Washington, July 14: New research suggests that telomere shortening is one of the most prevalent changes on a cell's path to cancer.
According to studies presented at the 94th Annual Meeting of the American Association for Cancer Research, telomeres, which are the ubiquitous safety caps on the ends of chromosomes help maintain genomic integrity.

As cells multiply the telomere DNA is lost and telomeres keep getting cropped. The new study suggests that telomere dysfunction from the shortening may play a causal role in human intraepithelial neoplasia (IEN) found in precancers.


"Normal human cells have systems that monitor telomere length, either halting cell division or causing the cell to commit suicide, should telomeres become too short," said Alan K.


Meeker, postdoctoral fellow in urology at the Johns Hopkins School of Medicine in Baltimore, and lead author of the studies.



Using a high-resolution, fluorescent in-situ hybridization method for direct telomere length assessment, the scientists found that in greater than 90 per cent of the cases, there was evidence of significantly shorter telomeres in precancerous lesions compared to normal tissue.

Dramatic telomere shortening occurs in breast luminal epithelial cells in subsets of non-malignant, normal-appearing lobules and small ducts: a potential early molecular mechanism underlying breast tumorigenesis To further understand the disease process in breast cancer, Meeker, DeMarzo and colleagues attempted to shortening was observed in nine of 12 cases.


Menstrual cycle is also assumed to be a key player since the cell division that occurs during that regular process causes normal ductal epithelial cells to lose telomeric DNA. Bureau Report