Book contents
- Frontmatter
- Dedication
- Contents
- List of Contributors
- Preface
- Part 1.1 Analytical techniques: analysis of DNA
- Part 1.2 Analytical techniques: analysis of RNA
- Part 2.1 Molecular pathways underlying carcinogenesis: signal transduction
- Part 2.2 Molecular pathways underlying carcinogenesis: apoptosis
- Part 2.3 Molecular pathways underlying carcinogenesis: nuclear receptors
- Part 2.4 Molecular pathways underlying carcinogenesis: DNA repair
- 34 The ATM-mediated DNA-damage response
- 35 Werner syndrome: association of premature aging and cancer predisposition
- 36 Hereditary disorders of DNA repair and DNA damage tolerance that predispose to neoplastic transformation
- 37 Telomerase: target for cancer treatment
- Part 2.5 Molecular pathways underlying carcinogenesis: cell cycle
- Part 2.6 Molecular pathways underlying carcinogenesis: other pathways
- Part 3.1 Molecular pathology: carcinomas
- Part 3.2 Molecular pathology: cancers of the nervous system
- Part 3.3 Molecular pathology: cancers of the skin
- Part 3.4 Molecular pathology: endocrine cancers
- Part 3.5 Molecular pathology: adult sarcomas
- Part 3.6 Molecular pathology: lymphoma and leukemia
- Part 3.7 Molecular pathology: pediatric solid tumors
- Part 4 Pharmacologic targeting of oncogenic pathways
- Index
- References
37 - Telomerase: target for cancer treatment
from Part 2.4 - Molecular pathways underlying carcinogenesis: DNA repair
Published online by Cambridge University Press: 05 February 2015
- Frontmatter
- Dedication
- Contents
- List of Contributors
- Preface
- Part 1.1 Analytical techniques: analysis of DNA
- Part 1.2 Analytical techniques: analysis of RNA
- Part 2.1 Molecular pathways underlying carcinogenesis: signal transduction
- Part 2.2 Molecular pathways underlying carcinogenesis: apoptosis
- Part 2.3 Molecular pathways underlying carcinogenesis: nuclear receptors
- Part 2.4 Molecular pathways underlying carcinogenesis: DNA repair
- 34 The ATM-mediated DNA-damage response
- 35 Werner syndrome: association of premature aging and cancer predisposition
- 36 Hereditary disorders of DNA repair and DNA damage tolerance that predispose to neoplastic transformation
- 37 Telomerase: target for cancer treatment
- Part 2.5 Molecular pathways underlying carcinogenesis: cell cycle
- Part 2.6 Molecular pathways underlying carcinogenesis: other pathways
- Part 3.1 Molecular pathology: carcinomas
- Part 3.2 Molecular pathology: cancers of the nervous system
- Part 3.3 Molecular pathology: cancers of the skin
- Part 3.4 Molecular pathology: endocrine cancers
- Part 3.5 Molecular pathology: adult sarcomas
- Part 3.6 Molecular pathology: lymphoma and leukemia
- Part 3.7 Molecular pathology: pediatric solid tumors
- Part 4 Pharmacologic targeting of oncogenic pathways
- Index
- References
Summary
Introduction
Telomerase, a cellular reverse transcriptase that adds DNA to the ends of chromosomes, is reactivated or up-regulated in the vast majority of human advanced malignancies, and is thus an almost universal target for human cancer. Most human tumors not only express telomerase, but also have very short telomeres, whereas telomerase activity is absent or at lower levels in normal tissues, which also have longer telomeres. This relationship between activation of telomerase activity and short telomeres in human malignancies makes the inhibition of telomerase a novel target for cancer therapeutics. Importantly, the mode of action of telomerase inhibitors predicts minimal side effects on normal stem cells that can express telomerase. Here we summarize the role of telomeres and telomerase in cancer and review the current status of ongoing telomerase clinical trials. This chapter will also discuss the relationship of telomerase to cancer stem cells. Central questions remaining include: What are the key safety concerns, such as the effect of telomerase inhibitors on normal stem cells that express some telomerase? Do cancer stem cells express telomerase activity? What effect will telomerase inhibitors have if cancer stem cells are more quiescent than the bulk of the more differentiated tumor cells? Will human cancers become resistant to telomerase inhibitors?
- Type
- Chapter
- Information
- Molecular OncologyCauses of Cancer and Targets for Treatment, pp. 442 - 451Publisher: Cambridge University PressPrint publication year: 2013