The alternative lengthening of telomeres pathway may operate in non-neoplastic human cells |
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Authors: | 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 |
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Affiliation: | Department of Pathology, Dunedin School of Medicine, Health Sciences, University of Otago, Dunedin, New Zealand. |
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Abstract: | 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 ALT-associated PML bodies (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. |
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Keywords: | telomere maintenance alternative lengthening nuclear bodies non‐neoplastic cells |
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