Saturday, December 08, 2012

Drag-and-Drop DNA is Novel technique aiding development of new cancer drugs

Using a simple "drag-and-drop" computer interface and DNA self-assembly techniques, researchers have developed a new approach for drug development that could drastically reduce the time required to create and test medications.

In work supported by a National Science Foundation (NSF) Small Business Innovation Research grant, researchers from Parabon® NanoLabs of Reston, Va., recently developed and began evaluating a drug for combating the lethal brain cancer glioblastoma multiforme.

Now, with the support of an NSF Technology Enhancement for Commercial Partnerships (TECP) grant, Parabon has partnered with Janssen Research & Development, LLC, part of the Janssen Pharmaceutical Companies of Johnson & Johnson, to use the technology to create and test the efficacy of a new prostate cancer drug.

"We can now 'print,' molecule by molecule, exactly the compound that we want," says Steven Armentrout, the principal investigator on the NSF grants and co-developer of Parabon's technology. "What differentiates our nanotechnology from others is our ability to rapidly, and precisely, specify the placement of every atom in a compound that we design."

The new technology is called the Parabon Essemblix™ Drug Development Platform, and it combines their computer-aided design (CAD) software called inSçquio™ with nanoscale fabrication technology.

Scientists work within inSçquio™ to design molecular pieces with specific, functional components. The software then optimizes the design using the Parabon Computation Grid, a cloud supercomputing platform that uses proprietary algorithms to search for sets of DNA sequences that can self-assemble those components.

"When designing a therapeutic compound, we combine knowledge of the cell receptors we are targeting or biological pathways we are trying to affect with an understanding of the linking chemistry that defines what is possible to assemble," says Hong Zhong, senior research scientist at Parabon and a collaborator on the grants. "It's a deliberate and methodical engineering process, which is quite different from most other drug development approaches in use today."


Thought you were perfect? Think again!

Nobody Is Perfect: Study Shows People Have 400 Genetic Flaws In DNA

Perfection is something that all humans strive for at one time or another, be it scoring a perfect 100 on a test, making the perfect soufflé, having the perfect play in basketball, or even landing the perfect job. For others, perfection is a state of well-being—as in being perfectly healthy. While achieving perfect health may be plausible in sense of how one feels, new research shows that, at the genetic level, nobody will ever be perfect.

Researchers from the UK have found that, on average, a normal healthy person has no less than 400 potentially damaging DNA variants known to be associated with disease traits. In a study, these researchers also showed that one in 10 people is expected to develop a genetic disease as a result of carrying these variant genes.

Scientists have long known that all people carry some harmful genetic variants, but this is the first time researchers have been able to quantify how many variants each person has on average, and also list them. The study authors said this figure is likely to increase as more powerful genetic studies discover rare genetic variants more efficiently.

While most of these genetic variants are considered “silent” mutations and do not affect health, the team said they can cause problems as they pass down through generations. Some of the more harmful genetic variants found were linked to cancer and heart disease.

Dr. Yali Xue, lead author of the research from Wellcome Trust Sanger Institute at Cambridge, said: “For over half a century, medical geneticists have wanted to establish the magnitude of the damage caused by harmful variants in our genomes. Our study finally brings us closer to understanding the extent of these damaging mutations.”

The evidence comes from the 1,000 Genomes Pilot Project, which has been mapping normal human genetic differences, from tiny changes in DNA to major mutations. The researchers also gleaned data “from the Human Gene Mutation Database (HGMD), a detailed catalogue of human disease-causing mutations that have been reported in scientific literature,” said Xue.

Xue and his colleagues compared the genomes of 179 participants, who were healthy at the time their DNA was sampled, with a database of human mutations compiled at Cardiff University. The research found that along with the 400 average variations, most people also have two DNA changes known to be associated with disease.

“Ordinary people carry disease-causing mutations without them having any obvious effect,” said Dr. Chris Tyler-Smith, a lead researcher on the study from Wellcome. “In a population there will be variants that have consequences for their own health.”

This research gives insight into the “flaws that make us all different, sometimes with different expertise and different abilities, but also different predispositions in diseases,” study coauthor Prof. David Cooper of Cardiff, said in an interview with the BBC’s Helen Briggs.

“Not all human genomes have perfect sequences,” he said in the interview. “The human genome is packed with pervasive, architectural flaws.”

“In the majority of people we found to have a potential disease-causing mutation, the genetic condition is actually quite mild, or would only become apparent in the later decades of life,” Cooper said in a separate statement. “We now know that normal healthy people can possess many damaged or even completely inactivated proteins without any noticeable impact on their health. It is extremely difficult to predict the clinical consequences of a given genetic variant, but databases such as HGMD promise to come into their own as we enter the new era of personalized medicine.”

The work to catalog disease-causing variants has been ongoing for more than two decades, yet the work is still far from complete. Disease variants are extremely rare for the most part and comprehensive searches for such mutations have so far only scratched the surface.

But as DNA sequencing becomes more common in humans, geneticists must determine ethical ways to go about handling sensitive data. For this latest study, researchers anonymized the samples so as not to offer participants any information as to whether or not they may be at risk for a particular genetic disorder.

Tyler-Smith said currently there is no clear answer for what is ethical and what is not when it comes to sharing genetic variation data and potential incidental findings with volunteers in their study.

“All of our genomes contain flaws; some of us will carry deleterious variants but will not be at risk of acquiring the associated disease for one reason or another. For others, there will be health consequences, and early warning could be useful, but might still come as an unwelcome surprise to the participant,” he concluded.This study is published in the American Journal of Human Genetics.


New prenatal genetic test gives parents more answers

New applications of a genetic test could help parents learn more about the genetics of their unborn children.

Three studies released Wednesday in the New England Journal of Medicine highlight the use of microarray testing as the latest technology in chromosome analysis. Researchers suggest using this test to identify potential intellectual disabilities, developmental delays, autism and congenital abnormalities as well as determining why a pregnancy failed.

During pregnancy a number of tests are suggested by the American College of Obstetricians and Gynecologists based on the mother's age, medical history or ethnic or family background, along with results of other tests. Chromosomal microarray analysis is a genetic test that finds small amounts of genetic material that traditional testing such as karyotyping cannot detect.

The genetic material is obtained during a regular amniocentesis (where small amounts of amniotic fluid and cells are taken from the sac surrounding the fetus and tested during the second trimester of pregnancy) or another commonly used test called CVS, or chorionic villus sampling (where a small amount of cells is taken from the placenta during the first trimester).

According to one study, this prenatal testing surpassed standard testing to detect more genetic abnormalities. Lead study author Dr. Ronald Wapner, says with microarray, doctors don't look at chromosomes and are able to evaluate smaller pieces of DNA.

Read the rest of the article here:

We're Gypsies originally from India?

Katherine Harmon  recently published an article that the Romani people—once known as “gypsies” or Roma—have been objects of both curiosity and persecution for centuries. Today, some 11 million Romani, with a variety of cultures, languages and lifestyles, live in Europe—and beyond. But where did they come from?

Earlier studies of their language and cursory analysis of genetic patterns pinpointed India as the group’s place of origin and a later influence of Middle Eastern and Central Asian linguistics. But a new study uses genome-wide sequencing to point to a single group’s departure from northwestern Indian some 1,500 years ago and has also revealed various subsequent population changes as the population spread throughout Europe.

“Understanding the Romani’s genetic legacy is necessary to complete the genetic characterization of Europeans as a whole, with implications for various fields, from human evolution to the health sciences,” said Manfred Kayser, of Erasmus University in Rotterdam and paper co-author, in a prepared statement.

To begin the study, a team of European researchers collected data on some 800,000 genetic variants (single nucleotides polymorphisms) in 152 Romani people from 13 different Romani groups in Europe. The team then contrasted the Romani sequences with those already known for more than 4,500 Europeans as well as samples from the Indian subcontinent, Central Asia and the Middle East.

According to the analysis, the initial founding group of Romani likely departed from what is now the Punjab state in northwestern India close to the year 500 CE. From there, they likely traveled through Central Asia and the Middle East but appear to have mingled only moderately with local populations there. The subsequent doorway to Europe seems to have been the Balkan area—specifically Bulgaria—from which the Romani began dispersing around 1,100 CE.

These travels, however, were not always easy. For example, after the initial group left India, their numbers took a dive, with less than half of the population surviving (some 47 percent, according to the genetic analysis). And once groups of Romani that would go on to settle Western Europe left the Balkan region, they suffered another population bottleneck, losing some 30 percent of their population. The findings were published online December 6 in Current Biology.

The researchers were also able to examine the dynamics of various Romani populations as they established themselves in different parts of Europe. The defined geographic enclaves appear to have remained largely isolated from other populations of European Romani over recent centuries. And the Romani show more evidence of marriage among blood relatives than do Indians or non-Romani Europeans in the analysis.

But the Romani did not always keep to themselves. As they moved through Europe and set up settlements, they invariably met—and paired off with—local Europeans. And some groups, such as the Welsh Romani, show a relatively high rate of bringing locals—and their genetics—into their families.

Local mixing was not constant over the past several centuries—even in the same groups. The genetic history, as told through this genome-wide analysis, reveals different social mores at different times. For example, Romani populations in Romania, Hungary, Slovakia, Bulgaria and Croatia show genetic patterns that suggest a limited pairing with local populations until recently. Whereas Romani populations in Portugal, Spain and Lithuania have genetic sequences that suggest they had previously mixed with local European populations more frequently but have “higher levels of recent genetic isolation from non-Romani Europeans,” the researchers noted in their paper.

The Romani have often been omitted from larger genetic studies, as many populations are still somewhat transient and/or do not participate in formal institutions such as government programs and banking. “They constitute an important fraction of the European population, but their marginalized situation in many countries also seems to have affected their visibility in scientific studies,” said David Comas, of the Institut de Biologia Evolutiva at the Universitat Pompeu Fabra in Spain and co-author of the new paper, in a prepared statement.

Finer genetic analysis of various Romani populations as well as those from the putative founder region of India will help establish more concrete population dynamics and possibly uncover new clues to social and cultural traditions in these groups that have not kept historical written records.


Wednesday, December 05, 2012

Did humans really kill the Tasmanian Devil?

A real whodunit eh mate?

Contrary to popular belief that Humans caused the Devil Disease - studies have now found that Humans didn't cause devil disease!

Researchers at the University of Sydney have found the low immune gene diversity that enables the spread of the disease in Tasmanian devils, also existed in this species thousands of years ago.
Fossils reveal devil development through history

The team examined DNA from four different periods, as far back as 10,000 years ago when devils also ran around on the Australian mainland.

"We found that the immune gene diversity was actually low in Tasmania even before European arrival and also that mainland devils had low immune gene diversity," lead author Katrina Morris says. "So this wasn't caused by European settlers, it's a much longer historical trend in devils."

Devil fossils have been found in every Australian state and it is thought they became extinct on the mainland around 3000 years ago. However, it is unlikely that an earlier outbreak of the facial tumour, which has wiped out more than 80 per cent of the Tasmanian population in recent years, was to blame.

"It's possible that it has occurred previously but it wouldn't really leave evidence so we can't really be sure," Katrina says. "Nothing like DFTD has occurred in the last 200 years."

Katrina says diseases brought with the introduction of dingoes would have had a significant impact.
Dogs to blame for earlier population crashes

While devil populations in Tasmania have crashed several times over the past 200 years, DFTD did not first appear until 1996. Dogs, this time brought by Europeans, are again thought to be the culprits.

"Since devils had this lack of immune gene diversity they were very susceptible to disease epidemics," says Katrina.

"If the dogs brought anything like distemper with them they might have got into the devil population and then had quite a devastating impact."

The new study reinforces the importance of captive breeding programs for Tasmanian devils, which promote genetic diversity. "They have such a lack of immune gene diversity," Katrina says.

"They still do have some, though, so we need to maintain what they have left so that we don't make the problem any worse."

Pre-natal gene testing may become common

 A new study sets the stage for wider use of gene testing in early pregnancy. Scanning the genes of a fetus reveals far more about potential health risks than current prenatal testing does, say researchers who compared both methods in thousands of pregnancies nationwide.

A surprisingly high number -- 6 percent -- of certain fetuses declared normal by conventional testing were found to have genetic abnormalities by gene scans, the study found.

The flaws can cause anything from minor defects such as a clubfoot to more serious ones such as mental retardation and heart problems.

"This isn't done just so people can terminate pregnancies," because many choose to continue them even if a problem is found, said Dr. Ronald Wapner, reproductive genetics chief at Columbia University Medical Center in New York. "We're better able to give lots and lots of women more information about what's causing the problem and what the prognosis is and what special care their child might need."

He led the federally funded study, published in today's New England Journal of Medicine.

A second study in the journal found that gene testing could reveal the cause of most stillbirths, many of which remain a mystery.

The prenatal study of 4,400 women has long been awaited and could make gene testing a standard of care in cases where initial screening with an ultrasound exam suggests a defect in how the baby is developing, said Dr. Susan Klugman, director of reproductive genetics at New York's Montefiore Medical Center, which enrolled 300 women in the study.

Read more here:

Tuesday, December 04, 2012

4 new genetic regions that influence birth weight!

You're already determined to be a fat child!

Researchers have identified four new genetic regions that influence birth weight, providing further evidence that genes as well as maternal nutrition are important for growth in the womb. Three of the regions are also linked to adult metabolism, helping to explain why smaller babies have higher rates of chronic diseases later in life.

It has been known for some time that babies born with a lower birth weight are at higher risk of chronic diseases such as type 2 diabetes and cardiovascular disease. Three genetic regions have already been identified that influence birth weight, two of which are also linked to an increased susceptibility to type 2 diabetes.

The latest study analysed almost 70,000 individuals of European, Arab, Asian and African American descent from across 50 separate studies of pregnancy and birth. Their findings confirmed the three regions previously identified and also revealed four new genetic regions that are associated with birth weight. The study was part-funded by the Wellcome Trust, the Netherlands Organisation for Scientific Research, the European Union, the Medical Research Council (UK), the Academy of Finland and the National Institute of Health (USA).

One of the new genetic regions is also associated with blood pressure in adulthood, providing the first evidence of a genetic link between birth weight and blood pressure. Two of the regions are known to be linked to adult height, showing that genes involved in growth begin to take effect at a very early stage.

Professor Mark McCarthy, a co-author of the study from the Wellcome Trust Centre for Human Genetics, said: "Our findings add to the growing evidence that events during early growth in the womb can have a significant impact on our health as adults. However, these genes tell only part of the story. It's important that we understand how much is down to genetics and how much is due to the environment in which we grow so that we can target efforts to prevent disease later in life."

Researchers discover 15 new genetic regions linked with coronary artery disease

The University of Ottawa Heart Institute (UOHI) participated in the largest genetic study of Coronary Artery Disease (CAD) to date. Researchers from the CARDIoGRAMplusC4D Consortium report the identification of 15 genetic regions newly associated with the disease, bringing to 46 the number of regions associated with CAD risk.

The Ruddy Canadian Cardiovascular Genetics Centre, at the Heart Institute, was the main genetic centre in Canada contributing most patient cases involved in this study and analyzing patient cases from across North America.

In this unparalleled study, published today in the prestigious scientific magazine Nature, the team identified a further 104 independent genetic variants that are very likely to be associated with the disease, enhancing our knowledge of the genetic component that causes CAD.

Researchers, including Dr. George Wells and Dr. Alexandre Stewart from the Heart Institute, used their discoveries to identify biological pathways that underlie the disease and showed that lipid metabolism and inflammation play a significant role in CAD.

CAD and its main complication, myocardial infarction (heart attack), are some of the most common causes of death in the world and approximately one in five men and one in seven women die from the disease in the UK. CAD has a strong inherited basis.

"These findings show, for the first time, clear evidence that several of the genetic risk factors for CAD function through known inflammatory pathways," said Dr. Robert Roberts, President and CEO of the Heart Institute and Director of the Ruddy Canadian Cardiovascular Genetics Centre. "This identifies a novel pathway for the prevention of heart disease and establishes molecules that can now be targeted for developing new therapies."

Continue reading here:


Family member's DNA solves 1978 killing

A man who never knew his father was the missing link Santa Ana cold-case detectives needed to solve the apparent sexual assault and murder of a young mother and the shooting of her friend in 1978. The case was solved earlier this month using DNA taken from crime scenes to identify family members of a suspected criminal.

California is one of three states that permit the technique, called familial searching. It has led to the 2010 arrest of a man suspected of being the "Grim Sleeper," a serial killer who terrorized South Los Angeles for two decades, and the 2011 arrest of a young man linked to the sexual assault of a woman at a coffee shop near the Santa Cruz Harbor.
The Santa Ana case marks the first time familial DNA has led to an Orange County crime being solved.
Mary Hong, a forensic scientist at the Orange County Crime Lab in Santa Ana, has been trying to solve the homicide of then 26-year-old Lynda Susan Saunders since 1996, when she developed a DNA profile of the perpetrator using semen left on the victim.
In the early 2000s, Hong retested the evidence using new DNA technology that provided a better identification of the suspect. The DNA profile was sent to the California Department of Justice's data bank and to the FBI's Combined DNA Index System, but there was no match.
The decades-old sexual assault and killing of Saunders and shooting of her friend, Michael Scott Reynolds, then 28, went cold. But in 2006, the Santa Ana Police Department's Cold Case Unit was formed to review more than 250 unsolved deaths.

read the whole article here:

Monday, December 03, 2012

First Pics of DNA Photographed!

DNA's double-helix structure is on display for the first time in this electron microscope photograph of a small bundle of DNA strands. (Enzo Di Fabrizio)

A bundle of DNA is supported by two silicon pillars. (Enzo Di Fabrizio)

 Click on the images for a larger view.

Fifty-nine years after James Watson and Francis Crick deduced the double-helix structure of DNA, a scientist has captured the first direct photograph of the twisted ladder that props up life.
Enzo Di Fabrizio, a physics professor at the Magna Graecia University in Catanzaro, Italy, snapped the picture using an electron microscope.

Previously, scientists had only seen DNA's structure indirectly. The double-corkscrew form was first discovered using a technique called X-ray crystallography, in which a material's shape is reconstructed based on how X-rays bounce after they collide with it.

But Di Fabrizio and his colleagues developed a plan to bring DNA out of hiding. They built a nanoscopic landscape of extremely water-repellant silicon pillars. When they added a solution that contained strands of DNA into this scene, the water quickly evaporated and left behind cords of bare DNA that stretched like tightropes between the tiny mesas.

They then shone beams of electrons through holes in the silicon bed, and captured high-resolution images of the illuminated molecules.

Di Fabrizio's images actually show a thread of several interwoven DNA molecules, as opposed to just two coupled strands. This is because the energy of the electrons used would be enough to destroy an isolated double helix, or a single strand from a double helix.

But with the use of more sensitive equipment and lower energy electrons, Di Fabrizio thinks that snapshots of individual double helices will soon be possible, reports New Scientist

Molecules of DNA, or deoxyribonucleic acid, store the genetic instructions that govern all living organisms' growth and function.

Di Fabrizio's innovation will allow scientists to vividly observe interactions between DNA and some of life's other essential ingredients, such as RNA (ribonucleic acid). The results of Di Fabrizio's work were published in the journal NanoLetters.

How Childhood Trauma Can Affect and Alter DNA

Childhood trauma we know for a fact has deep reaching effects. Mostly believed to be limited to psycological, it seems now studies have shown it goes much deeper.

Traumatic experience can induce lasting changes to abused children’s gene regulation that can last through adulthood, putting them at high risk of anxiety and mood disorders. Scientists at the Max Planck Institute of Psychiatry report that genetic variants of the FKBP5 gene, an important regulator of the stress hormone system, can influence epigenetic alterations in this gene induced by early trauma.

The team found that in individuals with a certain allele of FKBP5, trauma causes long-term changes in DNA methylation. This demethylation was linked to increased stress-dependent gene transcription followed by a long-term dysregulation of the stress hormone system and a global effect on the function of immune cells and brain areas associated with stress regulation. As a result, those affected find themselves less able to cope with stressful situations throughout their lives, frequently leading to depression, post-traumatic stress disorder, or anxiety disorders in adulthood.

Research group leader Elisabeth Binder of the Max Planck Institute of Psychiatry examined the DNA of almost 2,000 Afro-Americans who had been repeatedly and severely traumatized as adults or in childhood. One-third of trauma victims had become ill and were now suffering from post-traumatic stress disorder. The risk of developing post-traumatic stress disorder rose with increasing severity of abuse only in the carriers of a specific genetic variant in the FKBP5 gene. The scientists hoped to cast light on the mechanisms of this gene-environment interaction by comparing modifications of the DNA sequence of victims who had not become ill with that of those who had.

The scientists were then able to demonstrate that the genetic FKBP5 variant does make a physiological difference to those affected, as seen in nerve cells. Extreme stress and the associated high concentrations of stress hormones bring about an epigenetic change. A methyl group is broken off the DNA at this point, causing a marked increase in FKBP5 activity. This lasting epigenetic change is generated primarily through childhood traumatization. Consequently, no disease-related demethylation of the FKBP5 gene was detected in participants who were traumatized in adulthood only.

“Depending on genetic predisposition, childhood trauma can leave permanent epigenetic marks on the DNA,” explains Torsten Klengel, M.D., one of the study authors. “The consequence is a permanent dysregulation of the victim’s stress hormone system, which can ultimately lead to psychiatric illness. Decisive for victims of childhood abuse, however, is that the stress-induced epigenetic changes can only occur if their DNA has a specific sequence.”

The investogators say this study improves our understanding of psychiatric illnesses that arise from the interaction of environmental and genetic factors. The study was published online yesterday in Nature Neuroscience under the title “Allele-specific FKBP5 DNA demethylation mediates gene–childhood trauma interactions”.

originally posted on:

Why Genetic Information Should be a Trade Secret

This has been a hot topic thats doing rounds. Why should genetic information be a trade secret?

National health systems and insurers, regulators, researchers, providers and patients all have a strong interest in ensuring broad access to information about the clinical significance of variants discovered through genetic testing.

The whole question of proprietary claims over genetic information is not limited to patents and is very much open to debate.  In essence, the authors say that the Myriad patent saga serves as an excellent case study of the importance of collecting clinical data and the implications of keeping those data private. Myriad’s imminent entry into Europe presents an opportunity to implement policies on access to data on the mutation of the BRCA gene which leads to breast cancer. Such policies would set a salutary precedent not only for BRCA but for genetic testing in general, including whole-genome analysis. Mutations on single point mutations on active stretches of the gene are clearly deleterious because they disrupt protein function. Data on these mutations are valuable to those tested and to their health providers, influencing decisions about treatment options. But other data is being withheld, report the authors, which could be essential for further research in the analysis and treatment of cancer caused by single point variations. These are  ‘variants of unknown significance’ (VUS). They occur between the active and inactive segments of the gene and are therefore particularly difficult to interpret. The paper reports that Myriad claims that the fraction of cases resulting in a VUS is 3% in its hands, and 20% for most EuropeanBRCA-testing services.

You can read the entire article here:


Sunday, December 02, 2012

A Little Variation Makes All the Difference in Human Genetics

Paul Diehl's Article

Genes make us who we are and the small variations between each person's genes do more than just make us look different. They influence our unique physiology, personality, intelligence, and health. They can also tell us where our ancestors originated.
The sequencing of the human genome--the genetic material contained in each person--was completed in 2003. However, this just provided a reference DNA sequence. While the DNA in different humans is more than 99% identical, each individual's genome is a little different. It is this small variation that makes each of us unique.
The less than 1% differences between the genomes of two individuals amounts to millions of variations in the 3 billion bases of DNA in each of their cells. Since the completion of the first human genome, researchers have been devoting massive efforts to work out the effect of these variations in different people's genomes. Of course they define our physical differences, but they also influence our susceptibility to diseases, determine our sensitivity to various chemicals and drugs, affect our metabolism, and influence our behavior and neurology.
Almost 10 years after the completion of the human genome sequence, science is starting to understand enough about how specific DNA variations produce different traits and predispose individuals to various health and lifestyle risks to impact individual healthcare.
Just a couple weeks ago, over 6,000 scientists met at the American Society of Human Genetics (ASHG) in San Francisco to discuss the latest research linking human DNA variations to diseases and other human characteristics. Sessions at the conference discussed the genetics of cancer, cardiovascular disease, metabolic disorders, neurodegenerative diseases, and pharmacogenetics--which deals with how people with different genetics can respond differently a drug. To get a sense of the conference, here are a couple blogs from attendees. Brigitte Ganter from DNANexus gives a general overview of the conference, and Razib Khan on the Discover website offers a more on-the-ground view of happenings at this event. A blog by Meg Byrne from the journal PLOS also highlights some interesting published genomic research (although not necessarily presented at the ASHG conference)
I was fortunate enough to stop in at the ASHG conference for a day to poke around. I just posted a couple articles that offer a bit of an introduction to genomics science. One talks about, Genetic Variation, Disease Genes, and Risk Factors, and the other, How Researchers Figure Out Which Genes Are Associated with Diseases. Hope you find them interesting. I will also add a couple other related pieces in coming weeks.

Stem Cells Now Being Harvested from Blood: Top Stem Cell Stocks

Stem cells therapies are currently used in bone marrow transplants that are used to treat leukemia, and scientists believe in the future, they can be used to treat cancer, Parkinson’s disease, and multiple sclerosis. Researchers at the at the University of Cambridge have developed a way of producing stem cells with blood. The research was published in the Stem Cells: Translational Medicine journal. With all the controversy about embryonic stem cells, scientists are looking for alternative sources, such a teeth and umbilical cord blood.

Several companies are involved in some aspect of stem cells and stem cell research. has turned up over a dozen stem cell stocks, and over half a dozen of which are generating profits.

Alexion Pharmaceuticals (ALXN) is a Connecticut based company with an $18.7 billion market capitalization that is involved in the development of biologic therapeutic products for the treatment of hematologic and cardiovascular disorders, auto-immune diseases, and cancer. The company licenses porcine embryonic stem cells for transgenic animals. The stock has a price to earnings ratio of 85 and a forward PE of 42.6. Earnings for the latest quarter were up an incredible 40.6%% on a 44.2% boost in revenues.

Integra Lifesciences Holdings (IART) is a New Jersey based company that develops, manufactures, and sells medical devices, implants, biomaterials, and instruments to the stem cell, surgery, and soft tissue repair markets. The stock trades at 33 times current earnings, and 12 times forward earnings. However, earnings for the latest quarter were up a strong 17.5% on a 3.9% rise in sales.

Cellgene (CELG) is a $29.8 billion market cap company involved in the discovery and production of therapies designed to treat cancer and immune-inflammatory-related diseases. One of the company’s main products is Thalomid, which is used for the treatment of erythema nodosum leprosum, a complication of leprosy. They also received a patent on placental stem cell recovery. The stock sports a PE ratio of 22 and a forward PE of 14. Quarterly earnings were up 13.7%% on a 13.6%% revenue increase.

For a free list of twenty stocks involved in stem cell research, along with some cord blood stocks, which you can download, sort, and update, go to

Disclosure: Author did not own any of the above at the time the article was written.