Ever since we broke up with chimpanzees, a change in one letter in our DNA seems to have made us more likely to get cancer, probably as a compromise on extra fertility.

Health


May 3, 2022

Illustration of DNA molecules

KATERINA KON / SCIENTIFIC PHOTO LIBRARY

A small change in our DNA that has occurred since we evolved from other primates has made us more susceptible to cancer, new research shows.

Cancer is relatively rare in other primates. For example, autopsies of 971 non-human primates that died at the Philadelphia Zoo in Pennsylvania between 1901 and 1932 found that only eight had tumors.

To learn why we are more susceptible to cancer, Christine Jacobusio-Donahue at the Memorial Sloan Kettering Cancer Center in New York, and her colleagues compared hundreds of genes between humans and 12 non-human primates.

They found that we had developed a slightly different version of a gene called BRCA2 since we broke up with the chimpanzees.

BRCA2 is known as the tumor suppressor gene because it is involved in DNA repair. However, researchers have found that a single DNA letter changes in humans BRCA2 The gene made it 20 percent worse at DNA repair than other versions of the primate gene, which may explain our higher levels of cancer.

The discovery complements existing knowledge about the role of BRCA2 in human cancer. For example, we know that people with certain variants of BRCA2 a gene that further inhibits its regenerative activity has an even greater risk of developing cancer, especially breast and ovarian cancer.

At this stage we do not know why BRCA2 evolved to become less active in humans than in other primates, says Jacobusio-Donahue. One possibility is to reduce this BRCA2 activity has been chosen for in humans to increase fertility, as studies show that women with BRCA2 cancer-related options seem to get pregnant easiershe says.

If so, this increase in fertility may have come at the cost of higher cancer rates, she added.

The discovery that a single mutation in BRCA2 The gene could be a major cause of human cancer, leading to new treatments, says Jacobusio-Donahue.

For example, although human gene editing is far away, in theory we could rewrite our BRCA2 gene to make it more like versions of non-human primates that are linked to lower levels of cancer, she says.

Reference in the magazine: Cell reports, DOI: 10.1016 / j.celrep.2022.110771

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