Catching cancer before it can spread through the human body almost always means the difference between life and death. Medical experts say that nearly all cancer patients whose disease has begun to spread at the time of detection have little chance of survival. But now, a team of researchers at the University of Western Ontario in London may have achieved a significant advance in science’s quest to defeat cancer. In an article published in the Feb. 17 issue of the respected U.S. journal Science, the team led by biochemist David Denhardt described research that points to a protein that may play a key role in preventing cancer. “This discovery is very exciting,” said Richard Schultz, a biochemist who works in the same field at Chicago’s Loyola University. “It may eventually lead to some drug which inhibits the spread of cancer.”
The protein that attracted the attention of Denhardt’s team is known as tissue inhibitor of
metalloproteinase (TIMP). British and American researchers first identified it in the late 1970s as a substance that they said was important in maintaining the connective tissue joining cells together. But Denhardt and his team now say that TIMP may also prevent cancer from occurring and rapidly spreading through the body. Using genetic engineering techniques to clone mouse genes, the team then supressed the gene that produced TIMP. They discovered that when cells were unable to make TIMP, they became cancerous. That discovery emphasizes the role of genes in cancer, and the fact that some people are genetically more susceptible to some kinds of cancer than other people. Said Denhardt, a Sacramento, Calif.-born scientist who headed Western’s cancer research laboratory from 1980 to 1988: “We speculate that some human tumors will be found to result from the loss of the gene [responsible for producing TIMP].”
The findings emerged after Denhardt’s 12member team began examining the cellular substances known as metalloproteinases—a group of enzymes found in animal and human cells. Enzymes act as catalysts of cellular change. The metalloproteinase enzymes, which some cancerous cells produce in large quantities, can break down the tissues that bind cells together. As a result, cancer cells are able to enter the bloodstream and invade other parts of the body. Said Denhardt: “Cancer is simply a disease of aberrant, or runaway, cell growth. So we felt that a better understanding of cell growth was essential to understanding how that regulatory process may break down in cancer.”
Other researchers, including Schultz, have increased the amount of TIMP in cancerous mice, which significantly retarded the spread of the disease. If the findings about TIMP are correct, the way might be open to using a laboratory-produced version of the protein. Still, Denhardt said that the testing of TIMP in human beings may be some years away because further clinical trials are needed. As well, Denhardt said that even if the protein were to prove effective in checking a cancer’s growth, the disease would still have to be detected before it had spread to other parts of the body.
The findings of Denhardt’s team also seemed likely to help scientists studying other diseases that involve enzyme deficiencies. In rheumatoid arthritis, for one, a lack of TIMP is suspected to lead to an early onset of the disease in those genetically disposed to it. Researchers at Synergen Inc., a biotechnology firm in Boulder, Colo., have already discovered that arthritic mice show a 50-per-cent improvement rate after being injected with TIMP. Meanwhile, Denhardt said that his team’s findings provide new clues to the intricate workings of the human cell. He added, “We can’t really understand cancer until we know how the normal cell functions, just like you can’t fix your car if you don’t know how it works.” For Canada’s estimated 96,300 cancer sufferers diagnosed each year, more understanding can only mean more hope.
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