Johns Hopkins findings could reshape research on cancer origins

Research suggests cancer mutation likely triggers scleroderma

Johns Hopkins scientists have found evidence that cancer triggers the autoimmune disease scleroderma, which causes thickening and hardening of the skin and widespread organ damage.

A report on the discovery, published Dec. 5 in Science, suggests that a normal immune system is critical for preventing the development of common types of cancer. These findings revive the decades-old cancer theory that everyone develops mutation-laden cells with the potential to morph into cancer. According to this theory, through a process called immunosurveillance, the immune system detects and kills these cancer-prone cells. Full-blown cancers arise when immunosurveillance fails.

"Our study results could change the way many physicians evaluate and eventually treat autoimmune diseases like scleroderma," says study investigator Antony Rosen, a professor at the Johns Hopkins University School of Medicine.

Scientists have previously found that some patients with scleroderma have a higher incidence of cancer.

"As early cancers grow, the body is exposed to novel proteins caused by the mutations in the cancer and potentially opens a window to development of autoimmune disease," says Bert Vogelstein, professor of oncology at the Johns Hopkins Kimmel Cancer Center.

According to investigators, while evidence supporting and rebutting this theory had been gathered in mice, the new study provides the first evidence that this principle may be important in common human tumors. Study results may also help explain why, in some cases, people cured of cancer have also seen their scleroderma disappear.

"This study speaks to the power of the immune system and the emerging picture of harnessing the immune system to treat cancer, adding support to the notion that the immune system may be keeping cancers in check naturally," says Kenneth Kinzler, professor of oncology at the Kimmel Cancer Center.

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