We've updated our Privacy Policy to make it clearer how we use your personal data. We use cookies to provide you with a better experience. You can read our Cookie Policy here.

Advertisement

New Gene Target for Treatment-Resistant Brain Cancer

An abstract image of the human brain.
Credit: DeepMind on Unsplash.
Listen with
Speechify
0:00
Register for free to listen to this article
Thank you. Listen to this article using the player above.

Want to listen to this article for FREE?

Complete the form below to unlock access to ALL audio articles.

Read time: Less than a minute

Doctors and scientists at UCLA Jonsson Comprehensive Cancer Center and the UCLA Jane and Terry Semel Institute for Neuroscience and Human Behavior have identified a gene that may provide a therapeutic target for the deadly, treatment-resistant brain cancer glioblastoma multiforme.


The gene, P300, enables cancer cells that have been damaged by radiation therapy to recover by rearranging DNA and initiating a molecular mechanism that refortifies tumor cells for growth and survival.


In studies using mice and in human glioblastoma multiforme cells, the scientists discovered that blocking P300 disrupted its ability to set that process in motion. The research is published online  in Nature Communications.


Glioblastoma is considered rare — about 13,000 new cases are expected to be diagnosed in the U.S. this year, according to the National Brain Tumor Society — but it is the most common primary brain tumor in adultsm, and there is no known cure. Glioblastoma multiforme cells and their precursors, glioma stem cells, quickly adapt and recover from injury, so chemotherapy and radiation therapy, which may initially slow a tumor’s progress, can ultimately contribute to growth and recurrence.


Reference: Muthukrishnan SD, Kawaguchi R, Nair P, et al. P300 promotes tumor recurrence by regulating radiation-induced conversion of glioma stem cells to vascular-like cells. Nat Comms. 2022;13(1):6202. doi: 10.1038/s41467-022-33943-0.


This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.