Not all precancerous epithethial lesions are capable of fully advancing to malignant cancers, Meeker says.  One reason for this may be that if genetic instability gets too high, the cells die, thus blocking cancer progression.  Only cells that find a way to balance their telomere length - allowing unlimited cell division and a limited degree of genomic stabilization - can progress to becoming an invasive, life-threatening tumor.

The Hopkins research team examined 35 precancerous lesions from 25 patients, including 11 lesions from eight bladders, three lesions from three uterine cervixes, seven lesions from five large intestines, six lesions from three esophagi and eight lesions from six mouths.  They scored the telomere lengths on a five-point scale ranging from very short to very long.

Overall, the group found telomere length abnormalities in 34 of 35 lesions studied (97 percent).  Short or very short telomeres were observed in all lesions of the esophagus, large intestine and uterine cervix; in eight of 11 (72 percent) lesions of the bladder; and in seven of eight lesions of the oral cavity, which includes the mouth and throat.  Ten of 35 (29 percent) lesions, particularly those of the bladder, displayed a variety of telomere lengths.

More than one million human epithelial cancers are diagnosed every year, Meeker says, and these cancers cause a half-million deaths each year.

Previous studies by the research team and others at Johns Hopkins found shortened telomeres in more than 90 percent of precancerous lesions of the prostate, pancreas and breast.

The current study was funded by the U.S. Public Health Service.  Coauthors were Jessica L. Hicks, Christine A. Iacobuzio-Donahue, Elizabeth A. Montgomery, William H. Westra, Theresa Y. Chan and Brigitte M. Ronnett.

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