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Cancer researchers identify the ‘switch’ that allows intestinal cells to regenerate after injury

Cancer researchers identify the 'switch' that allows intestinal cells to regenerate after injury
Suppressing H3K36 methylation induces the accumulation of abnormal secretory cells. Credit: Nature Cell Biology (2025). DOI: 10.1038/s41556-024-01580-y

Researchers from the University of Colorado Cancer Center have solved a cellular mystery that may lead to better therapies for colorectal and other types of cancer.

Peter Dempsey, Ph.D., professor of pediatrics–developmental biology in the CU School of Medicine, and Justin Brumbaugh, Ph.D., assistant professor of molecular, cellular, and developmental biology at CU Boulder, recently published a paper in the journal Nature Cell Biology showing the importance of the H3K36 methylation process in regulating plasticity and regeneration in intestinal cells.

“The intestine has an enormous ability to regenerate itself after injury, an...

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Researchers Identify ‘Switch’ to Activate Cancer Cell Death

A graphic shows two circles in blue and gold representing tumor cells and a red circle representing CAR-T immunotherapy.
An antigen-negative tumor cell, shown in the golden color on the right, is killed by Fas-mediated “bystander” killing.

A research team from the UC Davis Comprehensive Cancer Center has identified a crucial epitope (a protein section that can activate the larger protein) on the CD95 receptor that can cause cells to die. This new ability to trigger programmed cell death could open the door for improved cancer treatments. The findings were published Oct. 14 in the Nature journal Cell Death & Differentiation.

CD95 receptors, also known as Fas, are called death receptors. These protein receptors reside on cell membranes. When activated, they release a signal that causes the cells to self-destruct.

Modulating Fas may also extend the benefits of chimeric antigen receptor (CAR) T-cell th...

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