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Inflammation can Lead to Cancer

evidence indicates that antibodies may signal specific receptors on leukocytes to enhance the cancer-promoting pathway. Part of the receptor for the antibody known as immunoglobulin appears to be involved, Coussens said.

The good news, she adds, is that potential drugs to block this pathway are already being tested in clinical trials to treat B cell lymphoma and auto-immune diseases made worse by inflammation, such as rheumatoid arthritis.

"We already know that inflammation accelerates skin, cervical and colon cancer, and most likely also lung and breast cancer," she said. "If we confirm that what we've discovered in the mice studies also occurs in human cancers, we may soon be in a good position to slow this cancer process using drugs already under study for severe immune disorders."

Coussens envisions a therapeutic strategy similar to treating people with HIV. The goal would not be to necessarily eliminate every last cancer cell, but to control the inflammation process needed for the cancer to progress to a more threatening stage.

The new UCSF finding comes from studies with mice genetically engineered to carry some of the genes of the human papilloma virus (HPV), a pathogen that is known to cause human cervical cancer. By comparing cancer progression in these mice compared with gene "knock-out mice" that lacked the antibody receptors normally active on the leukocyte surfaces, Coussens and her colleagues discovered that the receptors were involved for the cancer to progress rapidly.

Coussens stresses that because of the unique antibody makeup of each person, there is no evidence and no likelihood that periodic booster shots of the immunoglobulin antibody, or even blood transfusions from someone with precancerous tissue could trigger cancer progression in a recipient.

Source-Eurekalert
PRI
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