Categories: Health

They learned how to predict whether leukemia patients will respond to epigenetic drugs – Society

A study from the Josep Carreras Leukemia Research Institute answers the question of why some leukemia patients respond to treatment with epigenetic cancer drugs while others do not.

The study, conducted by the team of director of the Leukemia Research Institute Josep Carreras Manel Esteller, was published in the journal Cancer Research Communications.

“We decided to focus our research on a type of bone marrow cancer that produces leukemia blood cells, called myelodysplastic syndrome, because its treatment option is an epigenetic drug called azacitidine, a DNA methylation inhibitor. We looked at what was happening at DNA and protein levels in thousands of cells isolated from these patients at two points in time: before and after receiving epigenetic therapy,” Esteller explained.

The researcher explained that they were able to characterize more than 30 cell subtypes and 50 genes, which allowed them to observe that patients in whom pharmacological treatment had an effect had a specific profile at the level of individual cells.

In particular, they observed a decrease in the number of mutations in progenitor stem cells and immature granulocytes (a type of immune cell that has small particles) and monocytes (a type of white blood cell), suggesting that epigenetic therapy evolved from modifications. in gene expression – according to researchers, has little chance of success.

However, for those patients resistant to the epigenetic drug, the good news is that they have discovered that some of the new mutations may be targets for other drugs specifically targeting them.

“As if it were a game of cat and mouse between the doctor and the cancer, the tumor’s strength against one drug creates its vulnerability to another drug. Hence the importance of molecular studies at the level of individual cells, which allow us to predict not only the prognosis of the disease, but also what the leukemia may be sensitive to, Esteller concluded.

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