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New potential target for leukemia therapy. « Medicine in the Library

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New potential target for leukemia therapy.  « Medicine in the Library

New potential target for leukemia therapy.

Posted by giorgiobertin on May 10, 2024

A group of researchers from Dana-Farber Cancer Institute discovered that a subgroup of myeloid and lymphoid leukemias depends on a molecular complex called PI3Kgamma for survival.

The study published in “Nature“, provides both mechanistic and preclinical evidence to support the rapid initiation of clinical trials for patients with acute myeloid leukemia (AML) to test an existing drug that inhibits the complex, called eganelisbboth alone and in combination with the most widely used chemotherapy for AML, cytarabine.

This is a drug ready to be tested in AML patients,” says the professor. Lane. “It has already been used in clinical trials for many patients with solid tumors.”
Luo, who initiated this research to improve existing therapies for AML, has also treated animal models of leukemia with cytarabine alone and with eganelisib plus cytarabine. The team found that those treated with a combination di eganelisib e citarabina had longer survival than those treated with cytarabine alone, regardless of the sensitivity of the leukemia to PI3Kgamma inhibition alone.

The observations suggested that the two drugs worked synergistically. The researchers discovered and found that inhibition of PI3Kgamma also leads to the suppression of a metabolic process in leukemia cells called oxidative phosphorylation (OXPHOS). Leukemia cells depend on OXPHOS for energy, and suppression of OXPHOS can lead to their death.

Read abstract of the article:
Targetable leukaemia dependency on noncanonical PI3Kγ signalling.
Luo Q, Raulston EG, Prado MA, et al.
Nature. Published: 08 May 2024. doi: 10.1038/s41586-024-07410-3

Source: Dana-Farber Cancer Institute

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This entry was posted on Maggio 10, 2024 a 6:10 am and is filed under News-research. Tagged: biochemistry, hematology, pharmacology, oncology. You can follow any responses to this entry through the RSS 2.0 feed.

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