New data published in Nature describe researchers' discovery of the mechanism through which drug resistance to cancer treatment for acute myeloid leukemia (AML) develops. In particular, the study results implicated a gene called GLI1 in the development of drug resistance to anticancer therapies such as ribavirin or cytarabine. GLI1 appeared to be overactive in cells taken from patients with AML or head and neck cancer, which led to an alteration in the drugs' chemical composition. According to the researchers, these data have spurred investigation into treatment approaches that would prevent the development of drug resistance and may have broad application for treatment of other cancers.
A mechanism that enables the development of resistance to Acute Myeloid Leukemia (AML) anticancer drugs, thereby leading to relapse, has been identified by researchers. The new discovery constitutes a major breakthrough in the fight against AML, one of the deadliest forms of leukemia, because it immediately suggests strategies to overcome drug resistance.