Melanoma is a type of skin cancer that develops in the cells (melanocytes) that produce pigment in the skin. It is a more aggressive form of skin cancer and can spread (metastasize) to other parts of the body if not detected and treated early.
A team of scientists from the University of Pittsburgh School of Medicine has found the missing puzzle piece in the mystery of how melanoma tumors control their mortality.
In a paper published in Science, they describe how they identified the specific genetic changes that allow tumors to grow rapidly while also preventing their own death. This discovery could have significant implications for the way melanoma is understood and treated by oncologists.
Telomeres, protective caps at the end of the chromosome, are required to prevent DNA from degrading. In healthy cells, telomeres become shorter with each cycle of replication until they become so short that the cell can no longer divide. Disruptions in maintenance of the length of the telomeres can lead to severe disease. Short telomere syndromes lead to premature aging and death, but extra-long telomeres are associated with cancer.
For years, scientists have observed strikingly long telomeres in melanoma tumors, especially in comparison with other cancer types.
“There’s some special link between melanoma and telomere maintenance,” said Alder. “For a melanocyte to transform into cancer, one of the biggest hurdles is to immortalize itself. Once it can do that, it’s well on its way to cancer.”
The telomerase protein is responsible for elongating telomeres, protecting them from damage, and preventing cell death. Telomerase is inactive in most cells, but many types of cancers use mutations in the telomerase gene, TERT, that activate this protein and allow cells to continue growing. Melanoma is particularly well-known for doing just this.
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