanin. Researchers don&#8217;t yet understand how this same protein impacts pain sensitivity and anesthetic needs.
People carrying one or two of the MC1R variants had 2.46 times greater odds of avoiding routine dental care compared to those who carry none. The authors speculate that this might be because prior dental experiences have left them in pain.
The researchers recommend that dentists evaluate all patients, especially those with natural red hair, for dental procedure-related anxiety and take whatever steps are necessary to help them manage their feelings and make it to their regular check-ups, because as the saying goes, &#8220;Ignore your teeth and they&#8217;ll go away.&#8221;

Link Between Red Hair and Avoiding The Dentist

<img loading="lazy" decoding="async" class="alignright size-full wp-image-4273" title="blooddonation" src="https://blog-api.23andme.com/wp-content/uploads/2009/08/blooddonation.jpg" alt="blooddonation" width="350" height="232" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/08/blooddonation.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2009/08/blooddonation-300x199.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
Editor&#8217;s note: This post has been edited to reflect the current product. 
When it comes to blood transfusions, what&#8217;s good for one person might be deadly for another.
This might seem obvious today, but until 1900 the idea of &#8220;blood types&#8221; wasn’t understood. A person in need of a transfusion could find himself getting a donation from just about anyone, and sometimes even an animal!
But in 1900 Austrian scientist <a href="http://nobelprize.org/nobel_prizes/medicine/laureates/1930/" target="_blank" rel="noopener noreferrer">Karl Landsteiner</a> noticed that when the blood of different people was mixed together the cells would often clump up, a process he correctly attributed to an immune reaction between the two blood samples. By the next year he had used this clumping reaction to define three main types of blood, which he named A, B and O. (The fourth blood type, AB, was identified in 1902 by two other scientists, Decastello and Struli.)

After hundreds of years of performing blood transfusions unguided, scientists finally had what they needed to safely transfer blood between people. In 1907, the first blood transfusion utilizing the new typing techniques was successfully carried out, and by World War I transfusions were being performed safely on a large scale.
But knowing what blood to give someone and having it on hand are two different things.
Blood banks are faced with the daunting task of making sure there is enough blood of the right type for everyone who needs it at all times. Blood type O, the &#8220;universal donor,&#8221; tends to be overused. This presents a problem for the approximately 40% of Americans are type O and thus can receive only this type in a transfusion. If supplies run low, their lives could be in danger. At the same time, donated blood with the rare B and AB types can sit unused for so long that it becomes outdated and must be discarded.
One solution to managing the blood supply would be to transform all blood into type O, thus making it suitable for everyone. In the early 1980&#8217;s scientists found a way to do this using an enzyme from coffee beans that could strip certain sugars off of type B blood cells. Clinical trials showed that this method was safe and effective, but the method itself was too time consuming and costly to ever be of clinical use. <a href="http://www.bioedonline.org/news/news.cfm?art=3239" target="_blank" rel="noopener noreferrer">New research, however, has identified bacterial enzymes</a> that can carry out this same process more efficiently. Research with this new method is still in progress.

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