Texas researchers identify new pathways contributing to cancer treatment resistance

Researchers in Texas have identified new cellular mechanisms that contribute to cancer resistance in preclinical studies.

At The University of Texas MD Anderson Cancer Center, scientists discovered a pathway where prostate tumors use cancer-associated fibroblasts to create physical barriers. This process limits the ability of T cells to infiltrate tumors and may explain why certain immunotherapies, such as those targeting the B7-H3 immune checkpoint, show limited efficacy alone. The study suggests that combining B7-H3-targeted therapy with MEK inhibition could improve antitumor responses in models of castration-resistant prostate cancer.

Separately, researchers at Texas A&M University identified enzymes that activate a stress-protection system in human cells, which may help liver cancer cells survive chemotherapy. The study found that the protein URM1 helps cells respond to oxidative stress. In laboratory experiments, blocking the enzymes NAE1/UBA3 or UBE2M with an experimental drug, pevonedistat, alongside the chemotherapy drug cisplatin, killed liver cancer cells more effectively than using either treatment alone. These findings are based on cell experiments and do not currently change clinical treatment protocols.