PHILADELPHIA — (April 25, 2018) — Targeting telomerase was effective at killing NRAS-mutant melanoma cells, and the impact was further enhanced when the strategy was paired with an inhibitor of mitochondrial function, according to study results by The Wistar Institute published in Oncogene.
“Many melanoma patients do not benefit from new treatment options or experience disease progression because of resistance. Our research advances the search for novel therapeutic strategies to treat NRAS-mutant melanoma, which is highly resistant to most therapies and associated with poor prognosis,” said lead researcher Jessie Villanueva, Ph.D., assistant professor in the Molecular & Cellular Oncogenesis Program at Wistar.
Targeting NRAS as well as the other oncogenes of the Ras family has proven extremely challenging, according to Villanueva, and researchers have resorted to searching for vulnerabilities in NRAS-mutant cancer cells that can provide alternative therapeutic targets.
Mutations in the regulatory element of the TERT gene, which encodes the catalytic subunit of telomerase, are found in more than 70 percent of melanomas. Telomerase is an enzyme that protects the integrity of chromosome ends during replication and represents a promising target for cancer therapy because it is absent in most normal adult cells while its reactivation in malignant
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