London: A drug developed for breast cancer treatment that blocks the activity of CDK6 enzyme in the body has been found to be highly effective against acute myeloid leukaemia (AML) with FLT3 mutations, a study said.
According to Iris Uras from the Institute of Pharmacology and Toxicology at the Vetmeduni Vienna, the first author of the study, the myeloid leukaemia cells growth depends on an activating mutation in the FLT3 tyrosine kinase and the cancer cells die if FLT3 is blocked.
In her study, published recently in the journal Blood, Uras found that another tumour-promoting factor, the enzyme CDK6, directly regulates and initiates the production of FLT3 and thus causes the disease.
The active agent developed for breast cancer treatment blocks the activity of CDK6 and subsequently down regulates FLT3.
“We found a novel therapeutic window that attacks the dependency of a cancer cell on its growth regulator,” said Uras.
The compound from breast cancer therapy deprives the cancer cells of “nutrients”. AML cancer cells carrying the mutation died immediately in the experiments.
The advantage of having this agent at hand is the fact that it has already been approved for the therapy of breast cancer in 2015.
It significantly enhanced the lifespan of patients with breast cancer. Hence, clinical studies can be rapidly initiated without passing a long series of tests in advance.
AML is the most frequent form of leukaemia, also known as blood cancer. Patients with AML have poor prognosis and high mortality rate despite considerable advances in chemotherapy and haematopoietic stem cell transplantations.