New target for cancer therapy may improve treatment for so...( Targeting and killing the non-malign...),Health

Targeting and killing the non-malignant cells that surround and support a cancer can stop tumor growth in mice, reports a research team based at the University of Chicago Medical Center in the March 1, 2008, issue of the journal Cancer Research. The discovery offers a new approach to treating cancers that are resistant to standard therapy.

Many solid tumors develop elaborate mechanisms to prevent recognition and elimination by the immune system. Due to their genetic instability they often discard the tumor antigen-presenting cell-surface structures that alert the immune system that these cells are harmful. Without these flags, the white blood cells fail to recognize and kill infected or cancerous cells. These tumors then often grow rapidly and resist treatment with chemotherapy or efforts to boost the immune system's response to the tumor.

But the stroma, the layers of cells that surround a tumor, can accumulate tumor antigens and present them on their surface. These genetically stable surrounding cells retain the molecules that present tumor antigens, which makes them a good target for immunotherapy, and they often play an enabling role in tumor growth.

We already knew that targeting the stroma is essential for eradicating established large tumors, because the stroma is like the 'root of the tumor," said study author Hans Schreiber, MD, PhD, professor of pathology at the University of Chicago. However, effects of current treatments that target stroma are usually transient and not cancer-specific."

"Since cancer is a genetic disease," he said, "we wondered whether mutant proteins are released into the surroundings and picked up by the stroma. If so, we can target the root of the cancer in a cancer-specific way to arrest or eradicate a tumor."

They injected T cells, the immune system's warriors, into mice with large established cancers. These T cells, specifically engineered to recognize the tumor antigen, had no di
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