Aging appears to be intrinsically related to carcinogenesis. Genomic instability due to telomere shortening plays an important role in carcinoma development. In order to clarify telomere dysfunction in carcinoma development, we examined the uninvolved epithelium adjacent to carcinoma in situ (CIS), i.e. background of CIS, and CIS itself, compared to control without carcinoma, using an improved quantitative fluorescence in situ hybridization (Q-FISH) method. We also estimated anaphase bridge (AB), which is inferred to be related to chromosomal instability. In all cell types (basal, parabasal, and suprabasal), mean telomere lengths were significantly shorter in the background than in the control. We also demonstrated increased incidences of AB, not only in CIS, but also in the background and control epithelia with excessively shortened telomeres. Thus we have conclusively demonstrated that CIS arises from epithelium with short telomeres.
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