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Archive - Apr 6, 2015

Clue to Cancer Wasting (Cachexia) from Fruit Fly Studies; Results Could Lead to Targeted Treatments; Key Is Tumor-Secreted ImpL2 Protein in Fly, Analogous to Human IGFBPs

The progressive wasting of muscle and fat tissue throughout the body is one of the most visible and heart-breaking manifestations of cancer, yet little is known about how tumors cause distant tissues to degenerate. Two independent studies published in open-access articles in the April 6, 2015 issue of Developmental Cell reveal that a tumor-secreted molecule called ImpL2 drives the loss of fat and muscle tissue in fly cancer models that replicate key features of tumor-induced wasting in humans. The findings could lead to the development of much-needed targeted therapies for wasting syndrome in cancer patients. "Many cancer patients die, not because of the local effects of tumors, but rather from more broad, systemic changes to the entire body that are induced by these tumors. One of the worst of these long-range effects is wasting syndrome, also known as cachexia, which is a major obstacle to cancer treatment," says developmental biologist Dr. David Bilder of the University of California, Berkeley, one of the study authors. "The two new studies illustrate the power of using simple model organisms to provide new insights relevant to the most important questions of human cancer biology." About 20% of cancer deaths are due to cachexia, which mostly affects patients with advanced cancer, making them too weak for some types of chemotherapy and radiation therapy and more susceptible to the toxic effects of chemotherapy. An increase in food intake does not fully reverse tissue loss, and available therapies are so limited that the National Cancer Institute highlighted cachexia as a perplexing problem that has slowed progress against cancer. To tackle the complexities of cancer cachexia, two independent research teams. One consists of Dr. Bilder and Dr.

Cells Take Sub-Optimal Metabolic Approaches to Maximize Survival Chances

There are few times in life when one should aim for suboptimal performance, but new research at Rice University in Texas suggests scientists who study metabolism and its role in evolution should look for signs of just that. A study published online on April 3, 2015 in an open-access article in BMC Systems Biology details a computational method called corsoFBA. FBA stands for flux balance analysis and the program predicts internal cell flux -- the rate at which cells process and store energy -- at what researchers call suboptimal growth. The ultimate goal of the study is to discover how organisms, including humans, adapt to changing environments, including the body's response during exercise. The method allows researchers to model how metabolic pathways, chains of chemical reactions in the cells of all living beings, will react in the presence or absence of certain conditions, like the availability of oxygen or the acidity of the environment. It does so by measuring how a cell spends its fixed energetic resources -- its protein cost -- to preserve flux in more than one pathway. The work springs from the mind and talents of a Rice graduate student André Schultz who spent years training his body for absolutely optimal performance. Schultz is a former member of the Brazilian national swim team who trained alongside U.S. Olympic legend Michael Phelps at the University of Michigan. As an undergraduate there, Schultz divided his time between competitive swimming and academics, particularly his love for mathematics. At Rice, where he is a student of bioengineering in the laboratory of co-author Amina Qutub, Ph.D., Schultz turned his attention to biophysics, specifically mathematical models of metabolic pathways.

HIV-1 Infection Accelerates Certain Aging Changes by 14 Years, According to UCLA Analysis of Aging-Related Methylation Patterns

People undergoing treatment for HIV-1 have an increased risk for earlier onset of age-related illnesses such as some cancers, renal and kidney disease, frailty, osteoporosis and neurocognitive disease. But is it because of the virus that causes AIDS or the treatment? To answer that question, researchers at the UCLA AIDS Institute and Center for AIDS Research and the Multicenter AIDS Cohort Study (MACS) investigated whether the virus induces age-associated epigenetic changes -- that is, changes to the DNA that, in turn, lead to changes in expression of gene levels without changing the inherited genetic code. These changes affect biological processes and can be brought on by environmental factors or by the aging process itself. In a study published online on March 25, 2015 in an open-access article in PLOS ONE, the researchers suggest that HIV itself accelerates these aging-related changes by more than 14 years. "While we were surprised by the number of epigenetic changes that were significantly associated with both aging and HIV-infection, we were most surprised that the data suggests HIV-infection can accelerate aging-related epigenetic changes by 13.7 to 14.7 years," said Dr. Beth Jamieson, Professor of Medicine in the Division of Hematology/Oncology at the David Geffen School of Medicine at UCLA and one of the study's senior authors. "This number is in line with both anecdotal and published data suggesting that treated HIV-infected adults can develop the diseases of aging mentioned above, approximately a decade earlier than their uninfected peers." The researchers examined samples of white blood cells stored by UCLA's MACS site, which has been collecting biological samples as well as clinical, behavioral, and socioeconomic data on men infected with HIV and men at risk for HIV infection since 1983.