Mutations associated with cancer are common in normal human esophagus
Mutations associated with cancer are common in normal human esophagus
Mutations associated with cancer are common in normal human esophagus
A new study reveals that genetic mutations associated with cancer are surprisingly common in normal esophageal tissue of human donors, especially among those from middle age. The results broaden our understanding of cancer and aging, but at the same time highlight how little is known about the prevalence and evolution of somatic mutations in normal tissues.
As they get older, people accumulate mutations in healthy cells. In general, these mutations accumulate passively and do not alter cellular behavior. However, if a genetic mutation provides a mutant cell with a competitive advantage, these cells will generate more daughter cells than those that lack the mutation.
It is believed that the expanded population of mutant cells (or "clones") is the origin of cancer. Human skin exposed to ultraviolet light from the sun is the normal tissue with the greatest mutation: almost 25% of skin cells exposed to the sun of middle-aged people carry mutations that cause cancer. Little is known about the degree to which cells accumulate somatic mutations in tissues not exposed to potent mutagens such as ultraviolet light.
To explore the mutational load of a tissue protected from the sun, Iñigo Martincorena and his colleagues performed a directed gene sequencing of the normal esophageal epithelium, a tissue with a structure and properties similar to those of the skin, from nine human donors of ages between 20 and 75 years old.
Although the mutation rate was lower in the esophageal tissue than in the skin, Martincorena et al. found that there was strong positive selection in favor of cell clones that carried mutations in 14 genes associated with cancer. In tissue samples from donors of middle age or older, more than half of the esophageal epithelial tissue contained mutant clones.
Most striking was the high frequency of mutations in the cancer-leading gene NOTCH1 in the esophageal epithelium of older donors. These mutations were more common in normal cells than in esophageal cancer cells, which led the authors to speculate that esophageal cancers could evolve from epithelial cells lacking mutations in NOTCH1. (Source: AAAS)
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