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Clues To Molecular Cancer Switches Probed

HANOVER, NH-A genetic variation in human cells could facilitate cancer invasion and spread by boosting production of agents that dissolve the framework that holds the body together, report Dartmouth Medical School researchers. Their findings offer clues to molecular switches that control cancer progression and provide tools for cancer detection and treatment.

The study, headed by Dr. Constance Brinckerhoff, Nathan Smith Professor of Medicine and of Biochemistry, was reported in the Dec. 1 issue of Cancer Research.

The work builds on Brinckerhoff's studies of the enzymes called collagenases that break down collagen, the body's most abundant protein. The rigid collagen molecule gives the body shape and structure.

A family of at least 15 enzymes have essential roles in the modeling of connective tissues-the network of skin, bones, and blood vessels that mold the body. These enzymes are active in normal physiological processes such as wound healing and in diseases such as arthritis. Several have the unique ability to degrade collagens in the connective tissue matrix outside cells.

The team studied two different versions of a particular collagenase in normal skin cells and in cells from melanoma, the most serious form of skin cancer and one of the fastest growing cancers, according to Brinckerhoff, with more than 40,000 new cases a year.

Both the normal and cancer cells with one particular version had high levels of the collagenase, while those with the other version did not. Collagenase destroys tissue and its increased production could be a factor in the ability of tumor cells to invade other tissues and migrate.

The enzymes require metals and are also known as matrix metalloproteinases. The most ubiquitous of these is matrix metalloproteinase-1 (MMP-1), also called collagenase-1. Too much of the emzyme is associated with irreversible cartilage damage in arthritis. Cancer pati
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Contact: Hali Wickner
Hali.Wickner@dartmouith.edu
603-650-1481
Dartmouth Medical School
14-Dec-1998


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