Melanoma Wants To Kill – Here Is How It Changes To Do So

Source: Science 2.0, November 2022

A new paper describes the perfect combination of genetic alterations that tumors use to promote explosive growth and prevent their own demise, a development that could change the way oncologists understand and treat melanoma.

Telomeres, protective caps at the of 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. 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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