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Inflammatory protein converts glioblastoma cells into most aggressive version
Date:8/29/2013

r MES signatures had greater invasion by immune cells called macrophages /microglia elements of the glioblastoma microenvironment than did PN areas.

"We know we have to control inflammation in this disease," Bhat said. NF-κB is known to play an important role in promoting inflammation in multiple cell types.

"Surprisingly we found that activation of NF-κB was prevalent in the MES subtype even before surgery and radiation, which in turn can cause inflammation and further activation of NF-κB."

Bhat is investigating downstream targets of NF-κB that promote radiation resistance in glioblastoma.

Inhibitors of NF-κB are in clinical trials for inflammatory and autoimmune diseases, Aldape noted.

"One can imagine a clinical trial in which patients are evaluated for MES status and given an NF-κB inhibitor if they have the MES subtype. You can look at improving radiation response, and also whether you can reverse the MES subtype," Aldape said.


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Contact: Scott Merville
smerville@mdanderson.org
713-792-0661
University of Texas M. D. Anderson Cancer Center
Source:Eurekalert

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