Death to Blood Cancer Cells: New Drug Combination Could Revive the Power of Leading Treatment — Future clinical trials wil |
Researchers found that resistance to the leukemia drug venetoclax occurs due to increased breakdown and turnover of mitochondria in cancer cells, a process called mitophagy. They discovered that inhibiting mitophagy with chloroquine restores venetoclax’s ability to kill cancer cells, suggesting a potential future therapy for acute myeloid leukemia.
Recently, research conducted using both human tissue samples and mouse models has uncovered that the resistance of leukemia cells to the widely used drug venetoclax is due to an abrupt surge in the breakdown and turnover of mitochondria. These structures within the cell play a crucial role in generating energy and also signal the cell to undergo programmed cell death under certain adverse conditions.
“Overcoming resistance to BH3 mimetic drugs like venetoclax is of unique clinical significance because these medications are often used for treating people with acute myeloid leukemia,” said study co-lead investigator Christina Glytsou, Ph.D., a former postdoctoral researcher at NYU Grossman School of Medicine and now an assistant professor at Rutgers University.
Aifantis, the Hermann M. Biggs Professor and chair of the Department of Pathology at NYU Grossman and Perlmutter, says the research team plans to design a clinical trial to test whether chloroquine, when used in combination with venetoclax, prevents drug resistance in people with acute myeloid leukemia.
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