Scientists have shown a link between acute myeloid leukaemia (AML), an aggressive cancer of the blood, and mutant genes in the DNA mismatch repair pathway. The study, to be published online in Cell Research, could lead to more successful approaches to treating patients with AML.
Most patients with AML achieve complete remission after chemotherapy but then undergo relapse. This relapse may be due to minimal residual disease, in which a small number of drug-resistant cells persist in the patient after achieving complete remission. The molecular basis for the resistance of some AMLs to chemotherapy, however, has so far remained unclear.
Liya Gu and colleagues looked at different stages of the disease to find that loss of DNA mismatch repair function is associated with relapsed AML and AML that is resistant to treatment, and that it may contribute to the development of the disease. The researchers have found that the phenotype of these drug-resistant cells is similar to cells that show loss of mismatch repair function. An understanding of how disrupted mismatch repair sensitizes cells to drug treatments should lead to more successful treatments for AML.
Liya Gu (University of Kentucky College of Medicine, Lexington, KY, USA)
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