REHOVOT, Israel - May 11, 1999 -WeizmannInstitute researchers have discovered a molecular mechanism that may be involved in causing colon cancer,according to a study reported in the May 11 issue of the Proceedings of the National Academy of Sciences.
This research may one day contribute to the development of potential therapies for this type of malignancy and possibly for other types of cancer as well.
The discovery of the new mechanism has solved two seemingly unrelated molecular mysteries.
One concerned an important finding made some two years ago: the fact that colon cancer cells often have abnormally large quantities of a protein called beta- catenin, one of today's "hottest" research molecules. Beta-catenin has been dubbed a"moonlighter" because it holds down two distinct cellular jobs. In its better-known task, beta-catenin binds to adhesion molecules - those molecules that sit in the cellular membrane and allow cells to stick together. In its other role, beta-catenin is known to regulate the performance of genes in the nucleus. However, how exactly beta-catenin does this - and which genes it controls - remained unclear.
The second molecular mystery centered around the gene cyclin D1 - a major regulator of cell growth which, when mutated, can act as an oncogene, or gene that causes cancer. The levels of the protein produced by this gene are abnormally high in about 30 percent of colon cancers, indicating that cyclin D1 may be involved in malignant transformation. However, the cyclin D1 gene found in colon cancer cells is perfectly normal. This baffled researchers because usually oncogenes cause cancer only when they appear in mutated form.
A team of researchers led by Prof. Avri Ben-Ze'ev of the Weizmann Institute's
Molecular Cell Biology Department, in collaboration with the group of Dr. Richard
Pestell from the Albert Einstein College of Medicine in New York, has now put
these two mysterious puzzle pieces together
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