An international team of scientists has uncovered a mechanism by which acute myeloid leukemia (AML) cells sustain their growth. Researchers at Baylor College of Medicine, University of Veterinary Medicine in Austria and Josep Carreras Leukemia Research Institute in Spain discovered that AML cells prevent the synthesis of proteins that suppress their growth by forcibly isolating the mRNAs that encode such proteins within structures known as P-bodies. These findings, published in Nature Cell Biology , offer a novel perspective into the survival mechanisms of AML and possibilities for new anti-cancer therapies.
Despite important advances in cancer research, the prognosis for most AML patients remains poor. Our goal was to identify and mechanistically understand new vulnerabilities of leukemia cells that could potentially be therapeutically targeted in AML." Dr.
Bruno Di Stefano, co-corresponding author, assistant professor of molecular and cellular biology and part of the Stem Cell and Regenerative Medicine (STaR) Center at Baylor Previous studies have shown that leukemia cells corrupt the process that translates mRNAs into proteins in ways that facilitate their growth, but the underlying mechanisms are poorly understood. "Our first insight into how leukemia cells might derail normal translation control was the discovery that they harbored more P-bodies than their normal counterparts," said Di Stefano, member of the Dan L Duncan Comprehensive Cancer Center. "Excitingly, P-bodies.