In Early Study, Procedure Helps Teens Halt Insulin Injections

June 11, 2012 (Philadelphia) -- In an early study, an experimental stem cell procedure helped 15 teens with type 1 diabetes stay off of insulin injections for about 1.5 years, on average.

The study was very small, and the procedure is not ready for widespread use. "We now have a unique approach with some positive findings, but it's still early. We need to better understand the biology behind the treatment and follow patients for long-term side effects," Robert E. Ratner, MD, chief scientific and medical officer of the American Diabetes Association, tells WebMD.

This is the latest of several stem cell studies to show promising results for the treatment of type 1 diabetes, Ratner notes.

In the new study, 15 of 28 teens with type 1 diabetes who got an experimental treatment using their own stem cells went into remission and did not need insulin injections for an average of about 1.5 years.

The "cocktail treatment" combines stem cell therapy with drugs that suppress the body's immune system. In type 1 diabetes, the immune system attacks and destroys insulin-producing cells within the pancreas.

The experimental treatment is called autologous nonmyeloablative hematopoietic stem cell transplantation (HSCT). It aims to kill the destructive immune system cells and replace them with immature stem cells not programmed to destroy insulin-producing cells.

First, patients are given drugs to stimulate production of blood stem cells. The blood stem cells are then removed from the body and frozen. Then, patients are hospitalized and given drugs to kill the destructive immune system cells. The harvested blood stem cells are then put back into the patient.

Eight teens who took part in the study have remained insulin-free for two years, on average. One patient has gone without insulin injections for 3.5 years.

"All our patients considered the [treatment] to be worthwhile and beneficial, though some patients experienced side effects," study head Weiqiong Gu, MD, of Ruijin Hospital in Shanghai, tells WebMD.

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Experimental Stem Cell Treatment Tested for Type 1 Diabetes

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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.

###

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

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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

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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

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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

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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

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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

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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

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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

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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

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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.

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Preclinical Research Shows Normal Gene Hinders Breast Cancer Chemotherapy

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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 ...

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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

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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

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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?

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The cure that helped Good Morning America co-host Robin Roberts beat breast cancer may have caused the new disease shes battling, experts said Monday.

And before Roberts undergoes a bone marrow transplant to combat MDS, or myelodysplastic syndrome, she will need to subject her already weakend body to even more chemotherapy.

I know it seems counterintuitive, said Dr. Azra Raza, who heads the MDS Center at New York-Presbyterian Hospital/Columbia. But this is the only way we know how to get rid of these damaged cells before we can start treatment.

MDS is a disease of the blood and bone marrow that if left untreated can lead to leukemia and death.

It is a relatively rare condition, said Raza. The are 15,000 cases diagnosed annually every year in the U.S.

Patients who have been exposed to benzene or who have undergone chemotherapy or radiation treatments for cancer are the most susceptible to MDS, said Azra.

Sometimes stem cells are damaged during radiation or chemotherapy, Raza said. MDS is a bad disease to have.

There are different degrees of severity, added Robert Bona, Professor of Medical Sciences at Quinnipiac University. The ones that are most severe are treated with bone marrow transplants, if theyre young enough and a donor can be found.

Bone marrow donors are scarce, especially for African-American women.

Luckily for Roberts, her sister Sally-Ann Roberts, an anchor at a New Orleans TV station, is a match. And the 51-year-old newscasters age and otherwise good physical condition greatly improve her chances of licking this disease, the experts said.

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Robin Roberts’ breast cancer cure may have caused new illness

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istock

"Good Morning America's" Robin Roberts announced this morning that she has myelodysplastic syndrome, or MDS. The syndrome is also known as preleukemia.

MDS can be broken down by its name: Myeloid refers to a type of blood cell; dysplasia means a problem with the development of those cells.

The condition occurs when "something goes wrong in your bone marrow -- the spongy material inside your bones where blood cells are made," according to the Mayo Clinic.

A healthy person's bone marrow produces stem cells that mature into blood cells. But the bone marrow of a person with MDS produces abnormal stem cells that turn into defective blood cells.

Deformed cells get into the bloodstream and eventually outnumber healthy blood cells, according to the National Cancer Institute. Often the deformed blood cells don't live as long as they should, producing a shortage in the body.

There are several types of MDS, depending on the kind of myeloid cells - red blood cells, white blood cells or platelets - that are being affected. Having too few red blood cells results in anemia; having too few white blood cells can result in frequent infections.

The term "preleukemia" is a bit misleading, as most MDS cases do not become cancerous. Certain types of MDS can progress to acute myeloid leukemia, however.

MDS can be caused by exposure to chemotherapy and radiation, common cancer treatments. (Roberts is a breast cancer survivor.)

Symptoms are rare during the early stage of the disease, but can include tiredness, shortness of breath and easy bruising/bleeding. Doctors generally diagnose through a blood test and a bone marrow biopsy.

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What is preleukemia or MDS?

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"Good Morning America" co-host Robin Roberts, who five years ago beat breast cancer, said Monday that she has now been diagnosed with myelodysplastic syndrome, a blood disorder caused by chemotherapy for her cancer. She is now taking chemotherapy in preparation for receiving a bone marrow transplant from her sister later this year. Because she is relatively young and healthy, the combination of treatments should cure the condition, doctors have told her.

Myelodysplastic syndrome is sometimes known as pre-leukemia, and many researchers now believe that, if untreated, it will progress to acute myeloid leukemia. It most commonly strikes people between the ages of 58 and 75, but can occur at any age, particularly if the patient has had cancer chemotherapy. It is estimated to affect as many as 50 Americans per 100,000, with about 20,000 new cases each year.

It is a disease of the bone marrow -- the semi-liquid tissue inside bones that produces blood cells. Stem cells in the bone marrow develop into two types of cells, myeloid and lymphoid. Lymphoid cells go on to become white blood cells that fight infections. Myeloid cells develop into three different types of cells: red blood cells, which carry oxygen; platelets, which control bleeding by forming clots; and white blood cells. In myeloplastic syndrome the myeloid cells stop developing; they do not function normally and either die in the bone marrow or soon after they enter the blood. The dysfunctional cells crowd out healthy cells.

Symptoms are often not apparent, but can include shortness of breath, weakness or tiredness, pale skin, easy bruising and bleeding, and fever or frequent infections. The best treatment for the type of disorder Roberts is suffering is to kill all the stem cells with chemotherapy, then replace them with functioning stem cells from a donor -- in this case, her sister. Treatment is usually more effective when the disorder has been caused by chemotherapy.

Roberts announced her condition on the show and on the ABC blog, saying she will continue her job at "Good Morning America" and that "My doctors tell me Im going to beat this and I know its true."

LATimesScience@gmail.com

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'Good Morning America' co-host Robin Roberts has blood disorder

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061112_RobinRobertsABC_ftrGood Morning America host Robin Roberts announced June 11 that she was diagnosed with Myelodysplastic Syndrome (MDS), a blood disorder affecting the stem cells in the bone marrow. Celebrities and first lady Michelle Obama have already offered their support on Twitter!

Robin Robertshas a special connection to The Obamas: She found out she was interviewingPresident Obama on the very same day she underwent a painful bone marrow extraction. The combination of landing the biggest interview of my career and having a drill in my back reminds me that God only gives us what we can handle and that it helps to have a good sense of humor when we run smack into the absurdity of life, Robin wrote on her blog. And First Lady Michelle Obama was quick to offer her condolences to the GMA host.

.@RobinRoberts, Barack and I have you in our prayers. We believe in you and thank you for bringing awareness and hope to others. mo, Michelletweeted June 11.

Heres what other celebs tweeted about Robin:

prayers for Robin Roberts tweeted hip-hop mogul Russell Simmons.

We all love you & are cheering you on!! tweeted fellow journalist Katie Couric.

I wish my friend@RobinRobertsthe strength, faith & love she will need on this new journey. I send all that and more. tweeted Maria Shriver.

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Michelle Obama & More Celebs Tweet At Robin Roberts After MDS Diagnosis

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Verinata Health CEO Caren Mason has resigned but will continue to provide the company with consultative services. Mason joined Verinata in November 2010. She was previously the president and CEO of Quidel, president and CEO of MiraMedica, CEO of eMed Technologies, and general manager of GE Healthcare. The firm plans to recruit a new CEO.

Bruker has named Charles Wagner to be its new executive VP and chief financial officer, beginning at the end of June, Bruker said this week. Current CFO William Knight will continue to serve on the company's management team and will work with Wagner to ensure a smooth transition. Wagner also has stepped down from his positions on Bruker's board of directors and its audit committee, where he has served since 2010.

CLC Bio said this week that it has appointed Richard Lussier as director of business for the Americas region. He has worked in life sciences sales and commercial operations, most recently as VP of worldwide sales at RainDance Technologies. He formerly held leadership positions in sales, service, and support at Solexa, Fluidigm, Applied Biosystems, and Celera Genomics.

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Follow-Up Guide To Personalized Medicine Hits All The Right Notes

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11-06-2012 18:26 Strengths of the Saban Research Institute Developmental Biology/Regenerative Medicine Retreat by: David Warburton OBE, DSc, MD, MMM, FRCP, FRCS, FRCPCH Professor of Pediatrics, Surgery and Craniofacial Biology Director, Developmental Biology and Regenerative Medicine Program Director, California Institute for Regenerative Medicine Training Program and Shared Laboratory Saban Research Institute Children¹s Hospital Los Angeles Keck School of Medicine and Ostrow School of Dentistry University of Southern California

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Warburton Strengths of Saban Developmental Biology Regenerative Medicine Dept. - Video

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SAN DIEGO, June 11, 2012 /PRNewswire/ --

Shire plc, the global specialty biopharmaceutical company, announced today that its Regenerative Medicine business, Advanced BioHealing, Inc., has entered into a lease agreement with BioMed Realty Trust, Inc. which will allow the company to further expand its operational footprint and presence in the San Diego area over the next several years.

The new campus will provide Shire's Regenerative Medicine business the increased capacity it needs to meet future demand for its lead product, DERMAGRAFT, while offering additional space and infrastructure to manufacture new regenerative medicine products, in alignment with the business' strategic growth plan.

"We are committed to investing in and expanding our Regenerative Medicine business and with the signing of this lease, we are pleased to confirm and build our presence in San Diego with BioMed Realty as our real estate partner," said Kevin Rakin, Shire's Regenerative Medicine President. "This new campus will give us the flexibility and increased capacity we need to develop and manufacture new regenerative medicine therapies and build our foundation for continued growth in this exciting field."

Phase I of the site development will be in excess of 150,000 square feet and will house the company's manufacturing and associated support operations, commercial operations, corporate, and administrative functions. This expansion could create several hundred local jobs once the regenerative medicine campus is operational.

"Shire's commitment to growing its Regenerative Medicine business in San Diego is important to a region where one-in-10 people remain unemployed," said Congressman Brian Bilbray (CA-50). "This investment will not only provide additional opportunities for rewarding, high-paying jobs, but will ensure that San Diego remains a leader in the development of innovative patient care."

Shire expects to begin construction of the new campus in Sorrento Mesa in 2013, with initial occupancy targeted for 2014.

"We are pleased to enter into this partnership with Advanced BioHealing, which is the culmination of extensive, collaborative efforts by both companies to identify and execute on a real estate solution which will fully support their development and manufacturing needs," said Alan D. Gold, Chairman and Chief Executive Officer of BioMed Realty. "We look forward to working closely with the Advanced BioHealing and Shire teams to develop this future multi-phase campus for the development and commercialization of important regenerative medicine therapies."

The company plans to maintain its current DERMAGRAFT manufacturing facility on North Torrey Pines Road in La Jolla, CA, which currently employs nearly 200 people.

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Shire's Advanced BioHealing Commits to Developing Regenerative Medicine Campus in San Diego

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Newswise UCLA stem cell scientists purified a subset of stem cells found in fat tissue and made from them bone that was formed faster and was of higher quality than bone grown using traditional methods, a finding that may one day eliminate the need for painful bone grafts that use material taken from the patient during invasive procedures.

Adipose, or fat, tissue is thought to be an ideal source of cells called mesenchymal stem cells - capable of developing into bone, cartilage, muscle and other tissues - because they are plentiful and easily attained through procedures such as liposuction, said Dr. Chia Soo, vice chair for research at UCLA Plastic and Reconstructive Surgery. The co-senior authors on the project, Soo and Bruno Pault, are members of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

Traditionally, cells taken from fat had to be cultured for weeks to isolate the stem cells which could become bone, and their expansion increases risk of infection and genetic instability. A fresh, non-cultured cell composition called stromal vascular fraction (SVF) also is used to grow bone. However, SVF cells taken from adipose tissue are a highly heterogeneous population that includes cells that arent capable of becoming bone.

Pault and Soos team used a cell sorting machine to isolate and purify human perivascular stem cells (hPSC) from adipose tissue and showed that those cells worked far better than SVF cells in creating bone. They also showed that a growth factor called NELL-1, discovered by Dr. Kang Ting of the UCLA School of Dentistry, enhanced the bone formation in their animal model.

People have shown that culture-derived cells could grow bone, but these are a fresh cell population and we didnt have to go through the culture process, which can take weeks, Soo said. The best bone graft is still your own bone, but that is in limited supply and sometimes not of good quality. What we show here is a faster and better way to create bone that could have clinical applications.

The study appears June 11, 2012 in the early online edition of the peer-reviewed journal Stem Cells Translational Medicine, a new journal that seeks to bridge stem cell research and clinical trials.

In the animal model, Soo and Paults team put the hPSCs with NELL-1 in a muscle pouch, a place where bone is not normally grown. They then used X-rays to determine that the cells did indeed become bone.

The purified human hPSCs formed significantly more bone in comparison to the SVF by all parameters, Soo said. And these cells are plentiful enough that patients with not much excess body fat can donate their own fat tissue.

Soo said if everything goes well, patients may one day have rapid access to high quality bone graft material by which doctors get their fat tissue, purify that into hPSCs and replace their own stem cells with NELL-1 back into the area where bone is required. The hPSC with NELL-1 could grow into bone inside the patient, eliminating the need for painful bone graft harvestings. The goal is for the process to isolate the hPSCs and add the NELL-1 with a matrix or scaffold to aid cell adhesion to take less than an hour, Soo said.

Excitingly, recent studies have already demonstrated the utility of perivascular stem cells for regeneration of disparate tissue types, including skeletal muscle, lung and even myocardium, said Pault, a professor of orthopedic surgery Further studies will extend our findings and apply the robust osteogenic potential of hPSCs to the healing of bone defects.

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A Better Way to Grow Bone: Fresh, Purified Fat Stem Cells Grow Bone Better, Faster

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

Contact: Kim Irwin kirwin@mednet.ucla.edu 310-206-2805 University of California - Los Angeles Health Sciences

UCLA stem cell scientists purified a subset of stem cells found in fat tissue and made from them bone that was formed faster and was of higher quality than bone grown using traditional methods, a finding that may one day eliminate the need for painful bone grafts that use material taken from the patient during invasive procedures.

Adipose, or fat, tissue is thought to be an ideal source of cells called mesenchymal stem cells - capable of developing into bone, cartilage, muscle and other tissues - because they are plentiful and easily attained through procedures such as liposuction, said Dr. Chia Soo, vice chair for research at UCLA Plastic and Reconstructive Surgery. The co-senior authors on the project, Soo and Bruno Pault, are members of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

Traditionally, cells taken from fat had to be cultured for weeks to isolate the stem cells which could become bone, and their expansion increases risk of infection and genetic instability. A fresh, non-cultured cell composition called stromal vascular fraction (SVF) also is used to grow bone. However, SVF cells taken from adipose tissue are a highly heterogeneous population that includes cells that aren't capable of becoming bone.

Pault and Soo's team used a cell sorting machine to isolate and purify human perivascular stem cells (hPSC) from adipose tissue and showed that those cells worked far better than SVF cells in creating bone. They also showed that a growth factor called NELL-1, discovered by Dr. Kang Ting of the UCLA School of Dentistry, enhanced the bone formation in their animal model.

"People have shown that culture-derived cells could grow bone, but these are a fresh cell population and we didn't have to go through the culture process, which can take weeks," Soo said. "The best bone graft is still your own bone, but that is in limited supply and sometimes not of good quality. What we show here is a faster and better way to create bone that could have clinical applications."

The study appears June 11, 2012 in the early online edition of the peer-reviewed journal Stem Cells Translational Medicine, a new journal that seeks to bridge stem cell research and clinical trials.

In the animal model, Soo and Pault's team put the hPSCs with NELL-1 in a muscle pouch, a place where bone is not normally grown. They then used X-rays to determine that the cells did indeed become bone.

"The purified human hPSCs formed significantly more bone in comparison to the SVF by all parameters," Soo said. "And these cells are plentiful enough that patients with not much excess body fat can donate their own fat tissue."

Read the rest here:
A better way to grow bone: Fresh, purified fat stem cells grow bone faster and better

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DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/pqrlwc/analysis_of_the_st) has announced the addition of Frost & Sullivan's new report "Analysis of the Stem Cell Markets-Unlocking the New Era in Therapeutics" to their offering.

This Frost & Sullivan research service titled Analysis of the Stem Cell Markets-Unlocking the New Era in Therapeutics focuses on prospects for the stem cell therapeutics market in Europe and provides valuable recommendations and conclusions for market participants. Market segmentation is based on regulatory framework in Europe relating to research on adult and embryonic stem cells. The main countries discussed are the United Kingdom, Germany, France, Spain, Sweden, Finland, and the remaining parts of Europe.

Market Overview

New Applications in Drug Discovery Platforms to Drive Stem Cells Market

Stem cells offer exciting potential in regenerative medicine, and are likely to be widely used by mid-2017. Pharmaceutical, biotech and medical device companies are showing increased interest in stem cell research. The market will be driven by stem cell applications in drug discovery platforms and by successful academia -commercial company partnership models.

The high attrition rates of potential drug candidates has piqued the interest of pharmaceutical and biotech industries in stem cell use during the drug discovery phase, notes the analyst of this research. Previously, animal cell lines, tumours, or genetic transformation have been the traditional platform for testing drug candidates; however, these abnormal' cells have significantly contributed to a lack of translation into clinical studies. Many academic institutes and research centres are collaborating with biotechnology and pharmaceutical companies in stem cell research. This will provide impetus to the emergence of novel cell-based therapies.

Host of Challenges Need to be Confronted before Stem Cell Therapeutics can Realise its Potential

Key challenges to market development relate to reimbursement, ethics and the complexity of clinical trials. Securing reimbursement for stem cell therapeutic products is expected to be critical for commercial success. However, stem cell therapies are likely to be expensive. Insurers, therefore, may be unwilling to pay for the treatment. At the same time, patients are unlikely to be able to afford these treatments. The use of embryonic stem cells raises a host of thorny ethical, legal, and social issues, adds the analyst. As a result, market prices for various products may be affected. Moreover, many research institutes are adopting policies promoting the ethical use of human embryonic tissues. Such policies are hindering the overall research process for several companies working in collaboration with these institutes.

In addition to apprehensions about how many products will actually make it through human-based clinical trials, companies are also worried about which financial model can be applied to stem cell therapies, cautions the analyst. Possibly low return on investment (ROI) is also resulting in pharmaceutical companies adopting a cautious approach to stem cell therapeutics. To push through policy or regulatory reforms, the technology platform and geographical location of stem cell companies should complement the terms laid down in EMEA. The methodology for cell expansion and synchronisation must be optimised to acquire a large population of the desired cell at the right differentiation point, adds the analyst. More research is needed in human pluripotent and multi potent stem cell as it differs from mice to humans. Completion of clinical trials will be essential to ensure the safety and efficacy of the stem cell therapy.

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Research and Markets: Analysis of the Stem Cell Markets-Unlocking the New Era in Therapeutics

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