Extending the Models of Tumor Suppression and Telomere Integrity Interaction: Focusing on the Bone MarrowFernando Pires Hartwig*
Postgraduate Program in Epidemiology, Federal University of Pelotas Oncology Research Group, Technology Development Center (Biotechnology Unit), Federal University of Pelotas, Brazil
- *Corresponding Author:
- Fernando Pires Hartwig
Postgraduate Program in Epidemiology
Federal University of Pelotas Oncology Research Group
Technology Development Center (Biotechnology Unit)
Federal University of Pelotas, Brazil
E-mail: [email protected]
Received May 02, 2013; Accepted June 10, 2013; Published June 12, 2013
Citation: Hartwig FP (2013) Extending the Models of Tumor Suppression and Telomere Integrity Interaction: Focusing on the Bone Marrow. J Bone Marrow Res 1:123. doi:10.4172/2329-8820.1000123
Copyright: © 2013 Hartwig FP. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Telomeres have been receiving attention given their roles in cancer and aging. Germline genetic variants that result in accelerated telomere dysfunction are often associated with bone marrow diseases, with bone marrow failure being the main cause of death for dyskeratosis congenita. It is well-established that telomere dysfunction activates tumor suppression pathways, thus limiting cell viability. Hartwig and Collares recently reviewed the literature on the differential roles of senescence and apoptosis in detecting telomere dysfunction, proposing biological models regarding tissue renewal impairment and cancer. Based on this paper, the present commentary extends the hypothesis to levels of telomerase activity/telomere integrity others than down-regulated, thus adding to the understanding of the effects of the interactions of senescence and apoptosis. Given the relevance of the bone marrow for the clinical manifestation of telomere syndromes, this commentary focuses on the implications of the proposed extensions for bone marrow impairments, suggesting a hematopoietic stem cell-based model according to which environmental factors plausibly add an extra degree of complexity to the effects of the interactions between telomere biology and tumor suppression responses on the balance between hematopoietic stem cell impairment and hematological malignancies in both telomere syndromes and physiological aging.