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The alternative lengthening of telomeres pathway may operate in non‐neoplastic human cells
Author(s) -
Slatter Tania L,
Tan Xin,
Yuen Yi Ching,
Gunningham Sarah,
Ma Sally SiYan,
Daly Erin,
Packer Stephen,
Devenish Celia,
Royds Janice A,
Hung Noelyn A
Publication year - 2012
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.2981
Subject(s) - telomere , telomerase , biology , dna , cancer research , stromal cell , dna damage , microbiology and biotechnology , genetics , gene
The alternative lengthening of telomeres (ALT) mechanism represents an alternative to the enzyme telomerase in the maintenance of mammalian telomeres in 25–60% of sarcomas and a minority of carcinomas (about 5–15%). ALT‐positive cells are distinguished by long and heterogeneous telomere length distributions by terminal restriction fragment (TRF) Southern blotting. Another diagnostic marker of ALT is discrete nuclear co‐localized signals of telomeric DNA and the promyelocytic leukaemia protein (PML), referred to as A LT‐associated P ML b odies (APBs). Recently, we detected smaller sized co‐localized PML and telomere DNA (APB‐like) bodies in endothelial cells adjacent to astrocytoma tumour cells in situ . In this study, we examined a wide variety of non‐neoplastic tissues, and report that co‐localized signals of PML and telomere DNA are present in endothelial, stromal, and some epithelial cells. Co‐localized signals of PML and telomere DNA showed an increased frequency in non‐neoplastic cells with DNA damage. These results suggest that a mechanism similar to that in ALT‐positive tumours also operates in non‐neoplastic cells, which may be activated by DNA damage. Copyright © 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.