TREATMENT

Melanoma, A new study provides critical molecular information that could aid researchers in developing more effective therapy and prevention techniques for a difficult-to-treat form of melanoma skin cancer.

Researchers from The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC – James) uncover and characterize critical aspects of a gene mutation that is responsible for 15 to 20% of all melanomas in this new article.

The research proves, using a preclinical laboratory model, that the frequency of a given NRAS gene mutation occurring in human melanoma is closely connected to that gene mutation’s potential to cause spontaneous melanoma formation.

“This means that the properties of the mutant itself, rather than the ease with which that specific gene mutation occurs,” said corresponding author Christin Burd, an associate professor of molecular genetics in The Ohio State University College of Arts and Sciences, Department of Molecular Genetics, and a member of the OSUCCC – James Molecular Carcinogenesis and Chemoprevention Program.

OSUCCC – James researchers created genetically altered models that allowed them to activate one of nine distinct NRAS-mutant variants in melanocytes, the pigment cells that produce melanoma.

“Amazingly, only those identified in human disease caused melanoma to develop when we activated these gene alterations,” Burd added. “Some mutations never resulted in melanoma, but we know they cause leukaemia. This discovery demonstrates that NRAS mutation selection is distinct to each tumour type and occurs during cancer initiation, rather than in response to a single mutagenic event such as sun exposure.”

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Burd’s team discovered that slight differences in the outward facing structure of NRAS mutants capable of initiating melanoma made these proteins better able to interact with the signalling pathways that drive melanoma growth, in collaboration with Sharon Campbell, a structural biologist at the University of North Carolina (UNC) Chapel Hill, and Debbie Morrison at the National Institutes of Health.

“We will now attempt to target this specific structural property of the melanoma-inducing NRAS mutations in order to prevent and/or treat the disease,” Burd added. “Our findings also reveal and corroborate what was previously simply speculation: that tiny changes between RAS mutations decide which ‘flavours’ can induce cancer. A similar approach could be utilised to identify vulnerabilities in other RAS-driven tumour types.”

To promote such discoveries, the team created eight unique and freely available genetically modified mouse models that will serve as a valuable resource for the global RAS community. These models, according to Burd, can be used to activate and research the involvement of NRAS in additional cancer types such as colon cancer, leukaemia, myeloma, and thyroid cancer. They can also be used to test new medications for certain disorders.

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