Archive for the ‘Gene Therapy Research’ Category

Public release date: 11-Jun-2012 [ | E-mail | Share ]

Contact: Susan Martonik smartonik@snm.org 703-652-6773 Society of Nuclear Medicine

Miami Beach, Fla.Finding a way to restore hair growth after substantial hair loss is something of an obsession worldwide. Investigators at the Society of Nuclear Medicine's 2012 Annual Meeting presented how stem cell research for the development of new hair follicles can be monitored with an optical imaging technique that uses bioluminescence, the same process that allows fireflies to light up.

There is a host of treatments available for hair loss, including creams and drugs, but these have not shown to be very effective for hair growth. Hair stem cells signal the actual regeneration of hair follicles and natural hair. A molecular imaging technique called bioluminescence is used to display processes at the cellular level. Bioluminescent signal is generated in specific chemical substances called substrates. These signals are easily recognized with very sensitive optical imaging systems that can see what is happening in the smallest placesin this case in hair stem cells.

"Hair regeneration using hair stem cells is a promising therapeutic option emerging for hair loss, and molecular imaging can speed up the development of this therapy," saysByeong-Cheol Ahn, M.D., Ph.D., professor and director of the department of nuclear medicine at Kyungpook National University School of Medicine and Hospital in Daegu, South Korea. "This study is the first study of hair follicle regeneration using an in vivo molecular imaging technique."

The current research involves grafting hair stem cells in animal models to investigate if they can grow and proliferate as normal cells do. The progress of hair stem cell therapy is non-invasivelytracked with bioluminescentreporter genes in specialized substrates. There are several bioluminescent reporter genes originating fromnot only fireflies, but also beetles, glowworms and other bioluminescent organisms. The strategy of using bioluminescent reporter genesis ideal for stem cell research, because bioluminescence works only in living cells.

In this study, researchers used bioluminescence imaging usingfirefly luciferase coupled with D-luciferin to monitor the engraftment of hair follicle stem cellscalled newborn fibroblastsin mice to track their viability and development into hair folliclesover time. Bioluminescence imaging was performed five times over the course of 21 days after transplantation of the stem cells.

Results of the study showed successful bioluminescence imaging forhair regeneration with hair stem cell transplantation, and new hair follicles were apparent on the surface of skin samples under microscope. More studies will have to be conducted before clinical trials could be initiated to verify whether this therapy would work for human hair regeneration.

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Scientific Paper 74: Jung Eun Kim, Byeong-Cheol Ahn, Ho Won Lee, Mi-hye Hwang, Sang-Woo Lee and Jaetae Lee, Nuclear Medicine, Kyungpook National University School of Medicine, Daegu, Republic of Korea; Seng Hyun Shin and Young Kwan Sung, Immunology, Kyungpook National University School of Medicine, Daegu, Republic of Korea, "In vivo monitoring of survival and proliferation of hair stem cells in hair follicle regeneration animal model," SNM's 59th Annual Meeting, June 9, 2012, Miami Beach, Fla.

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Bioluminescence imaging lights up stem cell therapy for hair growth

Newswise A study led by Vanderbilt-Ingram Cancer Center (VICC) investigators has identified a gene expression pattern that may explain why chemotherapy prior to surgery isnt effective against some tumors and suggests new therapy options for patients with specific subtypes of breast cancer.

The study by lead author Justin Balko, Pharm.D., Ph.D., was published online June 10, 2012 in Nature Medicine in advance of print publication. Balko is a postdoctoral fellow in the laboratory of Carlos L. Arteaga, M.D., associate director for Clinical Research and director of the Breast Cancer Program at VICC, who led the study.

About 30 percent of breast cancer patients have a pathological complete response when chemotherapy is used to shrink tumors prior to surgery. However, many patients still have residual cancer in the breast after neoadjuvant chemotherapy (NAC) is completed. These patients are at a higher risk of cancer recurrence and death.

The investigators suspected that profiling tumors after neoadjuvant chemotherapy would identify genes associated with resistance to this form of treatment. They studied gene expression patterns in 49 breast tumors obtained during surgery after four months of NAC.

They identified and analyzed specific groups of genes associated with high-grade, chemotherapy-resistant tumors, labeling their 244 unique genes the CLUSTER signature, and combined this panel with previously identified gene signatures to search for distinctive patterns of behavior.

The investigators found that low concentrations of dual specificity protein phosphatase 4 (DUSP4) is strongly correlated with faster tumor cell growth following neoadjuvant chemotherapy. Low DUSP4 was also correlated with a type of breast cancer known as basal-like breast cancer (BLBC). DUSP4 promoter methylation and gene expression patterns of Ras-ERK pathway activation were also higher in BLBC relative to other breast cancer subtypes.

When DUSP4 was present, chemotherapy was effective against cancer cells, whereas when DUSP4 was experimentally deleted, there was a much lower response to chemotherapy.

These data suggest that cells with low DUSP4 expression are enriched during NAC and that low DUSP4 expression in residual resected breast tumors is a potential biomarker for drug resistance and a high likelihood of tumor recurrence, said Balko.

The group also hypothesized that DUSP4 may be a potential biomarker for response to drugs that inhibit the MEK kinase. Using DUSP4-deficient tumors established in mice, they compared treatment with the chemotherapy drug docetaxel, with and without the MEK inhibitor selumetinib. This study showed that the combination was much more effective than docetaxel alone at eliminating the mouse tumors.

These data support exploratory clinical trials combining chemotherapy and MEK inhibitors in patients with DUSP-deficient basal-like breast cancer, said Balko.

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Study Identifies Genes Linked to Resistance to Breast Cancer Chemotherapy

11-06-2012 11:02 A study led by Vanderbilt-Ingram Cancer Center investigators has identified a gene expression pattern that may explain why chemotherapy prior to surgery isn't effective against some tumors and suggests new therapy options for patients with specific subtypes of breast cancer.

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Breast Cancer Study Identifies Genes Linked to Chemotherapy Resistance - Video

10-06-2012 11:01 Listen to Matt Moneymaker,the founder of the BFRO as he speaks on the subject of Bigfoot. Matt does seem to confirm my own research efforts in that the Sasquatch did migrate out of Asia and throughout the world..just as we Humans have done.There has also been no Neanderthal Gene found in anyone tested that came out of Africa. Unfortunately it may appear that he has failed to connect all the scientific evidence in that it has been scientifically proven that what they are (or could be) is a genetic interbreeding between Neanderthal Man and early modern man,the result was that these two human species did produce an offspring and that they continued reproducing. It has also been scientifically proven that each of us still carry the Neanderthal Gene in us...every Human outside of Africa has this Gene. So it has already been proven scientifically what these "creatures" are. The Sasquatch are real and they are of Human descent. Because we Humans still carry that gene it may also still be possible for it to surface from time to time through us in certain circumstances. All the scientific evidence is out there..all that is needed is to find it and study it. Peace

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SquatchEvidence: Matt Moneymaker speaks on Bigfoot - Video

11-06-2012 19:07 Dr Shireen Lamande presents on her study on the gene for arthritis at the Annual General Review 2012, Murdoch Childrens Research Institute

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Dr Shireen Lamande_Gene for Arthritis.mp4 - Video

11-06-2012 23:11 GENE V GLASS is a Research Professor in the School of Education at the University of Colorado at Boulder and Regents' Professor Emeritus at Arizona State University. Having made substantial contributions to education statistics and educational policy research, his work as a pioneer of meta-analysis has been recognized as one of 40 scholarly contributions that have changed psychology. As past president of the American Educational Research Association and the author of more than a dozen books and nearly two hundred scholarly articles, Dr. Glass now advocates for the expansion of open access to scholarship through free, online publications. BlueDream Production,

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Inside the Academy Dr. Gene Glass - Video

Public release date: 11-Jun-2012 [ | E-mail | Share ]

Contact: Dagny Stuart Dagny.stuart@vanderbilt.edu 615-936-7245 Vanderbilt University Medical Center

A study led by Vanderbilt-Ingram Cancer Center (VICC) investigators has identified a gene expression pattern that may explain why chemotherapy prior to surgery isn't effective against some tumors and suggests new therapy options for patients with specific subtypes of breast cancer.

The study by lead author Justin Balko, Pharm.D., Ph.D., was published online June 10, 2012 in Nature Medicine in advance of print publication. Balko is a postdoctoral fellow in the laboratory of Carlos L. Arteaga, M.D., associate director for Clinical Research and director of the Breast Cancer Program at VICC, who led the study.

About 30 percent of breast cancer patients have a pathological complete response when chemotherapy is used to shrink tumors prior to surgery. However, many patients still have residual cancer in the breast after neoadjuvant chemotherapy (NAC) is completed. These patients are at a higher risk of cancer recurrence and death.

The investigators suspected that profiling tumors after neoadjuvant chemotherapy would identify genes associated with resistance to this form of treatment. They studied gene expression patterns in 49 breast tumors obtained during surgery after four months of NAC.

They identified and analyzed specific groups of genes associated with high-grade, chemotherapy-resistant tumors, labeling their 244 unique genes the CLUSTER signature, and combined this panel with previously identified gene signatures to search for distinctive patterns of behavior.

The investigators found that low concentrations of dual specificity protein phosphatase 4 (DUSP4) is strongly correlated with faster tumor cell growth following neoadjuvant chemotherapy. Low DUSP4 was also correlated with a type of breast cancer known as basal-like breast cancer (BLBC). DUSP4 promoter methylation and gene expression patterns of Ras-ERK pathway activation were also higher in BLBC relative to other breast cancer subtypes.

When DUSP4 was present, chemotherapy was effective against cancer cells, whereas when DUSP4 was experimentally deleted, there was a much lower response to chemotherapy.

"These data suggest that cells with low DUSP4 expression are enriched during NAC and that low DUSP4 expression in residual resected breast tumors is a potential biomarker for drug resistance and a high likelihood of tumor recurrence," said Balko.

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Vanderbilt-led study identifies genes linked to resistance to breast cancer chemotherapy

ScienceDaily (June 11, 2012) Why do some cancers spread rapidly to other organs and others don't metastasize? A team of UNC researchers led by Norman Sharpless, MD, have identified a key genetic switch that determines whether melanoma, a lethal skin cancer, spreads by metastasis.

Treating melanoma is extremely challenging. The cancer spreads rapidly and to sites in the body that are remote from the original cancer site. Melanoma is the most deadly form of skin cancer, and advanced melanoma kills more than 8600 Americans each year. It is the most common form of cancer in young adults, aged 25-29 and the incidence of people under 30 developing melanoma is increasing fast -- more than 50 percent in young women since 1980.

In a paper published June 11 in the journal Cancer Cell, a team from UNC Lineberger Comprehensive Cancer Center demonstrates that inactivating a gene called LKB1 (or STK11) causes non-aggressive melanoma cells to become highly metastatic when tested in a variety of models using tumors from humans and mice. While Sharpless and his colleagues showed a role for LKB1 inactivation in lung cancer metastasis, the effects of LKB1 loss on melanoma spread is even more dramatic.

"Although we are not totally certain how LKB1 loss promotes metastasis in multiple cancer types, one important effect is the loss of LKB1 starts a chain reaction, activating a family of proteins called SRC kinases, which are known to drive metastasis," said Sharpless, who is associate director for translational research at UNC Lineberger.

"Loss of LKB1 occurs in about 30 percent of lung cancer and 10 percent of melanoma, and ongoing studies at UNC and elsewhere will determine if these LKB1 deficient tumors have a worse prognosis. These data suggest LKB1 deficient cancers will be more likely to metastasize, and therefore more likely to be incurable."

"The work is exciting because the laboratory model reliably replicates distant metastases, helping us better understand what treatments may work for melanoma that has spread. While several targeted drugs have recently been approved by the FDA for metastatic disease, these targeted mutations don't indicate whether the disease is likely to metastasize," said Stergios Moschos, MD, clinical associate professor of hematology/oncology. Moschos works in the area of drug development for melanoma but was not involved in this research project.

Other members of the research team from UNC-Chapel Hill include Wenjin Liu, PhD; Kimberly Monahan, PhD; and Jessica Sorrentino, BS, from the department of genetics; Adam Pfefferle, BS, and Ryan Miller, MD, from the department of pathology and laboratory medicine; Keefe Chan, PhD, David Roadcap, PhD, and James Bear, PhD; from the department of cell and developmental biology; David Ollila, MD, from the division of surgical oncology and endocrine surgery; and Charles Perou, PhD, of the departments of genetics and pathology and the Carolina Genome Sciences Center. Dr. Miller, Bear, Ollila, and Perou are also members of UNC Lineberger Comprehensive Cancer Center and Dr. Bear is a Howard Hughes Medical Institute investigator.

Kwok-Kin Wong, MD PhD, from the Dana-Farber Cancer Institute and Harvard Medical School and Diego Castrillon, MD PhD, from the University of Texas Southwestern Medical Center also contributed to the finding.

The research was funded by the National Cancer Institute and the NCI's Mouse Model of Human Cancer Consortium (MMHCC), the National Institute on Aging and the National Institute of Environmental Health Sciences (all part of the National Institutes of Health.

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Gene inactivation drives spread of melanoma

ScienceDaily (June 11, 2012) Presence of normal p53, a tumor suppressor gene, instead of a mutated version, makes breast cancer chemotherapy with doxorubicin less effective. The preclinical study led by MD Anderson scientists was published June 11 in the journal Cancer Cell.

The research, which challenges the existing paradigm, is another step closer to personalized cancer medicine for breast cancer.

"It's really important to understand the genetic defects a tumor cell has before we treat it," said lead author Guillermina Lozano, Ph.D., professor and chair of the Department of Genetics. "What we learned here is the complete opposite of what we expected. We thought tumors would respond better to treatment if the p53 gene were normal. But the opposite was true, and for a really interesting reason."

Lozano said the research in mouse models showed that non-mutated p53 halted cell division, initiating a senescence (cell aging) process that allowed cells to survive. These senescent cells produce factors that stimulate adjacent cells to grow, fueling the relapse. Mutant p53 cells do not arrest and proceed through the cell cycle into cell division with broken chromosomes caused by the chemotherapy.

"That's a signal for the cell to die," she said. "It can't go any farther."

P53 status crucial to predicting response

The tumor suppressor p53 is mutated or inactivated in the majority of cancers, and about one-third of breast cancers have mutations in the gene. It has long been thought that normal p53 results in a better chemotherapy response, but the evidence in breast cancer has been conflicting.

According to the National Cancer Institute, about 227,000 women in the United States are diagnosed with breast cancer each year.

In this study, doxorubicin-treated p53 mutant tumor cells did not stop cell proliferation, leading to abnormal mitoses and cell death, whereas tumors with normal p53 arrested, avoiding mitotic catastrophe.

"There are a lot of data out there on responses of women to doxorubicin and other drugs that break DNA," Lozano said. "The response rates were mixed, and we never understood the difference. Now we understand that we need to know the p53 status to predict a response."

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Normal gene hinders breast cancer chemotherapy

Mutated tumor suppressor gene p53 leads to better results

Newswise HOUSTON - Presence of normal p53, a tumor suppressor gene, instead of a mutated version, makes breast cancer chemotherapy with doxorubicin less effective. The preclinical study led by MD Anderson scientists was published today in the journal Cancer Cell.

The research, which challenges the existing paradigm, is another step closer to personalized cancer medicine for breast cancer.

"It's really important to understand the genetic defects a tumor cell has before we treat it," said lead author Guillermina Lozano, Ph.D., professor and chair of the Department of Genetics. "What we learned here is the complete opposite of what we expected. We thought tumors would respond better to treatment if the p53 gene were normal. But the opposite was true, and for a really interesting reason."

Lozano said the research in mouse models showed that non-mutated p53 halted cell division, initiating a senescence (cell aging) process that allowed cells to survive. These senescent cells produce factors that stimulate adjacent cells to grow, fueling the relapse. Mutant p53 cells do not arrest and proceed through the cell cycle into cell division with broken chromosomes caused by the chemotherapy.

"That's a signal for the cell to die," she said. "It can't go any farther."

P53 status crucial to predicting response

The tumor suppressor p53 is mutated or inactivated in the majority of cancers, and about one-third of breast cancers have mutations in the gene. It has long been thought that normal p53 results in a better chemotherapy response, but the evidence in breast cancer has been conflicting.

According to the National Cancer Institute, about 227,000 women in the United States are diagnosed with breast cancer each year.

In this study, doxorubicin-treated p53 mutant tumor cells did not stop cell proliferation, leading to abnormal mitoses and cell death, whereas tumors with normal p53 arrested, avoiding mitotic catastrophe.

Originally posted here:
Preclinical Research Shows Normal Gene Hinders Breast Cancer Chemotherapy

Critics caution against opening a 'Pandora's box' which could lead to a trend towards 'designer babies'

By Fiona Macrae

PUBLISHED: 19:56 EST, 11 June 2012 | UPDATED: 19:56 EST, 11 June 2012

The creation of babies with three genetic parents would be an amazing opportunity for families whose lives have been blighted by incurable diseases, say an eminent group of experts on ethics in science.

The influential Nuffield Council on Bioethics conceded that while those with religious views might view the advance as an abomination, there is no ethical reason to stop it, provided it is proved to be safe and effective.

The approval comes as pressure builds on the Government to amend the law to allow the genetic engineering of eggs and embryos, creating babies free of devastating genetic diseases.

Three parents? Ethicists have decided that mixing DNA from more than two parents is acceptable if it is used to cure hereditary diseases

The children would effectively have two mothers and one father. Those in favour say it would give couples who have endured the heartbreak of miscarriages and stillbirths, and children who have died while still young, the option of having a healthy family.

But critics say the science is too risky and the safety of the baby should take precedence over a womans desire to be a mother.

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Experts on ethics back creation of babies with three parents saying it is 'amazing opportunity' for families blighted ...

Newswise ATHENS, Ohio (June 11, 2012)Scientists have found new genetic information that shows how harmful bacteria cause the acute diarrheal disease shigellosis, which kills more than a million people worldwide each year.

The research, which could lead to the development of future treatments, was published today in the journal PLoS ONE. The study was led by Ohio University scientist Erin Murphy and doctoral student William Broach, with contributions from University of Nevada, Las Vegas and University of Texas at Austin researchers.

When the disease-causing bacterium Shigella invades a human host, environmental conditions there, such as changes in temperature or pH, stimulate a genetic expression pathway within the bacterium that allows it to survive and cause disease. Central to this genetic pathway are two proteins, VirF and VirB. VirF functions to increase production of VirB which, in turn, promotes the production of factors that increases the bacteriums virulence, or ability to cause illness in its host.

Its like a domino effect, said Murphy, assistant professor of bacteriology in the Ohio University Heritage College of Osteopathic Medicine.

Murphy and Broachs new study, however, suggests that production of VirB can be controlled independently of VirF. It also shows that the VirF-independent regulation is mediated by a specific small RNA, a special type of molecule whose job is to control the production of particular targets. This is the first study to demonstrate that transcription of virB is regulated by any factor other than VirF, Murphy explained.

The research not only reveals the intricate level of gene expression the bacteria employ to survive in the human body, but potentially could lead to new treatments. Currently, antibiotics are prescribed to patients with the disease.

These findings are feeding into the basic understanding of this gene expression so that future researchers can work to disrupt it, Broach said. The more we know about it, the more targets we have to disrupt it and to possibly develop targeted antibiotic treatments.

For those living in developing countries, where access to clean drinking water can be scarce, an improved medical treatment for shigellosis could mean the difference between life and death.

In the United States, if we get severe diarrhea we can go to the store and get Gatorade, Murphy said. But if you're already starving to begin with because you don't have access to good food and clean water, then you get shigellosis on top of thatand you dont have good water to rehydrate yourselfthats when the deaths happen.

The disease, which is transmitted person to person or through contaminated food or water sources, has an infectious dose of just 10 organisms, meaning as few as 10 organisms can cause disease in a healthy person. This infectious dose is exceedingly low compared to other bacteria that require tens of thousands of organisms to cause disease.

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Scientists Find New Genetic Path to Deadly Diarrheal Disease

June 11, 2012 in Health

Deborah L. Shelton Chicago Tribune (MCT)

The latest advance in prenatal genetic testing purports to offer parents more detailed information than ever about the child they are expecting. But for some, the new answers could lead to another round of questions.

The technology allows doctors to detect small or subtle chromosomal changes in a fetus such as missing or extra pieces of DNA that could be missed by standard tests.

Most parents will get results confirming a normal pregnancy. But some will learn that their baby has a birth defect, a developmental problem or other medical condition, and in a small number of cases the test will detect things that no one knows quite how to interpret.

The information can allow parents to prepare for early intervention and treatment, but it also could raise questions about terminating the pregnancy or lead to nagging worry over uncertain results.

The Reproductive Genetics Institute in Chicago, which has helped pioneer the rapidly developing field of prenatal diagnosis and testing, recently began offering the procedure array comparative genomic hybridization, or array CGH for short to any pregnant woman who wants it.

The technology has been available for a number of years but it has almost never been used prenatally, said Dr. Norman Ginsberg, an obstetrician specializing in prenatal genetic testing at the institute. We think this is the beginning of the next generation of how well look at things.

Other medical experts see the technology as promising but have concerns about using it as a first-line test because of the potential drawbacks and the lack of published research. The availability of array CGH also raises fundamental, sometimes delicate, questions for parents.

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Prenatal genetic test offers more information, raises questions - Mon, 11 Jun 2012 PST

Shares of Seattle Genetics (Nasdaq: SGEN) hit a 52-week high on Friday. Let's take a look at how it got there and see whether clear skies are still in the forecast.

How it got hereIf you're looking for one particular sector that's largely ignored the recent correction, biotechnology would be it.

Seattle Genetics is one of many cancer-focused biotechs tipping the scales at a new high. But it isn't just Seattle Genetics' drugs that have investors excited; it's the pathway by which they work that has both patients and Wall Street abuzz.

Seattle Genetics is one of a handful of biotechs focused on researching antibody-drug conjugates. These ADC's will have a toxin attached to them that only releases when it comes in contact with a very specific protein. For Seattle Genetics' lead drug, Adcetris, which is used to treat Hodgkin's lymphoma, this protein is CD30. When the ADCs come in contact with this protein, the cancer cell is destroyed with minimal side effects and considerably better efficiency (i.e., healthy cells remain predominantly unaffected).

Another firm that's had success with ADCs is ImmunoGen (Nasdaq: IMGN) , whose targeted antibody payload technology supplies the toxin and linker currently used in Genentech's advanced breast cancer treatment, T-DM1 (owned by Roche), which is currently in late-stage trials.

As always, the biggest concern with a company like Seattle Genetics is whether it can turn these aspirations into actual results. Too often we see drug hopefuls fizzle out as constant innovation in the sector and poor product launches doom a stock. Three years ago, Dendreon's (Nasdaq: DNDN) Provenge treatment was supposed to completely change the way we looked at late-stage prostate cancer and become a blockbuster treatment. Three years later, the treatment's $93,000 price tag and a pitiful product launch have Dendreon losing money hand over fist. At a price tag in excess of $100,000, Adcetris, and any future compounds, risks the same fate.

How it stacks upLet's see how Seattle Genetics stacks up next to its peers.

SGEN data by YCharts

In theory, there are only two companies utilizing ADC drug-combining technology: Seattle Genetics and ImmunoGen. I chose to include Pfizer (NYSE: PFE) here as well because it developed an ADC in 2010 called Mylotarg that it pulled from the market because the toxin would not stay linked to the antibody long enough to hit the target cancer cells.

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How High Can Seattle Genetics Fly?

SAN DIEGO , June 11, 2012 /CNW/ - Fate Therapeutics, Inc. in collaboration with BD Biosciences, a segment of BD (Becton, Dickinson and Company), today announced the introduction of the first induced pluripotent stem cell (iPSC)-related product resulting from the collaboration between the two companies. BD SMC4 is a patent protected, pre-formulated cocktail of small molecules for improving cellular reprogramming efficiencies and for enabling single-cell passaging and flow cytometry sorting of iPSCs in feeder cell-free and other pluripotent cell culture systems.

"iPSCs have the potential to redefine the way medical research is conducted," said Dr. Charles Crespi , Vice President at BD Biosciences. "However, most current reprogramming technologies are inefficient, which slows research efforts. BD SMC4 is an exciting complement to the BD portfolio of stem cell technologies that can accelerate the pace of research, and, ultimately, drug development."

The collaboration between BD Biosciences and Fate Therapeutics seeks to provide life science researchers and the pharmaceutical community reliable access to advanced iPSC tools and technologies. These technologies are for use in human disease research, drug discovery and the manufacture of cell-based therapies. The identification of the small molecule additives, and their use in an industrial platform for iPSC generation and characterization was recently published in the journal, Scientific Reports (Valamehr et al Scientific Reports 2, Article number: 213, 2012).

"Our research focus has uncovered novel technologies to enable the commercial and industrial application of iPS cells," said Dr. Peter Flynn , Vice President of Biologic Therapeutics at Fate Therapeutics. "The BD SMC4 media additive was developed at Fate to enable our scientists to internally perform high-throughput generation, clonal selection, characterization and expansion of pluripotent cells, and we are excited to empower the stem cell research community with these important iPSC technologies through our collaboration with BD."

iPSC technology holds great promise for disease modeling, drug screening and toxicology testing as well as for autologous and allogeneic cell therapy. Building on the foundational work of its scientific founders, Drs. Rudolf Jaenisch and Sheng Ding, Fate Therapeutics is developing a suite of proprietary products and technologies to overcome the remaining technical hurdles for iPS cell integration into the therapeutic development process. Under the three-year collaboration, Fate and BD will co-develop certain stem cell products using Fate's award-winning iPSC technology platform, and BD will commercialize these stem cell products on a worldwide basis. The iPSC product platform of Fate Therapeutics is supported by foundational intellectual property including U.S. Patent No. 8,071,369, entitled "Compositions for Reprogramming Somatic Cells," which claims a composition comprising a somatic cell having an exogenous nucleic acid that encodes an Oct4 protein introduced into the cell.

About Fate Therapeutics, Inc. Fate Therapeutics is an innovative biotechnology company developing novel stem cell modulators (SCMs), biologic or small molecule compounds that guide cell fate, to treat patients with very few therapeutic options. Fate Therapeutics' lead clinical program, ProHema, consists of pharmacologically-enhanced hematopoietic stem cells (HSCs), designed to improve HSC support during the normal course of a stem cell transplant for the treatment of patients with hematologic malignancies. The Company is also advancing a robust pipeline of human recombinant proteins, each with novel mechanisms of action, for skeletal muscle, beta-islet cell, and post-ischemic tissue regeneration. Fate Therapeutics also applies its award-winning, proprietary induced pluripotent stem cell (iPSC) technology to offer a highly efficient platform to recapitulate human physiology for commercial scale drug discovery and therapeutic use. Fate Therapeutics is headquartered in San Diego , CA, with a subsidiary in Ottawa , Canada . For more information, please visit http://www.fatetherapeutics.com.

About BDBD is a leading global medical technology company that develops, manufactures and sells medical devices, instrument systems and reagents. The Company is dedicated to improving people's health throughout the world. BD is focused on improving drug delivery, enhancing the quality and speed of diagnosing infectious diseases and cancers, and advancing research, discovery and production of new drugs and vaccines. BD's capabilities are instrumental in combating many of the world's most pressing diseases. Founded in 1897 and headquartered in Franklin Lakes , New Jersey, BD employs approximately 29,000 associates in more than 50 countries throughout the world. The Company serves healthcare institutions, life science researchers, clinical laboratories, the pharmaceutical industry and the general public. For more information, please visit http://www.bd.com.

SOURCE Fate Therapeutics, Inc.

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Fate Therapeutics And BD Biosciences Launch BD™ SMC4 To Improve Cellular Reprogramming And IPS Cell Culture Applications

OMAHA, Neb.--(BUSINESS WIRE)--

Transgenomic, Inc. (TBIO) announced that the US Patent and Trademark Office has issued patent number US 8,137,919 entitled Method of Determining the Sensitivity of Cancer Cells to EGFR Inhibitors including Cetuximab, Panitumumab and Erlotinib. The patent was exclusively licensed to Transgenomic by the Montefiore Medical Center (Bronx, NY, US) and includes all tumor types and targeted therapies that may be influenced by PIK3CA mutation status.

Montefiore inventors Drs. Sanjay Goel and John Mariadason have demonstrated that key mutations in the gene PIK3CA are powerful predictors for the efficacy of EGFR-targeted therapies such as cetuximab (Erbitux), panitumumab (Vectibix) and erlotinib (Tarceva). These findings were published in the June 2012 issue of Clinical Colorectal Cancer by the same researchers and have been reproduced in other independent studies.

Assays using Transgenomics proprietary SURVEYOR Scan, REVEAL ICE COLD-PCR and BLOCker-Sequencing for complete detection of PIK3CA mutations have been developed. The extremely high sensitivity of Transgenomics REVEAL ICE COLD-PCR technology enables the use of virtually any sample type including blood and circulating tumor cells. Non-invasive testing allows for more frequent and accurate profiling of a cancer as it responds to treatment and gains additional mutations.

The recent issuing of this important patent is a significant milestone in the continued development of our genetic biomarker intellectual property portfolio, said Craig Tuttle, CEO of Transgenomic. Since exclusively licensing this patent we have been able to effectively apply our high sensitivity mutation detection technologies, such as SURVEYOR Scan, REVEAL ICE COLD-PCR and BLOCker-sequencing, to PIK3CA assays in order to be able to detect genetic variations in very low mutant load samples, such as plasma, serum and circulating tumor cells.

Tuttle added that, The number of genes associated with the effectiveness of targeted cancer treatments is increasing; our strategy is to provide a complete portfolio of best-in-class kits for clinically relevant mutations using our proprietary and extremely sensitive technologies. These assays will also be available through our CLIA and Pharmacogenomics laboratories to support clinicians and pharmaceutical research and trials.

About Transgenomic

Transgenomic, Inc. (www.transgenomic.com) is a global biotechnology company advancing personalized medicine in cancer and inherited diseases through its proprietary molecular technologies and world-class clinical and research services. The Company has three complementary business divisions: Transgenomic Pharmacogenomic Services is a contract research laboratory that specializes in supporting all phases of pre-clinical and clinical trials for oncology drugs in development. Transgenomic Clinical Laboratories specializes in molecular diagnostics for cardiology, neurology, mitochondrial disorders, and oncology. Transgenomic Diagnostic Tools produces equipment, reagents, and other consumables that empower clinical and research applications in molecular testing and cytogenetics. Transgenomic believes there is significant opportunity for continued growth across all three businesses by leveraging their synergistic capabilities, technologies, and expertise. The Company actively develops and acquires new technology and other intellectual property that strengthen its leadership in personalized medicine.

Forward-Looking Statements

Certain statements in this press release constitute forward-looking statements of Transgenomic within the meaning of the Private Securities Litigation Reform Act of 1995, which involve known and unknown risks, uncertainties and other factors that may cause actual results to be materially different from any future results, performance or achievements expressed or implied by such statements. Forward-looking statements include, but are not limited to, those with respect to management's current views and estimates of future economic circumstances, industry conditions, company performance and financial results, including the ability of the Company to grow its involvement in the diagnostic products and services markets. The known risks, uncertainties and other factors affecting these forward-looking statements are described from time to time in Transgenomic's filings with the Securities and Exchange Commission. Any change in such factors, risks and uncertainties may cause the actual results, events and performance to differ materially from those referred to in such statements. Accordingly, the Company claims the protection of the safe harbor for forward-looking statements contained in the Private Securities Litigation Reform Act of 1995 with respect to all statements contained in this press release. All information in this press release is as of the date of the release and Transgenomic does not undertake any duty to update this information, including any forward-looking statements, unless required by law.

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PIK3CA Gene Patent for Predicting Response to Targeted Therapy Issued – Exclusively Licensed to Transgenomic

Public release date: 10-Jun-2012 [ | E-mail | Share ]

Contact: Dr. Aarno Palotie aarno.palotie@fimm.fi 358-041-501-5915 University of Helsinki

Researchers studied genetic data of more than 11 000 people and found altogether six genes that predispose to migraine without aura. Four of these genes are new and two of them confirm previous findings.

The new genes identified in this study provide further evidence for the hypothesis that dysregulation of molecules important in transmitting signals between brain neurons contribute to migraine. Two of the genes support the hypothesis of a possible role of blood vessels and thus disturbances in blood flow.

The researchers carried out what is known as a genome-wide association study (GWAS) to zoom in on genome variants that could increase susceptibility to migraine; they compared genomes of 4800 migraine patients with more than 7000 non-migraine individuals. The project was performed by the International Headache Genetics Consortium consisting of leading migraine researches from Europe and Australia.

This was the third report on genes predisposing people to common forms of migraine, but the first one on the most common migraine subtype. "The study establishes for the first time a specific gene that contributes to this common disease" said Professor Aarno Palotie at FIMM and the Wellcome Trust Sanger Institute, the chair of the International Headache Genetics Consortium.

The carefully studied migraine patients collected from specialized headache clinics were provided a strong basis for the success of this study.

Migraine affects approximately one in six women and one in eight men, making it a leading cause of work absence and short-term incapacity: 25 million school or work days are lost for migraine each year. A US report measures its economic costs as similar to those of diabetes and WHO lists it as one of the top twenty diseases with the causes of years lived with disability (YLDs). In up to one third of migraine patients, the headache phase may be preceded or accompanied by transient neurological disturbances, the so-called aura (i.e. migraine with aura), while the majority of patients suffer from migraine without aura.

"Studies of this kind are possible only through large-scale international collaboration - bringing together the wealth of data with the right expertise and resources. The identified genes open new doors to investigate how this type of migraine comes about," said Dr. Arn van den Maagdenberg, one of the senior authors on the paper.

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Researchers found 4 gene loci predisposing people to the most common subtype of migraine

ScienceDaily (June 10, 2012) An international research group from several European countries and Australia has identified four new gene loci predisposing people to the most common subtype of migraine, migraine without aura. About 2/3 of migraine sufferers belong to this group.

Researchers studied genetic data of more than 11,000 people and found altogether six genes that predispose to migraine without aura. Four of these genes are new and two of them confirm previous findings.

The new genes identified in this study provide further evidence for the hypothesis that dysregulation of molecules important in transmitting signals between brain neurons contribute to migraine. Two of the genes support the hypothesis of a possible role of blood vessels and thus disturbances in blood flow.

The researchers carried out what is known as a genome-wide association study (GWAS) to zoom in on genome variants that could increase susceptibility to migraine; they compared genomes of 4800 migraine patients with more than 7000 non-migraine individuals.

The project was performed by the International Headache Genetics Consortium consisting of leading migraine researches from Europe and Australia.

This was the third report on genes predisposing people to common forms of migraine, but the first one on the most common migraine subtype. "The study establishes for the first time a specific gene that contributes to this common disease" said Professor Aarno Palotie at FIMM and the Wellcome Trust Sanger Institute, the chair of the International Headache Genetics Consortium. The carefully studied migraine patients collected from specialized headache clinics were provided a strong basis for the success of this study.

Migraine affects approximately one in six women and one in eight men, making it a leading cause of work absence and short-term incapacity: 25 million school or work days are lost for migraine each year. A US report measures its economic costs as similar to those of diabetes and WHO lists it as one of the top twenty diseases with the causes of years lived with disability (YLDs). In up to one third of migraine patients, the headache phase may be preceded or accompanied by transient neurological disturbances, the so-called aura (i.e. migraine with aura), while the majority of patients suffer from migraine without aura.

"Studies of this kind are possible only through large-scale international collaboration -- bringing together the wealth of data with the right expertise and resources. The identified genes open new doors to investigate how this type of migraine comes about," said Dr. Arn van den Maagdenberg, one of the senior authors on the paper.

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Four new gene loci predisposing people to the most common subtype of migraine

09-06-2012 16:05 06/07-08/2012 Mom gave a blood sample. Dad spit. The entire genome of their fetus was born. Researchers at the University of Washington have, for the first time, done a near-total genome sequence of a fetus in this way. Scientists published the results of this study in the journal Science Translational Medicine, suggesting that thousands of genetic diseases could be detected in children while they are still in the fetal stage. More:

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Welcome to Gattaca: Genetic Discrimination Becomes Reality - Video

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/5f9pm7/bioinformatics_g) has announced the addition of the "Bioinformatics - Global Strategic Business Report" report to their offering.

This report analyzes the worldwide markets for Bioinformatics in US$ Million by following Product Segments: Software, Hardware, and Biocontent. The report provides separate comprehensive analytics for the US, Canada, Japan, Europe, Asia-Pacific, and Rest of World. Annual estimates and forecasts are provided for the period 2009 through 2017. Also, a six-year historic analysis is provided for these markets. Market data and analytics are derived from primary and secondary research. Company profiles are primarily based upon search engine sources in the public domain.

Companies Mentioned

- 3rd Millennium Inc.

- Accelrys Inc.

- Affymetrix Inc.

- Agilent Technologies

- Celera Group

- Gene Logic

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Research and Markets: Bioinformatics - Global Strategic Business Report - 2012 Study Profiles 206 Companies Including ...

07-06-2012 07:52 Stem cells differ from other types of cells as they are unspecialized cells that are capable of differentiating into almost any type of specialised cells. Stem cells have the ability to replace the diseased and damaged tissue in the body, without the risk of rejection and any side effects. Therapy performed using stem cells is termed as "Regenerative medicine" and has many potential benefits in treating a wide variety of diseases and injuries. The journal is the major open access forum for translational research in stem cell therapies.

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OMICS Group :: Journal of Stem Cell Research

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Stem cell therapy offers new treatment options for pets -- and humans

DUBLIN--(BUSINESS WIRE)--

Dublin - Research and Markets (http://www.researchandmarkets.com/research/p4qg7d/molecular_and_cell) has announced the addition of John Wiley and Sons Ltd's new book "Molecular and Cellular Therapeutics" to their offering.

Molecular and Cellular Therapeutics aims to bring together key developments in the areas of molecular diagnostics, therapeutics and drug discovery. The book covers topics including diagnostics, therapeutics, model systems, clinical trials and drug discovery. The developing approaches to molecular and cellular therapies, diagnostics and drug discovery are presented in the context of the pathologies they are devised to treat.

Key Topics Covered:

1 Cytochrome P450 pharmacogenetics: from bench to bedside

2 Cancer biomarkers for diagnosis, prognosis and therapy

3 HER2 targeted therapy-induced gastrointestinal toxicity: from the clinical experience to possible molecular mechanisms

4 Antibody-targeted photodynamic therapy

5 Anti-ageing strategy of the lung for chronic inflammatory respiratory disease - targeting protein deacetylases

6 RNA interference: from basics to therapeutics

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Research and Markets: Molecular and Cellular Therapeutics

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/xp9wx4/pharmacogenetics_a) has announced the addition of John Wiley and Sons Ltd's new book "Pharmacogenetics and Individualized Therapy" to their offering.

The One-Stop Reference To Pharmacogenetics And Its Impact On Pharmaceuticals, Therapeutics, And Clinical Practices

Pharmacogenetics and Individualized Therapy offers thorough coverage of the study of the genetic determinants of drug response at the single gene leveland its impact on pharmaceuticals, therapeutics, and clinical practice. Providing an overview of the molecular basis of pharmacogenetics, the book helps readers understand the implications of genetic variability on pharmacokinetics and pharmacodynamics, as well as other aspects such as adverse drug reactions. Providing coverage of specific disease areas, including cardiovascular concerns, cancer and asthma/COPD, transplantation, and pain medication, the book also looks at the clinical practices, along with the psychiatric and ethical issues that have come to dominate conversation about pharmacogenetics.

The technological applications of pharmacogenetics, including genotyping, drug disposition (metabolism and enzymes), and the impact of this research on the pharmaceutical industry and regulatory matters are all addressed in chapters by internationally recognized leaders from both academia and industry.

Including chapters on specific therapeutic areas and clinical aspects, Pharmacogenetics and Individualized Therapy helps readers, whether they're students or researchers, to understand the implications of genetic variability on pharmacokinetics and pharmacodynamics.

Authors

ANKE-HILSE MAITLAND-van der ZEE, PhD, is Associate Professor of Pharmacogenetics

Pharmacogenomics at Utrecht University, the Netherlands.

ANN K. DALY, PhD, is Professor of Pharmacogenetics at Newcastle University, UK.

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Research and Markets: Pharmacogenetics and Individualized Therapy

(CBS News) Parents designing babies is "a real risk" in the wake of new research that's given scientists the ability to map the genetic code of a fetus, according to Dr. Eric Schadt, chairman of the Genetics Department at New York's Mount Sinai Medical Center.

He said the test that requires only a blood sample from the mother and saliva from the father to diagnose more than 3,000 genetic disorders before a baby is born is a positive thing, but brings up many ethical and social questions that need to be discussed prior to the test's use, such as the potential for abortion for a variety of reasons following the test.

Schadt said on "CBS This Morning" that the test, utilized in a University of Washington study, will be available for wide use in five years or more. Until then, he said, it needs to be talked about extensively.

Researchers sequence fetus' entire genome from mom's blood and dad's saliva

He explained, "As we go through, how do we adapt to that kind of testing, the social implications; what sorts of policies should we be thinking about? Those are the discussions we should be having right now about how to leverage this information in ways that are benefiting humankind, not biasing the type of population through unnatural selection of traits."

Schadt said education of the general population and lawmakers on what's coming is needed to prevent what he called an "extreme designer baby mentality."

When asked if new laws are needed to avoid designing babies on traits not based on health, Schadt said, "It's not unlike choosing to terminate a pregnancy based on the sex of the child. Those are the sorts of things we want to avoid."

For more with Schadt on the test, watch the video in the player above.

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Expert on gene test: Baby designing a real risk