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Archive - Dec 10, 2018

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Study Supports Potential for Tailoring Patient-Specific Treatments for Acute Myeloid Leukemia (AML)

Advances in rapid screening of leukemia cells for drug susceptibility and resistance are bringing scientists closer to patient-tailored treatment for acute myeloid leukemia (AML). Research on the drug responses of leukemia stem cells may reveal why some attempts to treat are not successful or why initially promising treatment results are not sustained. AML is a serious disorder of certain blood-forming cells. In this disease, certain early precursor cells in the bone marrow that usually develop into white blood cells don't mature properly. They remain frozen as primitive cells called blasts, unable to further differentiate and mature. These can accumulate and cause low blood counts that reduce the ability to fight infections, and low platelet counts that cause risk of life-threatening hemorrhage. Leukemia stem cells - the progenitors for the immature, cancerous blood cells - propagate AML, and also play a role in the cancer returning after treatment. Cancer researchers are interested in how genes are expressed in this cell population, because this data may hold clues to resistance to standard therapies and answers to why some patients relapse. A study presented at the 60th Annual Meeting of the American Society of Hematology in San Diego (December 1-4, 2018) looked at the drug response patterns of stem cells and blast cells taken from individual patients diagnosed with AML. The information was gathered through high-throughput screening, a state-of-the-art method for quickly evaluating and testing many samples. The researchers found that leukemia stem cells and blast cells diverged in their drug susceptibility patterns, and also that these patterns differed from patient to patient.

Lifespan Extension at Low Temperatures Is Actively Controlled by Genes, Not by Passive Lowering of Metabolic Rate Reducing Reactive Oxygen Species (ROS), New Study Suggests

Why do we age? Despite more than a century of research (and a vast industry of youth-promising products), what causes our cells and organs to deteriorate with age is still largely unknown. One known factor is temperature: Many animal species live longer at lower temperature than they do at higher temperatures. As a result, "there are people out there who believe, strongly, that if you take a cold shower every day it will extend your lifespan," says Kristin Gribble (photo), PhD, an Assistant Scientist at the Marine Biological Laboratory(MBL) in Woods Hole, Massachusetts (the MBL is an affiliate of the University of Chicago). But a new study from Dr. Gribble's lab indicates that it's not just a matter of turning down the thermostat. Rather, the extent to which temperature affects lifespan depends on an individual's genes. The study from Dr. Gribble's group, which was published in Experimental Gerontology (114: 99-106; 2018), was conducted in the rotifer, a tiny animal that has been used in aging research for more than 100 years. Gribble's team exposed 11 genetically distinct strains of rotifers (Brachionus) to low temperature, with the hypothesis that if the mechanism of lifespan extension is purely a thermodynamic response, all strains should have a similar lifespan increase. However, the median lifespan increase ranged from 6 percent to 100 percent across the strains, they found. They also observed differences in mortality rate. The new study is titled “Congeneric Variability in Lifespan Extension and Onset of Senescence Suggest Active Regulation of Aging in Response to Low Temperature.” This study clarifies the role of temperature in the free-radical theory of aging, which has dominated the field since the 1950s.