title: Luminal and cancer cells in the breast show more rapid telomere shortening than myoepithelial cells and fibroblasts.
abstract: Critically shortened, dysfunctional telomeres may play a role in the genetic instabilities commonly found in cancer. We analyzed 30 surgical specimens of invasive breast carcinoma from women aged 34 to 91 years and estimated telomere lengths as telomere-to-centromere ratio values in the 5 different cell types comprising breast tissue in order to clarify telomere length variations within and between individuals using our tissue quantitative fluorescence in situ hybridization method. We obtained 3 novel findings. (1) In corresponding normal tissues, telomere length decreased in the order myoepithelial cells > normal-appearing fibroblasts > luminal epithelial cells, and telomere lengths were characteristic in these 3 cell types within each individual. (2) As expected, cancer cells had significantly shorter telomeres than myoepithelial cells (P < .0001) and normal-appearing fibroblasts (P = .0161), but there was no significant difference in telomere length between luminal cells and cancer cells (P = .6270). (3) Fibroblasts adjacent to cancer had longer telomeres than normal-appearing fibroblasts distant from cancer (P < .0001). This study, which represents the first reported assessment of telomere length variations in the 5 cell types comprising breast tissue within and between individuals, revealed that normal luminal epithelial cells and cancer cells had the shortest telomeres. Our new findings indicate that telomeres of background luminal cells are as short as those of cancer cells. Tissue quantitative fluorescence in situ hybridization, applicable to analysis of individual cells in tissue sections, is considered to be a powerful technique with considerable promise for studies in oncology.
authors.affiliation: Division of Metabolic Care and Endocrine Surgery, Department of Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. kurabar-tky@umin.ac.jp
authors.forename: Rie
authors.initials: R
authors.lastname: Kurabayashi
authors.forename: Kaiyo
authors.initials: K
authors.lastname: Takubo
authors.forename: Junko
authors.initials: J
authors.lastname: Aida
authors.forename: Naoko
authors.initials: N
authors.lastname: Honma
authors.forename: Steven S S
authors.initials: SS
authors.lastname: Poon
authors.forename: Makoto
authors.initials: M
authors.lastname: Kammori
authors.forename: Naotaka
authors.initials: N
authors.lastname: Izumiyama-Shimomura
authors.forename: Ken-ichi
authors.initials: K
authors.lastname: Nakamura
authors.forename: Ei-ichi
authors.initials: E
authors.lastname: Tsuji
authors.forename: Masaaki
authors.initials: M
authors.lastname: Matsuura
authors.forename: Toshihisa
authors.initials: T
authors.lastname: Ogawa
authors.forename: Michio
authors.initials: M
authors.lastname: Kaminishi
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001940:Breast / Q000473:pathology* / Q000648:ultrastructure; D001943:Breast Neoplasms / Q000473:pathology*; D004847:Epithelial Cells / Q000473:pathology / Q000648:ultrastructure; D005260:Female; D005347:Fibroblasts / Q000473:pathology / Q000648:ultrastructure; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D008875:Middle Aged; D016615:Telomere / Q000473:pathology* / Q000648:ultrastructure