Category Archives: Gene Medicine

ALAMEDA, Calif.--(BUSINESS WIRE)--LifeMap Sciences, Inc., a subsidiary of BioTime, Inc., announced today the recent release of MalaCards, Version 1.06. The new release is available at http://www.malacards.org/, and features greatly improved gene-disease associations. MalaCards is a database of human diseases and their annotations that is modeled on the architecture and richness of the popular GeneCards database of human genes (http://www.genecards.org/). The database consolidates disease data from 66 sources and in this version contains 19,663 disease entries, 11,808 of which include associated genes. LifeMap Sciences holds the exclusive worldwide license to market GeneCards and MalaCards from Yeda Research and Development Company Ltd., the commercial arm of the Weizmann Institute of Science.

MalaCards 1.06 includes the following features and improvements:

GeneCards, the Human Gene Compendium (www.genecards.org), has been updated to reflect the upgraded gene-disease associations.

The new MalaCards version further accentuates this databases role in providing users worldwide with a comprehensive birds eye view of human diseases and their gene connections, said Professor Doron Lancet, Ph.D., Head of the Crown Human Genome Center, at the Weizmann Institute of Science and principal investigator of MalaCards.

About LifeMap Sciences, Inc.

LifeMap Sciences (www.lifemapsc.com) core technology and business is based on its Integrated Biomedical Knowledgebase and discovery platform for biomedical research, which currently includesGeneCards: the leading human gene database;LifeMap Discovery, the database of embryonic development, stem cell research and regenerative medicine;MalaCards, the human disease database; and GeneAnalytics, a novel gene set analysis tool which leverages our Integrated Biomedical Knowledgebase. LifeMaps products are used in more than 3,000 institutions including academia, research hospitals, patent offices, and leading biotechnology and pharmaceutical companies.

LifeMap Sciences intends to continually improve the quality of its products, and is pursuing several new Internet and informatics products with substantial, rapid-revenue growth potential, leveraging its existing products and their large user base of life scientists. LifeMap also intends to extend its offerings to the field of mobile health via its subsidiaryLifeMap Solutions, Inc.

About the Weizmann Institute of Science and GeneCards

The Weizmann Institute of Science in Rehovot, Israel, is one of the world's top-ranking multidisciplinary research institutions. Noted for its wide-ranging exploration of the natural and exact sciences, the Institute is home to scientists, postdoctoral fellows, Ph.D. and M.Sc. students, and scientific, technical and administrative staff. In addition, visiting scientists and their families over 500 from 35 countries are regularly hosted at the Institute. The Institute was founded in 1934 following a donation to Dr. Chaim Weizmann, a noted biochemist and biotechnologist, who envisioned the establishment of a world-class scientific research center in Israel, and later also became the first President of the State of Israel. Weizmann Institutes Feinberg Graduate School, established in 1958, has 1000 M.Sc. and Ph.D. students enrolled in studies covering the Institutes five faculties: Biochemistry, Biology, Chemistry, Physics, and Mathematics and Computer Science. The Institutes technology transfer arm, Yeda Research and Development Co. was the first company of its kind in Israel, and is currently one of the most successful worldwide. Institute research efforts include the search for new ways of fighting disease and hunger, examining leading questions in mathematics and computer science, probing the physics of matter and the universe, creating novel materials and developing new strategies for protecting the environment. Particular excellence in bioinformatics and systems biology is manifested, among others, in the GeneCards project, initiated in 1996, under the leadership of Prof. Doron Lancet of the Dept. of Molecular Genetics, Head of the Crown Human Genome Center. A team of 10 led by Marilyn Safran continuously innovates and keeps GeneCards as a world-top human gene compendium, automatically mining and integrating 100 worldwide web resources.

About BioTime

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LifeMap Sciences, a Subsidiary of BioTime, Announces Release of MalaCards Version 1.06 With Greatly Improved Gene ...

It's an early lesson in genetics: we get half our DNA from Mom, half from Dad.

But that straightforward explanation does not account for a process that sometimes occurs when cells divide. Called gene conversion, the copy of a gene from Mom can replace the one from Dad, or vice versa, making the two copies identical.

In a new study published in the American Journal of Human Genetics, University of Pennsylvania researchers Joseph Lachance and Sarah A. Tishkoff investigated this process in the context of the evolution of human populations. They found that a bias toward certain types of DNA sequences during gene conversion may be an important factor in why certain heritable diseases persist in populations around the world.

Lachance is a postdoctoral fellow at Penn in Tishkoff's lab and will be starting his own lab at Georgia Tech in January. Tishkoff is a Penn Integrates Knowledge Professor with appointments in the Perelman School of Medicine's Department of Genetics and the School of Arts & Sciences' Department of Biology.

The study pins on the question of why humans have a genetic predilection for certain diseases. Some reasons have become clear to scientists. The Amish, for example, have a higher risk of several genetic diseases due in part to a phenomenon called founder effects, whereby certain genes rise to prevalence in populations that originated with a relatively small number of individuals.

Other genetic diseases can become relatively common if some aspect about them is advantageous.

"The classic example is sickle-cell anemia," Lachance said. "It's an evolutionary trade-off because people with one copy of a sickle-cell mutation are highly protected from malaria."

Less is known, however, about gene conversion events, which became the focus of Lachance and Tishkoff's study. Previously, researchers have found that during gene conversion DNA is more likely to be retained and copied if the allele that differs contains either a guanine (G) or a cytosine (C) nucleotide. Conversely, the DNA is more likely to be converted, or replaced, if the allele contains an adenine (A) or thymine (T).

"This bias is very small," Lachance said. "It's like a very slightly weighted coin. But over generations and across huge amounts of the genome, flipping the coin over and over again, we thought we would start to see an effect at the population level.

To see if this genetic preference, known as the GC bias, was having an effect, Lachance and Tishkoff analyzed the genomic sequences of 25 people -- five from each of five groups representing diverse populations. They identified 7.5 million single nucleotide polymorphisms, or SNPs, which are mutations involving a single nucleotide, and grouped them according to whether a change represented a shift from a G or C to an A or T or the reverse.

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DNA 'bias' may keep some diseases in circulation, biologists show

TUESDAY, Sept. 30, 2014 (HealthDay News) -- There's no genetic evidence that high levels of vitamin D can prevent type 2 diabetes, a new study says.

Some previous research had suggested that elevated levels of vitamin D might protect people against type 2 diabetes, raising the possibility of a link between vitamin D deficiency and the blood sugar disease.

In this study, British researchers investigated the association between diabetes risk and vitamin D by focusing on genes that control blood levels of vitamin D. They found no connection between different variants of these genes and the risk of developing type 2 diabetes.

The results were published Sept. 30 in The Lancet Diabetes & Endocrinology.

"Our findings suggest that interventions to reduce the risk of type 2 diabetes by increasing concentrations of vitamin D are not currently justified. Observational studies that show a strong and consistent higher risk of type 2 diabetes with lower levels of vitamin D may do so because they have thus far not been able to adequately control for distorting or confounding factors, such as physical activity levels," study author Dr. Nita Forouhi, of the University of Cambridge's School of Clinical Medicine, said in a journal news release.

The findings add to evidence showing that taking vitamin D supplements does not prevent diabetes. The only proven ways to prevent type 2 diabetes are diet and exercise, Forouhi said.

One expert noted that long-term trials that are still looking at any possible connection should be weighed in the final analysis.

The results "need careful interpretation, and long-term randomized trials of vitamin D supplementation, which are underway, remain important," Dr. Brian Buijsse, from the German Institute of Human Nutrition Potsdam-Rehbruecke in Germany, wrote in an accompanying commentary in the journal.

"The results of an [analysis] of 35 short-term trials, however, do not offer much hope that vitamin D supplementation can be used to prevent type 2 diabetes. The sky is becoming rather clouded for vitamin D in the context of preventing type 2 diabetes," he said.

-- Robert Preidt

Original post:
Gene Study Finds No Proof Vitamin D Guards Against Type 2 Diabetes

PUBLIC RELEASE DATE:

2-Oct-2014

Contact: Katherine Unger Baillie kbaillie@upenn.edu 215-898-9194 University of Pennsylvania @Penn

It's an early lesson in genetics: we get half our DNA from Mom, half from Dad.

But that straightforward explanation does not account for a process that sometimes occurs when cells divide. Called gene conversion, the copy of a gene from Mom can replace the one from Dad, or vice versa, making the two copies identical.

In a new study published in the American Journal of Human Genetics, University of Pennsylvania researchers Joseph Lachance and Sarah A. Tishkoff investigated this process in the context of the evolution of human populations. They found that a bias toward certain types of DNA sequences during gene conversion may be an important factor in why certain heritable diseases persist in populations around the world.

Lachance is a postdoctoral fellow at Penn in Tishkoff's lab and will be starting his own lab at Georgia Tech in January. Tishkoff is a Penn Integrates Knowledge Professor with appointments in the Perelman School of Medicine's Department of Genetics and the School of Arts & Sciences' Department of Biology.

The study pins on the question of why humans have a genetic predilection for certain diseases. Some reasons have become clear to scientists. The Amish, for example, have a higher risk of several genetic diseases due in part to a phenomenon called founder effects, whereby certain genes rise to prevalence in populations that originated with a relatively small number of individuals.

Other genetic diseases can become relatively common if some aspect about them is advantageous.

"The classic example is sickle-cell anemia," Lachance said. "It's an evolutionary trade-off because people with one copy of a sickle-cell mutation are highly protected from malaria."

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DNA 'bias' may keep some diseases in circulation, Penn biologists show

PUBLIC RELEASE DATE:

30-Sep-2014

Contact: Garth Sundem garth.sundem@ucdenver.edu University of Colorado Denver @CUDenver

The New England Journal of Medicine reports positive results of a phase 1 clinical trial of the drug crizotinib against the subset of lung cancer marked by rearrangement of the gene ROS1. In this multi-center study of 50 patients with advanced non-small cell lung cancer testing positive for ROS1 gene rearrangement, the response rate was 72 percent, with 3 complete responses and 33 partial responses. Median progression-free survival the time it takes for the disease to resume its growth after being slowed by treatment is estimated at 19.2 months with exactly half of patients remaining on observation for disease progression that has not yet occurred.

Over 200,000 people in the United States are diagnosed with lung cancer annually and advanced stage lung cancer has a 5-year survival rate of only about 2 percent. ROS1 rearrangements are found in approximately 1 percent of lung cancer patients, the majority of whom have never smoked.

"This is a major advance for the clinical treatment of lung cancer," says Robert C. Doebele, MD, PhD, investigator at the University of Colorado Cancer Center, associate professor of Medical Oncology at the CU School of Medicine, and one of the study authors. Doebele was involved primarily in the characterization of ROS1 gene rearrangements. Additional CU Cancer Center researchers involved in the project include Marileila Varella-Garcia, PhD, who developed a test for the ROS1 rearrangement in patient tumor samples, and Ross Camidge, MD, PhD, who was involved in the clinical testing of crizotinib against both ALK-positive and now ROS1-positive lung cancers.

In fact, current results follow similar activity seen earlier for the drug against lung cancers marked by rearrangement of the gene ALK. Crizotinib earned FDA approval for treatment of ALK-positive lung cancer in 2011. Both ALK and ROS1 are proteins in the family of tyrosine kinases that normally control the behavior of cells; in the case of these rearrangements, the altered genes continuously signal cells to improperly grow, spread and survive, making the cells act cancerous.

As in the case of ALK-positive lung cancer, in which the gene ALK improperly fuses with the nearby gene EML4, in this newly studied subtype of lung cancer, the gene ROS1 fuses with a nearby partner. Tumor samples studied in the current study showed 5 known gene partners for ROS1 fusion and 2 new partners. The most commonly rearrangement was of ROS1 with the gene CD74, but no matter the ROS1 partner, all rearrangements were equally susceptible to treatment with crizotinib.

"This is ongoing work in which the primary goal of this phase one study was to characterize the safety of the drug. Not only was the safety profile promising, but we saw anti-cancer activity that makes us extremely optimistic for future trials," Doebele says.

In fact, and though it will need to be confirmed by future trials, crizotinib may have an even more durable action against ROS1-positive lung cancer than it does against ALK-positive lung cancer, the disease for which the drug was initially developed and approved. Specifically, median progression free survival for crizotinib against ROS1-positive lung cancer is just more than double the progression free survival for the drug against ALK-positive lung cancer.

Read more:
NEJM: Crizotinib effective in Phase 1 trial against ROS1 lung cancer

PHILADELPHIA In the second of two papers outlining new gene-therapy approaches to treat a rare disease called MPS I, researchers from Perelman School of Medicine at the University of Pennsylvania examined systemic delivery of a vector to replace the enzyme IDUA, which is deficient in patients with this disorder. The second paper, which is published online in the Proceedings of the National Academy of Sciences this week, describes how an injection of a vector expressing the IDUA enzyme to the liver can prevent most of the systemic manifestations of the disease, including those found in the heart.

The first paper, published in Molecular Therapy, describes the use of an adeno-associated viral (AAV) vector to introduce normal IDUA to glial and neuronal cells in the brain and spinal cord in a feline model. The aim of that study was to directly treat the central nervous system manifestations of MPS while the more recent study aims to treat all other manifestations of the disease outside of the nervous system.

This family of diseases comprises about 50 rare inherited disorders marked by defects in the lysosomes, compartments within cells filled with enzymes to digest large molecules. If one of these enzymes is mutated, molecules that would normally be degraded by the lysosome accumulate within the cell and their fragments are not recycled. Many of the MPS disorders can share symptoms, such as speech and hearing problems, hernias, and heart problems. Patient groups estimate that in the United States 1 in 25,000 births will result in some form of MPS. Life expectancy varies significantly for people with MPS I.

The two main treatments for MPS I are bone marrow transplantation and intravenous enzyme replacement therapy (ERT), but these are only marginally effective or clinically impractical, and have significant drawbacks for patient safety and quality of life and do not effectively address some of the most critical clinical symptoms, such as life-threatening cardiac valve impairments.

Both of these papers are the first proof-of-principle demonstrations for the efficacy and practicality for gene therapies to be translated into the clinic for lysosomal storage diseases, says lead author James M. Wilson, MD, PhD, professor of Pathology and Laboratory Medicine and director of the Penn Gene Therapy Program. This approach may likely turn out to be better than ERT and compete with or replace ERT. We are especially excited about the use of this approach in treating the many MPS I patients who do not have access to ERT due to cost or inadequate health delivery systems to support repeated protein infusions, such as in China, Eastern Europe, India, and parts of South America.

Patients with mucopolysaccharidosis type I (MPS I), accumulate compounds called glycosaminoglycans in tissues, with resulting diverse clinical symptoms, including neurological, eye, skeletal, and cardiac disease.

Using a naturally occurring feline model of MPS I, the team tested liver-directed gene therapy via a single intravenous infusion as a means of establishing long-term systemic IDUA presence throughout the body.

The team treated four MPS I cats at three to five months of age with an AAV serotype 8 vector expressing feline IDUA. We observed sustained serum enzyme activity for six months at approximately 30 percent of normal levels in one animal and in excess of normal levels in the other three animals, says Wilson.

Remarkably, treated animals not only demonstrated reductions in glycosaminoglycans storage in most tissues, but most also exhibited complete resolution of aortic valve lesions, an effect which has not been previously observed in this animal model or in MPS I patients treated with current therapies.

Critical to the evaluation of these novel therapies is the feline model of MPS I, which was provided through coauthor Mark E. Haskins, School of Veterinary Medicine at Penn. Haskins and his colleagues maintain a variety of canine and feline models of human genetic diseases that have been instrumental in establishing proof of concept for a number of novel therapeutics, including the current enzyme replacement therapy.

Excerpt from:
Gene Therapy Targeting Liver Corrects Cardiovascular Symptoms in Animal Model of Rare Enzyme Deficiency Disease

A powerful new technology could be used to manipulate nature by changing a species gene pool through reproduction, and it has scientists proceeding with caution.

The technology is called gene drive by Harvard scientists who say it allows them to edit genes in wild organisms. Dr. Kenneth Oye, a professor at Massachusetts Institute of Technology, says gene drives are a game changer. Gene drives cheat, they play a game," he explained. "They bias inheritance so the odds of the gene being passed on are raised substantially.

For scientists, the possibilities of the technology are great. Gene drive lets researchers permanently block mosquitoes ability to spread malaria, for example. It can also be used to alter ticks, reducing the spread of Lyme disease.

But its not just malaria -- any disease spread by mosquitos we can combat in this way," said Oye. "So that means dengue, that means yellow fever, that means, potentially closer to home, West Nile Virus.

Because the technology has the potential to alter entire populations on a global scale scientists are proceeding with caution. The Harvard group is calling for public debate on the wisdom and safety of the technology before moving forward.

Ethically I think it's an open and shut case. A slam dunk. That if youre going to be taken actions that potentially affect the world, the world has a little voice in this, said Oye.

For scientists the extent of the risk -- and consequences associated with the technology are unknown. Scientists say that if this tech goes awry, it could mean accidental extinction for entire species, or unpredictable gene re-mutations spreading cross-species.

Kevin Esvelt, lead scientist in the research group, says the technology needs to be used wisely. Yes, we should be concerned. We should come together and discuss this because it has the potential to do a great deal of good, but it could also do harm if we use it unwisely.

But scientists say they have a plan B if something goes wrong. We can release a second drive that will undo that alteration and restore it pretty close to exactly the same sequence as it was originally, said Esvelt. But he warns the fix isnt absolute. Now that doesnt mean that its going to reverse all the potential ecological effects of that original change. But it does mean that we can take precautions.

The technology has even made waves internationally. A United Nations meeting of experts on biological weapons convened to review the benefits and potential implications of gene drive. Dr. Oye, who presented the tech to international delegates gathered in Geneva, said the tech especially piqued the interest of delegations from Malaria-inflicted regions. The reaction at Geneva from the biosecurity experts, these are the hard core folks, was very, very positive, he said.

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Powerful Gene-Mutating Tech Needs More Debate

PUBLIC RELEASE DATE:

30-Sep-2014

Contact: Emily Head emily.head@cancer.org.uk 44-203-469-6189 Cancer Research UK @CR_UK

A drug which targets a key gene fault could halt an aggressive womb cancer and shrink tumours, according to research published in the British Journal of Cancer*.

The scientists, from the Division of Gynaecologic Oncology at Yale School of Medicine funded by the National Institutes of Health, showed that the drug afatinib not only killed off uterine serous cancer cells after stopping their growth but also caused tumours to shrink.

The drug, a type of personalised medicine, attacks faults in the HER2 gene which lie at the heart of the cancer cells. This stops the disease in its tracks. Drugs which target HER2 are already used to treat breast cancer.

Uterine serous carcinoma is a fast-growing type of womb cancer. It is more likely than other womb cancers to come back after treatment, returning in one in two patients* even if it is caught early.

Although the cancer causes less than one in 10 womb cancers**, it accounts for 40 per cent of all deaths from womb cancer* which is around 800 deaths every year in the UK***.

The researchers looked at uterine serous carcinoma cell lines with normal and increased levels of the HER2 protein to see how afatinib affected the cancer. They found that the drug had a big impact on cancer cells with this gene fault, and could stop them growing and kill them. They also found that the drug shrank the size of uterine serous tumours when given to mice.

Afatinib works by targeting receptors that respond to growth signals. Cancers with high levels of the HER2 protein have too many of these receptors, allowing them to grow out of control. The drug is an example of personalised or tailored treatment, which works by specifically targeting the faulty genes and molecules in an individual's cancer. Afatinib is being tested in clinical trials for a number of cancers including bowel cancer and certain types of lung and breast cancer.

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Targeted treatment could halt womb cancer growth

PUBLIC RELEASE DATE:

29-Sep-2014

Contact: Karen Kreeger karen.kreeger@uphs.upenn.edu 215-349-5658 University of Pennsylvania School of Medicine @PennMedNews

PHILADELPHIA In the second of two papers outlining new gene-therapy approaches to treat a rare disease called MPS I, researchers from Perelman School of Medicine at the University of Pennsylvania examined systemic delivery of a vector to replace the enzyme IDUA, which is deficient in patients with this disorder. The second paper, which is published online in the Proceedings of the National Academy of Sciences this week, describes how an injection of a vector expressing the IDUA enzyme to the liver can prevent most of the systemic manifestations of the disease, including those found in the heart.

The first paper, published in Molecular Therapy, describes the use of an adeno-associated viral (AAV) vector to introduce normal IDUA to glial and neuronal cells in the brain and spinal cord in a feline model. The aim of that study was to directly treat the central nervous system manifestations of MPS while the more recent study aims to treat all other manifestations of the disease outside of the nervous system.

This family of diseases comprises about 50 rare inherited disorders marked by defects in the lysosomes, compartments within cells filled with enzymes to digest large molecules. If one of these enzymes is mutated, molecules that would normally be degraded by the lysosome accumulate within the cell and their fragments are not recycled. Many of the MPS disorders can share symptoms, such as speech and hearing problems, hernias, and heart problems. Patient groups estimate that in the United States 1 in 25,000 births will result in some form of MPS. Life expectancy varies significantly for people with MPS I.

The two main treatments for MPS I are bone marrow transplantation and intravenous enzyme replacement therapy (ERT), but these are only marginally effective or clinically impractical, and have significant drawbacks for patient safety and quality of life and do not effectively address some of the most critical clinical symptoms, such as life-threatening cardiac valve impairments.

"Both of these papers are the first proof-of-principle demonstrations for the efficacy and practicality for gene therapies to be translated into the clinic for lysosomal storage diseases," says lead author James M. Wilson, MD, PhD, professor of Pathology and Laboratory Medicine and director of the Penn Gene Therapy Program. "This approach may likely turn out to be better than ERT and compete with or replace ERT. We are especially excited about the use of this approach in treating the many MPS I patients who do not have access to ERT due to cost or inadequate health delivery systems to support repeated protein infusions, such as in China, Eastern Europe, India, and parts of South America."

Patients with mucopolysaccharidosis type I (MPS I), accumulate compounds called glycosaminoglycans in tissues, with resulting diverse clinical symptoms, including neurological, eye, skeletal, and cardiac disease.

Using a naturally occurring feline model of MPS I, the team tested liver-directed gene therapy via a single intravenous infusion as a means of establishing long-term systemic IDUA presence throughout the body.

Read this article:
Liver gene therapy corrects heart symptoms in model of rare enzyme disorder

Treatment with the targeted therapy drug crizotinib effectively halts the growth of lung tumors driven by rearrangements of the ROS1 gene. In an article receiving Online First publication in the New England Journal of Medicine to coincide with a presentation at the European Society for Medical Oncology meeting, an international research team reports that crizotinib treatment led to significant tumor shrinkage in 36 of 50 study participants and suppressed tumor growth in another 9.

"Prior to this study, there were a handful of reports describing marked responses to crizotinib in individual patients with ROS1-positive lung tumors," says Alice Shaw, MD, PhD, of the Massachusetts General Hospital (MGH) Cancer Center, lead author of the NEJM report. "This is the first definitive study to establish crizotinib's activity in a large group of patients with ROS1-positive lung cancer and to confirm that ROS1 is a bona fide therapeutic target in those patients."

Crizotinib currently is FDA-approved to treat non-small-cell lung cancers (NSCLC) driven by rearrangments in the ALK gene, which make up around 4 percent of cases. An MGH Cancer Center report published in 2012 reported that 1 to 2 percent of NSCLCs are driven by rearrangements in ROS1, which encodes a protein with significant structural similarities to that encoded by the ALK gene.

The current study, an expansion of the original phase 1 crizotinib trial, enrolled 50 patients with ROS1-positive NSCLC, beginning in late 2010. Patients received twice daily doses of crizotinib. As noted above, tumor size was significantly reduced in 72 percent of patients and tumor growth was halted in an additional 18 percent. The average duration of response was over 17 months. At the end of the study, 25 of the 50 patients were still receiving crizotinib with no evidence of tumor progression.

As with other targeted cancer therapy drugs, treatment resistance developed in a number of participants, but the effectiveness of crizotinib appeared to last longer in ROS1-positive patients than in patients with ALK-positive tumors. "Almost all patients treated with targeted therapies eventually develop resistance," explains Shaw, an associate professor of Medicine at Harvard Medical School (HMS). "Fortunately, the remissions induced by crizotinib in ROS1-positive patients are quite prolonged, and resistance appears to emerge much later, on average, than what we have seen with other targeted therapies for lung cancer and melanoma."

The authors note that development of efficient laboratory diagnostics has been critical to identification of ROS1 rearrangements and of other genetic alterations that drive tumor growth. John Iafrate, MD, PhD, medical director of the MGH Center for Integrated Diagnostics and associate professor of Pathology at HMS, who is senior author of the study comments, "This is a great example of success in personalized medicine. While NSCLC patients with ROS1 fusions are rare, if you devote the diagnostic laboratory resources to find that 1 to 2 percent of patients, you will make a real difference."

While crizotinib's FDA approval currently covers only ALK-positive NSCLC, Shaw notes that National Comprehensive Cancer Network guidelines recommend that patients with advanced lung cancer be considered for ROS1 testing and that crizotinib should be used to treat ROS1-positive patients.

Story Source:

The above story is based on materials provided by Massachusetts General Hospital. Note: Materials may be edited for content and length.

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Crizotinib treatment effective against ROS1-positive lung cancer, study suggests