|Life Extension Update Exclusive |
Colon cancer answer
A paper published online in the Journal of Biological Chemistry on September 8, 2004, explains why mutations in the adenomatous polyposis coli (APC) tumor suppressor gene cause the majority of cases of colon cancer. Researchers at the University of Utah's Huntsman Cancer Institute led by David Jones, PhD discovered that the gene controls the conversion of dietary vitamin A (retinol) into retinoic acid, which is necessary for normal cell growth in the lining of the intestines, without which colon cancer can develop.
The APC gene is mutated in individuals who have familial adenomatous polyposis, an inherited syndrome in which potentially thousands of precancerous polyps form in the colon, inevitably leading to colon cancer. Acquired mutations of the APC gene are also found in 85 percent of those with sporadic colon cancer.
The researchers blocked the APC gene in embryonic zebra fish, who share many genes with humans. They observed a lack of normal cells in the lining of their intestines, which was restored when the embryos were treated with retinoic acid.
Dr Jones commented, “For a long time, scientists believed they knew what the APC gene did – that it regulated cell growth and division – but now we know we've been missing a big piece of the picture... Implications of this study are far reaching. We have long suspected that vitamin A was helpful in preventing certain cancers, including colon cancer. With this new understanding, it may be possible to bypass a non-functioning APC gene by introducing retinoids as a form of chemoprevention, and thus control the undifferentiated and uncontrolled growth of colon cells that results in colon cancer."
If someone had the genetic defect, increasing dietary vitamin A would not overcome it, however, Dr Jones told Life Extension, “treatment with retinoic acid or retinoic acid derivatives might. “