![]() Researchers analyzed the 24 T-PLL samples using a novel technique called BH3 profiling, which gauges how likely a cell is to undergo apoptosis, and how functionally dependent it is on certain survival proteins. The challenge then became to find a targeted drug that could work synergistically with venetoclax. The temporary effectiveness of venetoclax in patients with T-PLL suggested that the tumor cells were sustained, in part, by BCL-2. BCL-2 is a survival protein - so-called because it inhibits cells from dying through a natural process known as apoptosis. Studies had shown that the drug venetoclax, which blocks a protein called BCL-2, produced brief responses in some patients with T-PLL. Researchers already had a clue to one of those vulnerabilities. These, combined with four from Dana-Farber, provided “a unique opportunity to study the molecular dependencies of this disease,” Davids remarks. are diagnosed with it each year - has made it difficult to obtain sufficient tissue samples to study.įor the current study, Charles Herbaux, MD, MSc - a postdoctoral fellow in Davids’ lab - utilized a collection of 20 T-PLL primary samples from patients across France that were banked at his home institution, Lille University School of Medicine. The relatively small number of patients - about 200 adults in the U.S. A ‘unique opportunity’Ī major obstacle to molecular research in T-PLL is the rarity of the disease. Our study is one of the first to do that.” “We urgently need to identify the molecular vulnerabilities of T-PLL cells so we can design clinical trials of drugs that target those weaknesses. The current treatments, such as chemotherapy and the antibody drug alemtuzumab, aren’t very effective and lead to considerable toxicities,” says Dana-Farber’s Matthew Davids, MD, senior author of the study. “T-PLL is an especially challenging cancer to treat. When they tested the combination in two patients with advanced T-PLL, the results were encouraging: one patient experienced a deep remission, and the other, whose cancer was rapidly worsening, saw the advance of the disease come to halt. In a recent study in the journal Blood, Dana-Farber researchers analyzed blood samples from two dozen patients with T-PLL and found that pairing the targeted drugs ruxolitinib and venetoclax caused T-PLL cells to die in the laboratory. It’s an approach that has now yielded a promising combination drug therapy for T-cell prolymphocytic leukemia (T-PLL), a rare, aggressive hematologic cancer. ![]() Scientists are finding ways to turn that survival instinct into a liability - by making the cells even more dependent on those pathways, then choking the pathways off. Cancer cells have a bias toward survival, often becoming heavily reliant on certain protein pathways to sustain themselves. ![]()
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