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New partnership to drive mass production of life-saving stem cells – Commercialization Impact Prize is first of its …

Posted: August 25, 2012 at 3:11 pm

TORONTO, ON Stem cells hold great promise for treating and curing numerous diseases; however, a major challenge facing scientists is how to produce stem cells in the massive quantities required for clinical use. The McEwen Centre for Regenerative Medicine (McEwen Centre) and the University of Toronto-based Centre for Commercialization of Regenerative Medicine (CCRM) are partnering to establish a fund that will drive research in this area. Several University of Toronto regenerative medicine scientists are affiliated with CCRM and the Scientific Director is Dr. Peter Zandstra of the Institute of Biomaterials and Biomedical Engineering.

The McEwen Centre-CCRM Commercialization Impact Prize launches today, and will solicit innovative ideas from regenerative medicine scientists working in labs throughout the McEwen Centre. The winning team(s) will be awarded up to $600,000 to pursue research that will determine how to manufacture stem cells for clinical use and drug screening.

This private-public funding partnership is an important step forward to accelerating the advance of a discovery from a lab bench to the patient and onto the global market. Scientists at the McEwen Centre are making significant progress towards finding a cure for diseases such as Type 1 diabetes and heart disease. Collaborative partnerships are the key to discovering the cures sooner! says Rob McEwen, co-founder of the McEwen Centre, and Chief Owner, McEwen Mining.

Deadline for submissions is October 15, 2012. The Prize will fund up to two, 2-year projects that address the following challenges:

Making the transition from pre-clinical to clinical mass production; and, Scaling up stem cell manufacturing for high throughput drug screening.

Overcoming the scale-up and manufacturing challenge of stem cells would be a huge advancement for the regenerative medicine [RM] industry and this initiative fits in perfectly with our mandate to bridge the RM commercialization gap, explains Dr. Michael May, CEO of the Centre for Commercialization of Regenerative Medicine. Were very pleased to be working with the McEwen Centre, already a partner of ours, to make this happen.

The Commercialization Impact Prize budget template and application form can be found here: http://ccrm.ca/Commercialization-Impact-Prize or http://mcewencentre.com/ccrm

About McEwen Centre for Regenerative Medicine The McEwen Centre for Regenerative Medicine was founded by Rob and Cheryl McEwen in 2003 and opened its doors in 2006. The McEwen Centre for Regenerative Medicine, part of Toronto-based University Health Network, is a world leading centre for stem cell research, facilitating collaboration between renowned scientists from 5 major hospitals in Toronto, the University of Toronto and around the world. Supported by philanthropic contributions and research grants, McEwen Centre scientists strive to introduce novel regenerative therapies for debilitating and life threatening illnesses including heart disease, spinal cord injury, diabetes, diseases of the blood, liver and arthritis.

About Centre for Commercialization of Regenerative Medicine (CCRM) CCRM, a Canadian not-for-profit organization funded by the Government of Canadas Networks of Centres of Excellence program and six institutional partners, supports the development of technologies that accelerate the commercialization of stem cell- and biomaterials-based technologies and therapies. A network of academics, industry and entrepreneurs, CCRM translates scientific discoveries into marketable products for patients. CCRM launched in Torontos Discovery District on June 14, 2011.

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Hormel Institute receives $1.7 million for skin cancer study

Posted: August 25, 2012 at 12:11 pm

By Kay Fate The Post-Bulletin, Austin MN

AUSTIN A five-year federal grant totaling more than $1.7 million has been awarded for skin cancer research led by Dr. Rebecca Morris, leader of the stem cells and cancer section at the Hormel Institute.

Morris, whose research uses adult, non-human stem cells, has been working to identify stem cell-regulating genes for 10 years. She now has found a gene that appears to be linked to stem cell numbers and helping to protect against skin tumor development.

The gene also might have an immune function in the skin that can fight bacteria and protect against environmental damage. As stem cell research leads to discoveries to improve health, these cells can be obtained through various ways such as from adult tissue stem cells or through bio-engineering to avoid the ethical issues of how to secure stem cells for treatment.

The new project, funded through 2017, will further Morris' research on that gene and the idea that, through using the gene, stem cells could be used to function as a way to protect the body.

The down side of stem cells is that they seem to be targets for cancer development, Morris said.

This is exciting for us because a gene whose function is to protect may do double duty by regulating stem cell activity related to the immune system, she said. If we can identify this gene, then maybe we could find a way to turn off the stem cells if theyre growing too fast, such as in cancer and other diseases involving too rapid cell growth.

With the title Identification of a Keratinocyte Stem Cell Regulatory Gene in the KSC2 Locus, the project is funded through the National Institute of Arthritis and Musculoskeletal and Skin Diseases, part of the National Institutes of Health.

The key is to find the genes that control the number and growth potential of epidermal stem cells, Morris said. Then scientists could create more stem cells or make them grow faster, for example, to heal an ulcer or the thinning of skin from aging.

Morris, who joined the institute in 2008, focuses her research on stem cells responsible for healing wounds, maintaining normal tissue integrity and cancer. Her lab uses adult stems cells isolated from the skin through a technique Morris developed when she was a post-doctorate at MD Anderson Cancer Center in Houston.

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Court: Gov't can fund embryonic stem cell research – Fri, 24 Aug 2012 PST

Posted: August 25, 2012 at 12:11 pm

August 24, 2012 in Health

Jesse J. Holland Associated Press

WASHINGTON (AP) A federal appeals court on Friday refused to order the Obama administration to stop funding embryonic stem cell research, despite complaints the work relies on destroyed humanembryos.

The U.S. Circuit Court of Appeals for the District of Columbia upheld a lower court decision throwing out a lawsuit that challenged federal funding for the research, which is used in pursuit of cures to deadly diseases. Opponents claimed the National Institutes of Health was violating the 1996 Dickey-Wicker law that prohibits taxpayer financing for work that harms anembryo.

But a three-judge appeals court panel unanimously agreed with a lower court judges dismissal of the case. This is the second time the appeals court has said that the challenged federal funding of embryonic stem cell research waspermissible.

Dickey-Wicker permits federal funding of research projects that utilize already-derived ESCs which are not themselves embryos because no human embryo or embryos are destroyed in such projects, Chief Judge David B. Sentelle said in the ruling, adding that the plaintiffs made the same argument the last the time the court reviewed the issue. Therefore, unless they have established some extraordinary circumstance, the law of the case is established and we will not revisit theissue.

Dr. Francis Collins, director of the National Institutes of Health, said in a statement after the decision, NIH will continue to move forward, conducting and funding research in this very promising area of science. The ruling affirms our commitment to the patients afflicted by diseases that may one day be treatable using the results of thisresearch.

Researchers hope one day to use stem cells in ways that cure spinal cord injuries, Parkinsons disease and other ailments. Opponents of the research object because the cells were obtained from destroyed human embryos. Though current research is using cells culled long ago, opponents say they also fear research success would spur new embryo destruction. Proponents say the research cells come mostly from extra embryos that fertility clinics would have discardedanyway.

The lawsuit was filed in 2009 by two scientists who argued that Obamas expansion jeopardized their ability to win government funding for research using adult stem cells ones that have already matured to create specific types of tissues because it will mean extracompetition.

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Court: Gov't can fund embryonic stem cell research - Fri, 24 Aug 2012 PST

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Court: Government can fund embryonic stem cell research

Posted: August 25, 2012 at 12:11 pm

WASHINGTON - A federal appeals court on Friday refused to order the Obama administration to stop funding embryonic stem cell research, despite complaints the work relies on destroyed human embryos.

The U.S. Circuit Court of Appeals for the District of Columbia upheld a lower court decision throwing out a lawsuit that challenged federal funding for the research, which is used in pursuit of cures to deadly diseases. Opponents claimed the National Institutes of Health was violating the 1996 Dickey-Wicker law that prohibits taxpayer financing for work that harms an embryo.

But a three-judge appeals court panel unanimously agreed with a lower court judge's dismissal of the case. This is the second time the appeals court has said that the challenged federal funding of embryonic stem cell research was permissible.

"Dickey-Wicker permits federal funding of research projects that utilize already-derived ESCs - which are not themselves embryos - because no 'human embryo or embryos are destroyed' in such projects," Chief Judge David B. Sentelle said in the ruling, adding that the plaintiffs made the same argument the last the time the court reviewed the issue. "Therefore, unless they have established some 'extraordinary circumstance,' the law of the case is established and we will not revisit the issue."

Researchers hope one day to use stem cells in ways that cure spinal cord injuries, Parkinson's disease and other ailments. Opponents of the research object because the cells were obtained from destroyed human embryos. Though current research is using cells culled long ago, opponents say they also fear research success would spur new embryo destruction. Proponents say the research cells come mostly from extra embryos that fertility clinics would have discarded anyway.

The lawsuit was filed in 2009 by two scientists who argued that Obama's expansion jeopardized their ability to win government funding for research using adult stem cells - ones that have already matured to create specific types of tissues - because it will mean extra competition.

President George W. Bush also permitted stem cell research, but limited the availability of taxpayer funds to embryonic stem cell lines that were already in existence and "where the life and death decision has already been made." Obama's order removed that limitation, allowing projects that involve stem cells from already destroyed embryos or embryos to be destroyed in the future. To qualify, parents who donate the original embryo must be told of other options, such as donating to another infertile woman.

Sentelle also rejected the opponent's two other arguments: that the same federal law prohibits funding for projects where embryos are "knowingly subjected to risk of injury or death," and that NIH issued guidelines on the funding without responding to complaints about the research.

"Because the executive order's entire thrust was aimed at expanding support of stem-cell research, it was not arbitrary or capricious for NIH to disregard comments that instead called for termination of all ESC research," including research the White House has permitted since 2001," said Sentelle, who wrote the majority opinion for Judges Karen Henderson and Janice Rogers Brown.

Sentelle was appointed by President Ronald Reagan, Henderson by President George H.W. Bush and Brown by President George W. Bush.

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Court: Embryonic stem cell research is legal

Posted: August 25, 2012 at 12:11 pm

By Maggie Fox, NBC News

The federal government may continue to pay for controversial human embryonic stem cell research, a federal appeals court ruled Friday.

The three-judge panel says the government has correctly interpreted a law that bans the use of federal funds to destroy human embryos for research. The ruling is unlikely to put the issue to rest and one of the judges pleaded for Congress to make clear what the government should and should not be able to do.

The hard-to-understand case pits science against mostly religious arguments against using embryos in medical research. It's even more confusing because there are so many differenlt types of cells called stem cells.

Dr. James Sherley of Boston Biomedical Research Institute and Theresa Deisher of AVM Biotechnology in Seattle, who both do research using adult stem cells and oppose the use of human embryonic stem cells, sued in 2009. They said federal guidelines violate the law and would harm their work by increasing competition for limited federal funding.

Its been back and forth in the federal courts since then, and Sherley has vowed to take the case all the way to the Supreme Court.

The embryonic stem cells at issue are the bodys master cells. Found in days-old embryos, they are the source of all the cells and tissues in the body blood, brain, bone and muscle. Researchers are studying them to investigate how disease develops and are using some as transplants to treat diseases from Parkinsons to cancer. They are being tested in people to repair spinal cord injuries and as a possible cure for some forms of blindness.

Opponents of the research say its unacceptable to destroy a human embryo to get the cells. The 1996 Dickey-Wicker amendment, added by Congress to budget language every year, forbids the use offederal funds in research that destroys embryos.

When he was president, George W. Bush decided that the ban extended to human embryonic stem-cell research and greatly limited the federal program.

As one of his first acts after he entered office, President Barack Obama issued an executive order reversing this and encouraging the National Institutes of Health to pay for embryonic stem-cell research, so long as federal money wasnt used to directly make the stem cells. To get the cells, someone in a private lab using private money has to take apart the embryos usually left over from fertility clinics and destined for the trash can. Federal funds may be used to work with the cells that private labs make available.

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Astrocytes control the generation of new neurons from neural stem cells

Posted: August 24, 2012 at 12:10 pm

24.08.2012 - (idw) University of Gothenburg

Researchers from the Laboratory of astrocyte biology and CNS regeneration headed by Prof. Milos Pekny just published a research article in a prestigious journal Stem Cells on the molecular mechanism that controls generation of new neurons in the brain. Astrocytes are cells that have many functions in the central nervous system, such as the control of neuronal synapses, blood flow, or the brains response to neurotrauma or stroke. Reduces brain tissue damage

Prof. Peknys laboratory together with collaborators have earlier demonstrated that astrocytes reduce the brain tissue damage after stroke and that the integration of transplanted neural stem cells can be largely improved by modulating the activity of astrocytes. Generation of new neurons

In their current study, the Sahlgrenska Academy researchers show how astrocytes control the generation of new neurons in the brain. An important contribution to this project came from bo Academy, one of Sahlgrenskas traditional collaborative partners.

In the brain, astrocytes control how many new neurons are formed from neural stem cells and survive to integrate into the existing neuronal networks. Astrocytes do this by secreting specific molecules but also by much less understood direct cell-cell interactions with stem cells, says Prof. Milos Pekny. Important regulator

Astrocytes are in physical contact with neural stem cells and we have shown that they signal through the Notch pathway to stem cells to keep the birth rate of new neurons low. We have also shown that the intermediate filament system of astrocytes is an important regulator of this process. It seems that astrocyte intermediate filaments can be used as a target to increase the birthrate of new neurons. Target for future therapies

The article Astrocytes Negatively Regulate Neurogenesis through the Jagged1-Mediated Notch Pathway is published in Stem Cells. function fbs_click() {u=location.href;t=document.title;window.open('http://www.facebook.com/sharer.php?u='+encodeURIComponent(u)+'&t='+encodeURIComponent(t),'sharer','toolbar=0,status=0,width=626,height=436');return false;} html .fb_share_link { padding:2px 0 0 20px; height:16px; background:url(http://static.ak.facebook.com/images/share/facebook_share_icon.gif?6:26981) no-repeat top left; } Share on Facebook Weitere Informationen: http://bit.ly/NCJEdI - article

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Human melanoma stem cells identified

Posted: August 24, 2012 at 12:10 pm

ScienceDaily (Aug. 23, 2012) Cancer stem cells are defined by three abilities: differentiation, self-renewal and their ability to seed a tumor. These stem cells resist chemotherapy and many researchers posit their role in relapse. A University of Colorado Cancer Center study recently published in the journal Stem Cells, shows that melanoma cells with these abilities are marked by the enzyme ALDH, and imagines new therapies to target high-ALDH cells, potentially weeding the body of these most dangerous cancer creators.

"We've seen ALDH as a stem cell marker in other cancer types, but not in melanoma, and until now its function has been largely unknown," says the paper's senior author, Mayumi Fujita, MD, PhD, investigator at the CU Cancer Center and associate professor in the Department of Dermatology at the CU School of Medicine.

Fujita's group transplanted ALDH+ and ALDH- melanoma cells into animal models, showing the ALDH+ cells were much more powerfully tumorigenic. In the same ALDH+ cells, the group then silenced the gene that creates this protein, finding that with ALDH knocked down, melanoma cells died in cultures and lost their ability to form tumors in animal models. In cell cultures, silencing this ALDH gene also sensitized melanoma cells to existing chemotherapies. When the group explored human tumor samples, they found distinct subpopulations of these ALDH+ cells, which made up about 0.1-0.2 percent of patients' primary tumors. In samples of metastatic melanoma -- the most aggressive form of the disease -- the percentage of ALDH+ cells was greater, even over 10 percent in some tumors, further implying the powerful danger of these cells.

"In these same ALDH+ cells, we find the markers of stem cells are upregulated and those of cell differentiation are downregulated. In addition to these clues, ALDH+ cells generate the heterogeneous cell types seen in the original tumor," says Fujita, meaning that in addition to self-renewal and tumorigenesis, ALDH+ cells fulfill the third criteria for a cancer stem cell: the ability to differentiate.

The study also shows how the ALDH gene and its protein act to create a cell's stem-like properties.

"One way ALDH makes a cancer stem cell is through the retinoic acid signaling pathway," Fujita says. The protein ALDH leads to the overproduction of retinoic acid, which in turn binds to a cell's nuclear receptors and influences the expression of many of the cell's genes -- for example, genes involved in regulating cell survival, repair, and proliferation, all of which combine to confer chemoresistance. Target cells with high ALDH and you target all the downstream effects, including the retinoic acid signaling pathway.

"Our hope is that we can intervene in this signaling, either at the level of ALDH or elsewhere in the pathway, especially to re-sensitize cells to chemotherapy. Using a new drug to take away a melanoma stem cell's chemoresistance could boost the effectiveness of existing drugs," Fujita says.

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Study Identifies Human Melanoma Stem Cells

Posted: August 24, 2012 at 12:10 pm

Cancer stem cells are defined by three abilities: differentiation, self-renewal and their ability to seed a tumor. These stem cells resist chemotherapy and many researchers posit their role in relapse. A University of Colorado Cancer Center study recently published in the journal Stem Cells, shows that melanoma cells with these abilities are marked by the enzyme ALDH, and imagines new therapies to target high-ALDH cells, potentially weeding the body of these most dangerous cancer creators.

Weve seen ALDH as a stem cell marker in other cancer types, but not in melanoma, and until now its function has been largely unknown, says the papers senior author, Mayumi Fujita, MD, PhD, investigator at the CU Cancer Center and associate professor in the Department of Dermatology at the CU School of Medicine.

KEY POINTS:

Fujitas group transplanted ALDH+ and ALDH- melanoma cells into animal models, showing the ALDH+ cells were much more powerfully tumorigenic. In the same ALDH+ cells, the group then silenced the gene that creates this protein, finding that with ALDH knocked down, melanoma cells died in cultures and lost their ability to form tumors in animal models. In cell cultures, silencing this ALDH gene also sensitized melanoma cells to existing chemotherapies. When the group explored human tumor samples, they found distinct subpopulations of these ALDH+ cells, which made up about 0.1-0.2 percent of patients primary tumors. In samples of metastatic melanoma the most aggressive form of the disease the percentage of ALDH+ cells was greater, even over 10 percent in some tumors, further implying the powerful danger of these cells.

In these same ALDH+ cells, we find the markers of stem cells are upregulated and those of cell differentiation are downregulated. In addition to these clues, ALDH+ cells generate the heterogeneous cell types seen in the original tumor, says Fujita, meaning that in addition to self-renewal and tumorigenesis, ALDH+ cells fulfill the third criteria for a cancer stem cell: the ability to differentiate.

The study also shows how the ALDH gene and its protein act to create a cells stem-like properties.

One way ALDH makes a cancer stem cell is through the retinoic acid signaling pathway, Fujita says. The protein ALDH leads to the overproduction of retinoic acid, which in turn binds to a cells nuclear receptors and influences the expression of many of the cells genes for example, genes involved in regulating cell survival, repair, and proliferation, all of which combine to confer chemoresistance. Target cells with high ALDH and you target all the downstream effects, including the retinoic acid signaling pathway.

Our hope is that we can intervene in this signaling, either at the level of ALDH or elsewhere in the pathway, especially to re-sensitize cells to chemotherapy. Using a new drug to take away a melanoma stem cells chemoresistance could boost the effectiveness of existing drugs, Fujita says.

SOURCE: University of Colorado Denver

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Repairing cartilage with fat: Problems and potential solutions

Posted: August 24, 2012 at 12:10 pm

Public release date: 23-Aug-2012 [ | E-mail | Share ]

Contact: Hilary Glover hilary.glover@biomedcentral.com 44-020-319-22370 BioMed Central

Stem cells isolated from fat are being considered as an option for treating tissue damage and diseases because of their accessibility and lack of rejection. New research published in BioMed Central's open access journal Stem Cell Research & Therapy shows that this is not as straightforward as previously believed, and that fat-derived stem cells secrete VEGF and other factors, which can inhibit cartilage regeneration. However pre-treating the cells with antibodies against VEGF and growing them in nutrients specifically designed to promote chondrocytes can neutralize these effects.

Chondrocytes make and maintain healthy cartilage but damage and disease including osteoarthritis can destroy cartilage resulting in pain and lack of mobility. Stem cell therapy using cells isolated from adult tissue (such as fat) are being investigated as a way of repairing this damage. Stem cells have the ability to become many different types of tissue so the real trick is persuading them to become cartilage rather than bone, or blood vessels, for example.

Researchers from the Georgia Institute of Technology found that adipose (fat) stem cells (ASCs) secrete large amounts of factors, especially the growth factor VEGF, which prevent cartilage regeneration and actually causes the death (apoptosis) of chondrocytes along with the formation of blood vessels. Treating ASCs with medium designed to encourage their differentiation into cartilage cells was able to reduce the amount of these secreted factors and also prevented the growth of blood vessels. Specifically, an antibody designed to neutralize VEGF prevented chondrocyte apoptosis.

Prof Barbara Boyan, who led this research, explained, "Non-treated ASCs actually impeded healing of hyaline cartilage defects, and although treating ASCs improved the situation they added no benefit to compared to cartilage allowed to heal on its own. However we only looked at cartilage repair for a week after treatment, and other people have shown that two to six weeks is required before the positive effect of ASCs on influence cartilage regeneration is seen."

So while stem cells from fat may be able to help repair damaged cartilage, careful handling and pre-treatment may be required to ensure a positive result.

###

Media contact

Dr Hilary Glover Scientific Press Officer, BioMed Central Tel: +44 (0) 20 3192 2370 Mob: +44 (0) 778 698 1967 Email: hilary.glover@biomedcentral.com

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Human melanoma stem cells identified

Posted: August 24, 2012 at 9:13 am

ScienceDaily (Aug. 23, 2012) Cancer stem cells are defined by three abilities: differentiation, self-renewal and their ability to seed a tumor. These stem cells resist chemotherapy and many researchers posit their role in relapse. A University of Colorado Cancer Center study recently published in the journal Stem Cells, shows that melanoma cells with these abilities are marked by the enzyme ALDH, and imagines new therapies to target high-ALDH cells, potentially weeding the body of these most dangerous cancer creators.

"We've seen ALDH as a stem cell marker in other cancer types, but not in melanoma, and until now its function has been largely unknown," says the paper's senior author, Mayumi Fujita, MD, PhD, investigator at the CU Cancer Center and associate professor in the Department of Dermatology at the CU School of Medicine.

Fujita's group transplanted ALDH+ and ALDH- melanoma cells into animal models, showing the ALDH+ cells were much more powerfully tumorigenic. In the same ALDH+ cells, the group then silenced the gene that creates this protein, finding that with ALDH knocked down, melanoma cells died in cultures and lost their ability to form tumors in animal models. In cell cultures, silencing this ALDH gene also sensitized melanoma cells to existing chemotherapies. When the group explored human tumor samples, they found distinct subpopulations of these ALDH+ cells, which made up about 0.1-0.2 percent of patients' primary tumors. In samples of metastatic melanoma -- the most aggressive form of the disease -- the percentage of ALDH+ cells was greater, even over 10 percent in some tumors, further implying the powerful danger of these cells.

"In these same ALDH+ cells, we find the markers of stem cells are upregulated and those of cell differentiation are downregulated. In addition to these clues, ALDH+ cells generate the heterogeneous cell types seen in the original tumor," says Fujita, meaning that in addition to self-renewal and tumorigenesis, ALDH+ cells fulfill the third criteria for a cancer stem cell: the ability to differentiate.

The study also shows how the ALDH gene and its protein act to create a cell's stem-like properties.

"One way ALDH makes a cancer stem cell is through the retinoic acid signaling pathway," Fujita says. The protein ALDH leads to the overproduction of retinoic acid, which in turn binds to a cell's nuclear receptors and influences the expression of many of the cell's genes -- for example, genes involved in regulating cell survival, repair, and proliferation, all of which combine to confer chemoresistance. Target cells with high ALDH and you target all the downstream effects, including the retinoic acid signaling pathway.

"Our hope is that we can intervene in this signaling, either at the level of ALDH or elsewhere in the pathway, especially to re-sensitize cells to chemotherapy. Using a new drug to take away a melanoma stem cell's chemoresistance could boost the effectiveness of existing drugs," Fujita says.

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