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A New AML Treatment Target

A New AML Treatment Target—The blood cancer acute myeloid leukemia (AML) is driven by leukemic stem cells (LSCs) that develop abnormally and proliferate excessively, until they ultimately displace healthy blood stem cells from the bone marrow. LSCs typically resist chemotherapy, so better strategies are needed to eliminate them. In a study published online on May 17 in the Journal of Experimental Medicine, researchers led by Ulrich Steidl, M.D., Ph.D., describe a promising target: a signaling protein called interleukin-1 receptor accessory protein (IL1RAP), which is often highly expressed on the surface of leukemic stem cells but is largely absent from normal blood stem cells. IL1RAP turned out to be crucial for leukemic stem cell survival. When AML cells (including leukemic stem cells) were isolated from patients, the researchers found they could kill those cells by targeting IL1RAP using techniques including anti-IL1RAP antibodies and gene deletion. Unexpectedly, the researchers found that IL1RAP has a much broader function in AML cells than previously realized: the protein, simultaneously stimulated multiple leukemia-promoting molecules, which makes therapeutically targeting IL1RAP particularly attractive. Dr. Steidl is the Diane and Arthur B. Belfer Faculty Scholar in Cancer Research, director of the Stem Cell Isolation and Xenotransplantation Facility and a professor of cell biology and of medicine at Einstein and associate chair for translational research in oncology at Montefiore.

Thursday, May 17, 2018
 
Functional Liver Grown in Placenta

Functional Liver Grown in Placenta—In the first use of human placenta for tissue engineering, Sanjeev Gupta, M.D., M.B.B.S., and colleagues seeded scaffold-supported human placentas with liver fragments from sheep, and the fragments developed into viable liver tissue. The achievement offers a new way to overcome donor liver shortages and help people awaiting liver transplants. The liver fragments that were transferred to the placentas contained all the cell types that comprise livers. The fragments grew within the placenta to form liver tissue with the same structure and functional ability (e.g., maintenance of albumin and urea synthesis) as the actual organ. When grafts of this liver tissue were transplanted into a sheep with liver failure, they rescued the sheep from liver failure and helped regenerate the damaged organ. The study was published online on March 26 in Hepatology. Dr. Gupta is professor of medicine and of pathology and is the Eleazar & Feige Reicher Chair in Translational Medicine at Einstein and is an attending physician at Montefiore Health System.

Tuesday, May 15, 2018
 
Reviving Old Blood-Making Cells

Reviving Old Blood-Making Cells—White cells, red cells and all other blood cells in the body are produced by hematopoietic (blood-forming) stem cells (HSCs) in bone marrow niches. Over time, HSCs age and produce fewer cells, which can lead to blood disorders and weakened immunity. In a study published online on May 7 in Nature Medicine, Paul Frenette, M.D., compared bone marrow from young and old mice. He found that age-related loss of sympathetic nerve signaling causes remodeling of blood vessels in the bone marrow, leading to aging of the marrow. Dr. Frenette and his team showed that stimulating old bone marrow with sympathetic nerve signaling reverses HSC aging by rejuvenating the niche. The findings could lead to new treatments for HSC-related blood disorders. Dr. Frenette is professor of medicine and of cell biology and director of the Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research at Einstein.

Monday, May 07, 2018
 
Treating Radiation Exposure

Treating Radiation Exposure—Exposure to high-dose radiation from nuclear accidents or terrorism can cause acute radiation syndrome (ARS)—illness due to the death of stem cells in specific tissues. The main cause of death from ARS—destruction of bone marrow—can be prevented with a bone marrow transplant. But survival is extremely unlikely when radiation exposure is high enough to damage the gastrointestinal tract. Chandan Guha M.B.B.S., Ph.D., has shown that ARS of the gastrointestinal tract can be treated with a bone marrow adherent stromal cell transplant (BMASCT), which consists mainly of stromal (connective tissue) and myeloid (bone marrow) cells. The National Institute of Allergy and Infectious Diseases has now awarded Dr. Guha a five-year, $2.7 million grant to develop strategies for applying BMASCT therapy in a mass-casualty situation. Dr. Guha is professor and vice chair of radiation oncology at Einstein and Montefiore Health System. Dr. Guha is also professor of urology and of pathology at Einstein and is director of Einstein’s Institute for Onco-physics. (1U01AI138324-01)

Wednesday, May 02, 2018
 
Studying the Dynamics of Cell Growth

Studying the Dynamics of Cell Growth—Dysregulated cell growth leads to cancer and many other diseases. In many cases, a mutation to the p53 tumor suppressor gene triggers aberrant cell growth. The National Institute of General Medical Sciences has awarded Robert Coleman, Ph.D., a four-year, $1.3 million grant to study the interplay between p53, chromatin (the complex of DNA and protein that forms chromosomes) and transcriptional bursting in single cells (when transcription from DNA to RNA occurs in bursts or pulses). Dr. Coleman and colleagues will use a single molecule live cell imaging system to directly visualize the p53 protein and the molecules it recruits to tightly regulate DNA repair, DNA replication and cell division. Insights into how this system is coordinated may lead to therapies to restore normal cellular growth in cancer and other diseases. Dr. Coleman is an assistant professor of anatomy and structural biology. (1R01GM126045-01A1)

Monday, April 30, 2018
 
Fat and Fit is a Myth

Fat and Fit is a Myth—Many studies over the past 20 years have found that a relatively low, or “normal,” body mass index (BMI) is associated with the lowest risk of dying. But other studies suggest a possible “obesity paradox”: a survival benefit for people who are overweight or even obese. In the first study to systematically examine how muscle mass might affect the BMI-mortality relationship, Einstein researchers, led by Matthew Abramowitz, M.D., analyzed the body composition of 11,687 participants in the National Health and Nutrition Examination Survey. In results published online on April 11 in PLOS ONE, they found that muscle mass—which is inversely associated with the risk of death—influences the association between BMI and mortality risk. When muscle mass is taken into account, any apparent survival advantage to being overweight or obese disappears, along with the obesity paradox— emphasizing the importance of weight loss and other anti-obesity interventions, even for people whose BMIs are only moderately elevated. Dr. Abramowitz is associate professor of medicine at Einstein and attending physician at Montefiore Health System.

Wednesday, April 25, 2018
 
Unlocking Food Craving

Unlocking Food Craving—The nucleus accumbens (NAc), a part of the brain associated with motivation and reward, may hold a key to understanding why people crave high-calorie foods. In a study published online on March 27 in eLife, Saleem M. Nicola, Ph.D., and his graduate student Kevin Caref found that the NAc’s naturally occurring opioids and opioid receptors activate neurons, which then promote the desire to eat palatable foods after animals reach satiety. In a series of trials, Dr. Nicola trained satiated and non-satiated rats to respond to cues indicating they’re about to receive high-fat food. He observed that the opioid system enhanced neuronal activity—and the desire to eat fatty foods—only in rats that were not hungry. The findings suggest that drugs that block the opioid receptors from stimulating neurons could potentially treat obesity. Dr. Nicola is an associate professor in the Dominick P. Purpura Department of Neuroscience and of psychiatry and behavioral sciences at Einstein.

Monday, April 23, 2018
 
Early Programming of Childhood Obesity

Early Programming of Childhood Obesity—More than one-third of U.S. children are classified as overweight or obese. Studies show that children born underweight are at higher risks for obesity, cardiovascular disease, and type 2 diabetes. Researchers believe that one cause of obesity involves changes in the nongenetic (i.e., epigenetic) influences on gene expression—in particular, changes in the pattern of DNA methylation. The Eunice Kennedy Shriver National Institute of Child Health & Human Development has awarded Maureen Charron, Ph.D., and Mamta Fuloria, M.B.B.S., a five-year, $3.4 million grant to study DNA methylation of blood cells of intrauterine growth restricted infants, who are at high risk for becoming obese. More specifically, Drs. Charron and Fuloria will examine the children’s blood at birth and at age two to determine how DNA methylation has affected their CD3+ T-cells--immune cells that plays a key role in the development of obesity. Dr. Charron is professor of biochemistry, of medicine, and of obstetrics & gynecology and women's health at Einstein. Dr. Fuloria is an associate professor of pediatrics at Einstein. (1R01HD092533-01A1)

Friday, April 20, 2018
 
New Approaches Against Zika Infection

New Approaches Against Zika Infection—The number of mosquito-borne Zika virus infections in humans are expected to increase, and drugs for protecting people are urgently needed.  In a study published online on March 23 in Virology, Felipe Diaz-Griffero, Ph.D., describes a family of therapeutic agents that halts the virus’ entry into cells. Theorizing that Zika requires a cellular protein called AXL to attach to cells, Dr. Diaz-Griffero found that cells in which the gene for AXL was deleted were resistant to infection. The drugs may also thwart Zika infection through a second mechanism: by neutralizing acidic compartments within the cells. This group of drugs could potentially treat people infected with Zika and thereby help prevent the well-established neurological problems associated with Zika. Dr. Diaz-Griffero is professor of microbiology & immunology and the Elsie Wachtel Faculty Scholar at Einstein.

Wednesday, April 18, 2018
 
Boosting T Cells’ Attack

Boosting T Cells’ Attack—Cell-membrane molecules called glycolipids help cells recognize one another and play an important part in launching immune responses. One class of glycolipids, called alpha-galactosylceramides, have been used as a drug to activate a portion of the immune system’s T cells and effectively treat cancers in laboratory mice, although so far this has been difficult to achieve in people with cancer. Steven Porcelli, M.D. and colleagues have found that simultaneously making two different chemical changes to the structure of alpha-galactosylceramides renders them more effective at stimulating T cells to attack cancers, especially in experiments that more accurately replicate cancer in humans. Their approach, described online on March 22 in Cell Chemical Biology, is a step toward improving current drugs and creating new immunotherapies for cancer. Dr. Porcelli is professor and chair of microbiology & immunology, professor of medicine and the Murray and Evelyn Weinstock Chair in Microbiology and Immunology at Einstein.

Monday, April 16, 2018
 
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