Posted: December 10, 2014 at 7:43 am
Stem cells: protectors of the brain | Tamir Ben-Hur | TEDxJaffa
This talk was given at a local TEDx event, produced independently of the TED Conferences. TEDxJaffa partnered with The British Council [http://www.britishcou...
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Stem cells: protectors of the brain | Tamir Ben-Hur | TEDxJaffa - Video
Posted: December 9, 2014 at 2:46 pm
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Newswise For a small percentage of cancer patients, treatment aimed at curing the disease leads to a form of leukemia with a poor prognosis. Conventional thinking goes that chemotherapy and radiation therapy induce a barrage of damaging genetic mutations that kill cancer cells yet inadvertently spur the development of acute myeloid leukemia (AML), a blood cancer.
But a new study at Washington University School of Medicine in St. Louis challenges the view that cancer treatment in itself is a direct cause of what is known as therapy-related AML.
Rather, the research suggests, mutations in a well-known cancer gene, P53, can accumulate in blood stem cells as a person ages, years before a cancer diagnosis. If and when cancer develops, these mutated cells are more resistant to treatment and multiply at an accelerated pace after exposure to chemotherapy or radiation therapy, which then can lead to AML, the study indicates.
The teams findings, reported Dec. 8 in the journal Nature, open new avenues for research to predict which patients are at risk of developing therapy-related AML and to find ways to prevent it.
About 18,000 cases of AML are diagnosed in the United States each year, with about 2,000 triggered by previous exposure to chemotherapy or radiation therapy. Therapy-related AML is almost always fatal, even with aggressive treatment.
Until now, weve really understood very little about therapy-related AML and why it is so difficult to treat, said corresponding author Daniel Link, MD, a hematologist/oncologist at Siteman Cancer Center at Washington University and Barnes-Jewish Hospital. This gives us some important clues for further studies aimed at treatment and prevention.
The researchers initially sequenced the genomes of 22 cases of therapy-related AML, finding that those patients had similar numbers and types of genetic mutations in their leukemia cells as other patients who developed AML without exposure to chemotherapy or radiation therapy, an indication that cancer treatment does not cause widespread DNA damage.
This is contrary to what physicians and scientists have long accepted as fact, said senior author Richard K. Wilson, PhD, director of The Genome Institute at Washington University. It led us to consider a novel hypothesis: P53 mutations accumulate randomly as part of the aging process and are present in blood stem cells long before a patient is diagnosed with therapy-related AML.
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Genetic Errors Linked to Aging Underlie Leukemia That Develops After Cancer Treatment
Posted: December 9, 2014 at 2:46 pm
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Michael Hadjiargyrou, Ph.D., of New York Institute of Technologys College of Arts and Sciences, an expert in engineering new musculoskeletal tissue, is available to discuss advanced bio-science predictions for 2015.
Undoubtedly, next year we will continue to see research advances in the realm of Tissue Engineering/Regenerative Medicine (TERM), says Hadjiargyrou, who specializes in molecular and cell biology, genetic engineering, biomaterials and stem cell research. Specifically, we will witness the formation of more tissues and possibly even organs fabricated in the laboratory with the use of 3D printers (Bioprinters).
Hadjiargyrou specifically identifies the heart valve, blood vessel, trachea, kidney, and liver, as the tissue or organs that will be printed with the use of 3D printers; kidneys, livers and hearts are most in demand.
Additionally, the successful transplantation of some of these laboratory tissues and organs will be achieved, particularly in Europe, as they have been more active in transplantation of biomaterials. With the emergence of such breakthroughs, we will begin to see more and more clinical and even cosmetic applications of TERM.
Hadjiargyrou focuses on studying the molecular mechanisms involved in bone regeneration as a way to better understand the healing of fractures. Hadjiargyrou teaches general biology, genetic engineering, contemporary biotechnology and biomedical research in Old Westbury, NY.
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NYIT Expert Predicts Growth in Demand for 3D Kidneys, Livers and Hearts
Posted: December 9, 2014 at 2:41 pm
MONDAY, Dec. 8, 2014 (HealthDay News) -- Some professional football players are seeking unproven stem cell therapies to speed their recovery from injuries. But experts are concerned that they may be unaware of the potential risks, a new report shows.
Stem cell therapy has attracted the attention of elite athletes. A number of National Football League (NFL) players have highlighted their use of those therapies and their successful recoveries.
Twelve NFL players are known to have received unapproved stem cell treatments since 2009.
"The online data on NFL players and the clinics where they obtained treatment suggest that players may be unaware of the risks they are taking," report co-author Kirstin Matthews, a fellow in science and technology policy at Rice University's Baker Institute for Public Policy, said in a university news release.
"Players who are official spokespersons for these clinics could influence others to view the therapies as safe and effective despite the lack of scientific research to support these claims," she added.
Most of the players receive treatment in the United States, but several have gone to other countries for stem cell therapies that aren't available in the United States.
"With the rise of new and unproven stem cell treatments, the NFL faces a daunting task of trying to better understand and regulate the use of these therapies in order to protect the health of its players," Matthews said.
The NFL and other sports leagues may need to evaluate and possibly regulate stem cell therapies in order to ensure the safety of their players, the report authors suggested.
The paper appears in a special supplement to the journal Stem Cells and Development.
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Some NFL players use unproven stem cell therapies
Posted: December 9, 2014 at 8:02 am
Big visions for cell biology prompted Paul Allen to launch the Allen Institute for Cell Science, and new director Rick Horwitz explains its new way of seeing cells.
Cell biologist Rick Horwitz will be the first director of the Allen Institute of Cell Science in Seattle, moving from his faculty job at the University of Virginia.
We have not been seeing cells as they really are, says Rick Horwitz, and it is time for that to change. Traditional laboratories focus on one or two aspects of cells, and not on the way the hundreds of different pieces of molecular machinery within the cell affect one another. To improve that perspective, Horwitz is leaving his cell biology lab at the University of Virginia to become the inaugural director of the Allen Institute for Cell Science in Seattle. The enterprise is being started today with a gift of $100 million from philanthropist Paul Allen, and will join the Allen Institute for Brain Science. Horwitz says the institute will kick off a large project, the Allen Cell Observatory, creating animated models of cells combined with an enormous database of cell parts that allows users to zoom into the genes and proteins that make these parts work in health and disease. It will be rather like a Google Maps for cells, he says. Horwitz spoke with Scientific American to describe the project, the new institute, and his hopes for the ways they can transform cell biology. [What follows is an edited version of the conversation.] What do we not know about cells? Scientists have been studying them for a long time. Cells are so very complicated, and we do not have any predictive models of their behavior and how that gets disturbed in disease. The cell comprises hundreds and hundreds of molecular machines, organelles like mitochondria and ribosomes. We do not know how genetic alterations in these machines change how they affect each other in time and space, and how that produces diseases like cancer. For example, a lot of cancer seems to be related to activities in the wrong place in the cell, at the wrong time. What has been holding scientists back? Traditionally, academic labs focus on small subsets of molecules, or small sets of cell activities. But to understand and predict cell behavior, you really need the overview. How many mitochondria are in a cell, for instance? How many ribosomes? When do they change in the cell cycle? How are these changes related to one another? We need to study them together because the cell is really an integrated system. How will the Allen Cell Observatory allow this? We want to create animated, visual models of the cell. We need to see how changes affect cells spatially and temporally. But why animation? The literature in cell biology has been presented as long stretches of text. Its like reading the phone book. What we want is something closer to Google Maps. We want to zoom in and see protein-scale structures. We want to zoom out and see connections between organelles. That will be very powerful. We can use this to build predictive models. At the moment, I havent heard anyone make a bold prediction about cell behavior that turned out to be right. But once you see how a cell behaves normally, you can perturb one gene, or a set of genes, and see how that affects the life of that cell. That calls for sophisticated IT, a big database, new biosensors, and new cell assays to measure activity. This is not happening elsewhere in cell biology? Not really. A lot of research now is trying to be very translational, focused on helping people with different diseases. We are building tools and infrastructure that will be open-access and available to everyone. We are not trying to develop a drug. So we are not restricted by funds that are only supposed to go to developing treatments. I think what we are doing will lead to treatments, but we need to build the basic tools to understand cells first. What cells will you use? Thats a very big deal. Weve decided to use human induced pluripotent stem cells. They can differentiate into any number of cell types, and they can go anywhere in the body. We think we can get pretty close to a real-life situation. But actually picking the right line of cells is going to be tricky. Why so tricky? If you pick the wrong cell line and it has an aberration, youll end up with a lot of very wrong stuff. We think that we will study three to five different lines and see if we keep getting consistent results. Then well figure out what to do next. When will you get started, and how long will it take before you get results? We will move into our new building in Seattle in the fall of 2015, and between now and then well be looking to hire about 75 people to work at the institute. Once were moved in and working, I think well be able to report significant progress in three years.
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Billionaire's New Science Institute Plans 'Google Maps' View Of Cells
Posted: December 9, 2014 at 7:59 am
SATURDAY, Dec. 6, 2014 (HealthDay News) -- In a small new trial, a form of treatment based on the body's immune system appears to be helping patients with Hodgkin lymphoma for whom other treatments had failed.
Hodgkin lymphoma -- a cancer of white blood cells called lymphocytes -- is one of the most common cancers in children and young adults in the United States, with about 10,000 new cases occurring each year. While current therapies are often successful in treating the disease, up to one-fourth of patients eventually suffer a relapse, experts say.
The disease "kills more than 1,000 people in the U.S. each year and is one of the rare cancers more common in young adults than in older patients," said one expert, Dr. Joshua Brody, director of the Lymphoma Immunotherapy Program at the Icahn School of Medicine at Mount Sinai, in New York City.
"Many people may know of actor Michael C. Hall, of television's 'Dexter,' who battled the disease in 2010," said Brody, who was not involved in the new study.
He stressed that Hodgkin lymphoma is often responsive to chemotherapy. However, in the minority of patients who do not respond to standard treatment, the disease is typically considered incurable and fatal.
The new study involved 23 such patients. According to researchers at Dana-Farber Cancer Institute, in Boston, more than one-third of the patients had tried -- and ultimately failed -- at least six lines of treatment. Four-fifths of the patients had also undergone stem cell transplant therapy in hopes of curing their disease, but also failed.
The new phase 1 trial involved a drug called nivolumab, a therapy that frees the immune system to attack cancer cells.
"Nivolumab is a novel therapy which blocks the protein PD-1 -- a 'brake pedal' of certain immune cells," Brody explained. "This allows patients' immune systems to attack their own cancer -- an old concept which has shown unprecedented results in recent years."
Following treatment, four of the patients had no detectable tumor left and the tumors in 16 other patients had shrunk to less than half of their original size, the researchers said. Six months after treatment, 86 percent of patients were alive and continued to show response to the therapy. One year after treatment, most of the patients continued to do well.
About 20 percent of the patients had serious treatment-related side effects, but none of them were life-threatening, the study's authors said.
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Hodgkin Lymphoma Treatment Shows Promise in Small Trial
Posted: December 9, 2014 at 7:59 am
In a small new trial, a form of treatment based on the body's immune system appears to be helping patients with Hodgkin lymphoma for whom other treatments had failed.
Hodgkin lymphoma -- a cancer of white blood cells called lymphocytes -- is one of the most common cancers in children and young adults in the United States, with about 10,000 new cases occurring each year. While current therapies are often successful in treating the disease, up to one-fourth of patients eventually suffer a relapse, experts say.
The disease "kills more than 1,000 people in the U.S. each year and is one of the rare cancers more common in young adults than in older patients," said one expert, Dr. Joshua Brody, director of the Lymphoma Immunotherapy Program at the Icahn School of Medicine at Mount Sinai, in New York City.
"Many people may know of actor Michael C. Hall, of television's 'Dexter,' who battled the disease in 2010," said Brody, who was not involved in the new study.
He stressed that Hodgkin lymphoma is often responsive to chemotherapy. However, in the minority of patients who do not respond to standard treatment, the disease is typically considered incurable and fatal.
The new study involved 23 such patients. According to researchers at Dana-Farber Cancer Institute, in Boston, more than one-third of the patients had tried -- and ultimately failed -- at least six lines of treatment. Four-fifths of the patients had also undergone stem cell transplant therapy in hopes of curing their disease, but also failed.
The new phase 1 trial involved a drug called nivolumab, a therapy that frees the immune system to attack cancer cells.
"Nivolumab is a novel therapy which blocks the protein PD-1 -- a 'brake pedal' of certain immune cells," Brody explained. "This allows patients' immune systems to attack their own cancer -- an old concept which has shown unprecedented results in recent years."
Following treatment, four of the patients had no detectable tumor left and the tumors in 16 other patients had shrunk to less than half of their original size, the researchers said. Six months after treatment, 86 percent of patients were alive and continued to show response to the therapy. One year after treatment, most of the patients continued to do well.
About 20 percent of the patients had serious treatment-related side effects, but none of them were life-threatening, the study's authors said.
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"Breakthrough" drug shows promise for Hodgkin lymphoma
Posted: December 9, 2014 at 7:58 am
In a small new trial, a form of treatment based on the body's immune system appears to be helping patients with Hodgkin lymphoma for whom other treatments had failed.
Hodgkin lymphoma -- a cancer of white blood cells called lymphocytes -- is one of the most common cancers in children and young adults in the United States, with about 10,000 new cases occurring each year. While current therapies are often successful in treating the disease, up to one-fourth of patients eventually suffer a relapse, experts say.
The disease "kills more than 1,000 people in the U.S. each year and is one of the rare cancers more common in young adults than in older patients," said one expert, Dr. Joshua Brody, director of the Lymphoma Immunotherapy Program at the Icahn School of Medicine at Mount Sinai, in New York City.
"Many people may know of actor Michael C. Hall, of television's 'Dexter,' who battled the disease in 2010," said Brody, who was not involved in the new study.
He stressed that Hodgkin lymphoma is often responsive to chemotherapy. However, in the minority of patients who do not respond to standard treatment, the disease is typically considered incurable and fatal.
The new study involved 23 such patients. According to researchers at Dana-Farber Cancer Institute, in Boston, more than one-third of the patients had tried -- and ultimately failed -- at least six lines of treatment. Four-fifths of the patients had also undergone stem cell transplant therapy in hopes of curing their disease, but also failed.
The new phase 1 trial involved a drug called nivolumab, a therapy that frees the immune system to attack cancer cells.
"Nivolumab is a novel therapy which blocks the protein PD-1 -- a 'brake pedal' of certain immune cells," Brody explained. "This allows patients' immune systems to attack their own cancer -- an old concept which has shown unprecedented results in recent years."
Following treatment, four of the patients had no detectable tumor left and the tumors in 16 other patients had shrunk to less than half of their original size, the researchers said. Six months after treatment, 86 percent of patients were alive and continued to show response to the therapy. One year after treatment, most of the patients continued to do well.
About 20 percent of the patients had serious treatment-related side effects, but none of them were life-threatening, the study's authors said.
Posted: December 9, 2014 at 7:56 am
Harvard scientists claim to have made a breakthrough in the obesity crisis Discovery could be 'the first step towards a pill that replaces the treadmill' Team found two compounds that turn white 'bad' fat cells into brown or 'good' fat cells in the human body When a person eats too many calories and doesn't burn them off, they're stored as white fat cells, causing a person to pile on the pounds New study found two molecules that convert fat stem cells, which would normally produce white fat, into brown fat cells The brown fat cells burn excess energy, reducing number of white fat cells
By Lizzie Parry for MailOnline
Published: 11:11 EST, 8 December 2014 | Updated: 17:07 EST, 8 December 2014
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An obesity pill that transforms 'bad' fat to 'good' could replace exercise, helping people shed pounds and with them their risk of type 2 diabetes, heart disease and cancer.
That is the claim by scientists who believe they have made a breakthrough in the battle against the bulge.
They said the discovery could be 'the first step towards a pill that can replace the treadmill'.
Harvard Stem Cell Institute at Havard and Massachusetts General Hospital have identified two compounds that can turn white or 'bad' fat cells into brown 'good' fat cells in the body.
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The obesity pill that could replace exercise by turning 'bad' fat to 'good'
Posted: December 9, 2014 at 7:56 am
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Tweet: Unresponsive triple-negative #breastcancer cells can be made susceptible to chemotherapeutic drugs.
Fast Facts: Only 20 percent of patients with so-called triple-negative breast cancer respond fully to chemotherapy. New research shows that chemotherapeutic drugs stimulate the HIF protein network in the cancer cells, enhancing their ability to survive. Giving HIF inhibitors together with traditional chemotherapy decreased tumor size in mice.
Newswise Triple-negative breast cancer is as bad as it sounds. The cells that form these tumors lack three proteins that would make the cancer respond to powerful, customized treatments. Instead, doctors are left with treating these patients with traditional chemotherapy drugs that only show long-term effectiveness in 20 percent of women with triple-negative breast cancer. Now, researchers at The Johns Hopkins University have discovered a way that breast cancer cells are able to resist the effects of chemotherapy and they have found a way to reverse that process.
A report of their findings was published online in the journal Proceedings of the National Academy of Sciences on Dec. 1.
Triple-negative breast cancers account for about 20 percent of all breast cancers in the United States, and 30 percent of all breast cancers in African-American women. In addition to being resistant to chemotherapy, they are known to include a high number of breast cancer stem cells, which are responsible for relapses and for producing the metastatic tumors that lead to the death of patients with cancer. Previous research revealed that triple-negative breast cancer cells show a marked increase in the activity of many genes known to be controlled by the protein hypoxia-inducible factor (HIF). Given these past results, a research team directed by Gregg Semenza, M.D., Ph.D., decided to test whether HIF inhibitors could improve the effectiveness of chemotherapy.
Our study showed that chemotherapy turns on HIF and that HIF enhances the survival of breast cancer stem cells, which are the cancer cells that must be killed to prevent relapse and metastasis, says Semenza, the C. Michael Armstrong Professor of Medicine at Johns Hopkins and a Johns Hopkins Kimmel Cancer Center expert. The good news is that we have drugs that block HIF from acting.
Semenzas study began by treating lab-grown triple-negative breast cancer cells with the chemotherapy drug paclitaxel and looking for changes in HIF levels. After four days of treatment, HIF protein and activity levels had increased, as had the percentage of breast cancer stem cells among the surviving cells. When Semenzas team, led by postdoctoral fellow Debangshu Samanta, Ph.D., genetically altered the cancer cells to have less HIF, the cancer stem cells were no longer protected from death by chemotherapy, demonstrating that HIF was required for the cancer stem cells to resist the toxic effects of paclitaxel, Semenza says.
At the molecular level, the team found that one of the ways HIF enhances the survival of the stem cells is by increasing the levels of a protein, multidrug resistance protein 1 (MDR1), which acts like a pump to expel chemotherapy from cancer cells. However, when triple-negative breast cancer cells were given paclitaxel plus the HIF inhibitor digoxin, MDR1 levels went down rather than up.
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Toughest Breast Cancer May Have Met Its Match
