In the Literature: New Lead in Treating ALL

The paper, published in Nature, has identified a "switch" that can be inhibited to restrict tumor growth.

Researchers at NYU Langone Medical Center and elsewhere say that blocking the action of an enzyme "switch" needed to activate tumor growth is emerging as a practical strategy for treating T-cell acute lymphoblastic leukemia.

An estimated quarter of the 500 U.S. adolescents and young adults diagnosed each year with this aggressive disease fail to respond to standard chemotherapy drugs that target cancer cells.


In a report on the work conducted with mice and human laboratory cells, and published in the Oct. 23 edition of the journal , the NYU Langone team concludes that the enzyme JMJD3 -- (pronounced ju-mon-ji D3) -- acts as a cancer "on" switch by splitting off a chemical methyl group of another protein that is usually methylated by a tumor-suppressing enzyme. This enzyme, known as polycomb repressive complex 2 (PRC2), acts, in turn, as an "off" switch for cancer cell proliferation.

It is this destabilizing and cutting loose of PRC2, the same researchers previously showed, that leads to the activation of the NOTCH1 biological pathway — a process common to many cancers but especially active in at least half of all people with T-cell acute lymphoblastic leukemia.

"Our investigations are showing incredible promise in fighting this disease at the transcriptional level," says senior study investigator and NYU Langone cancer biologist Iannis Aifantis, PhD. "We are blocking the action of enzymes controlling the transcription of proteins involved in leukemia rather than attempting to directly suppress cancer genes."

Read the complete press release:

Link to the paper:

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