| Literature DB >> 24411948 |
Hiroyuki Ikeda1, Junko Aida2, Atsushi Hatamochi3, Yoichiro Hamasaki3, Naotaka Izumiyama-Shimomura4, Ken-Ichi Nakamura4, Naoshi Ishikawa4, Steven S Poon4, Mutsunori Fujiwara5, Ken-Ichiro Tomita5, Naoki Hiraishi6, Mie Kuroiwa7, Masaaki Matsuura8, Yukihiro Sanada9, Youichi Kawano10, Tomio Arai11, Kaiyo Takubo12.
Abstract
Chromosomal and genomic instability due to telomere dysfunction is known to play an important role in carcinogenesis. To study telomere shortening in the epidermis surrounding actinic keratosis, we measured telomere lengths of basal, parabasal, and suprabasal cells in epidermis with actinic keratosis (actinic keratosis group, n = 18) and without actinic keratosis (sun-protected, n = 15, and sun-exposed, n = 13 groups) and in actinic keratosis itself as well as in dermal fibroblasts in the 3 groups, using quantitative fluorescence in situ hybridization. Among the 3 cell types, telomeres of basal cells were not always the longest, suggesting that tissue stem cells are not necessarily located among basal cells. Telomeres of basal cells in the sun-exposed group were shorter than those in the sun-protected group. Telomeres in the background of actinic keratosis and in actinic keratosis itself and those of fibroblasts in actinic keratosis were significantly shorter than those in the controls. Our findings demonstrate that sun exposure induces telomere shortening and that actinic keratosis arises from epidermis with shorter telomeres despite the absence of any histologic atypia.Entities:
Keywords: Actinic keratosis; Aging; Dermis; Epidermis; Photoaging; Q-FISH; Telomere
Mesh:
Year: 2013 PMID: 24411948 DOI: 10.1016/j.humpath.2013.10.009
Source DB: PubMed Journal: Hum Pathol ISSN: 0046-8177 Impact factor: 3.466