AYSE E. ERSON and ELIZABETH M. PETTY
- Published in print:
- 2006
- Published Online:
- September 2009
- ISBN:
- 9780195149616
- eISBN:
- 9780199865062
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780195149616.003.0004
- Subject:
- Public Health and Epidemiology, Public Health, Epidemiology
This chapter illustrates some of the basic molecular and genetic mechanisms that underlie the development of cancer. The chapter is organized into four main sections. The first section examines ...
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This chapter illustrates some of the basic molecular and genetic mechanisms that underlie the development of cancer. The chapter is organized into four main sections. The first section examines perspectives on the roles of oncogenes, tumor suppressor genes, and genomic instability genes in the pathogenesis of malignancy. The second section presents the genetic and epigenetic alterations that disrupt normal function of cancer genes. The third section discusses the alteration of cell cycle progression and checkpoint mechanisms relative to their possible contribution to carcinogenesis. The last section summarizes the phenotypic characteristics of cancer cells, including proliferation, apoptosis, angiogenesis, and metastasis as related to specific molecular events.Less
This chapter illustrates some of the basic molecular and genetic mechanisms that underlie the development of cancer. The chapter is organized into four main sections. The first section examines perspectives on the roles of oncogenes, tumor suppressor genes, and genomic instability genes in the pathogenesis of malignancy. The second section presents the genetic and epigenetic alterations that disrupt normal function of cancer genes. The third section discusses the alteration of cell cycle progression and checkpoint mechanisms relative to their possible contribution to carcinogenesis. The last section summarizes the phenotypic characteristics of cancer cells, including proliferation, apoptosis, angiogenesis, and metastasis as related to specific molecular events.
Jan Vijg
- Published in print:
- 2007
- Published Online:
- April 2010
- ISBN:
- 9780198569237
- eISBN:
- 9780191728242
- Item type:
- book
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780198569237.001.0001
- Subject:
- Biology, Evolutionary Biology / Genetics
Aging has long since been ascribed to the gradual accumulation of DNA mutations in the genome of somatic cells. However, it is only recently that the necessary sophisticated technology has been ...
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Aging has long since been ascribed to the gradual accumulation of DNA mutations in the genome of somatic cells. However, it is only recently that the necessary sophisticated technology has been developed to begin testing this theory and its consequences. This book critically reviews the concept of genomic instability as a possible universal cause of aging in the context of a new, holistic understanding of genome functioning in complex organisms resulting from recent advances in functional genomics and systems biology. It provides a synthesis of current research, as well as a look ahead to the design of strategies to retard or reverse the deleterious effects of aging. This is particularly important in a time when we are urgently trying to unravel the genetic component of aging-related diseases. Moreover, there is a growing public recognition of the imperative of understanding more about the underlying biology of aging, driven by continuing demographic change.Less
Aging has long since been ascribed to the gradual accumulation of DNA mutations in the genome of somatic cells. However, it is only recently that the necessary sophisticated technology has been developed to begin testing this theory and its consequences. This book critically reviews the concept of genomic instability as a possible universal cause of aging in the context of a new, holistic understanding of genome functioning in complex organisms resulting from recent advances in functional genomics and systems biology. It provides a synthesis of current research, as well as a look ahead to the design of strategies to retard or reverse the deleterious effects of aging. This is particularly important in a time when we are urgently trying to unravel the genetic component of aging-related diseases. Moreover, there is a growing public recognition of the imperative of understanding more about the underlying biology of aging, driven by continuing demographic change.
Jan Vijg
- Published in print:
- 2007
- Published Online:
- April 2010
- ISBN:
- 9780198569237
- eISBN:
- 9780191728242
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780198569237.003.0009
- Subject:
- Biology, Evolutionary Biology / Genetics
This epilogue presents some concluding thoughts from the author. Increased stochasticity, beginning at the level of the genome, may work its way through the system and eventually translate into aging ...
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This epilogue presents some concluding thoughts from the author. Increased stochasticity, beginning at the level of the genome, may work its way through the system and eventually translate into aging as a pattern of cells and tissues acting increasingly out of tune. It is now possible to explore a wealth of ever-more sophisticated tools in both cell and molecular biology and the computational sciences to systematically study these cascades of stochastic variation in the various model systems for aging that are now available. This is likely to finally unlock the door to a full understanding of how we grow old.Less
This epilogue presents some concluding thoughts from the author. Increased stochasticity, beginning at the level of the genome, may work its way through the system and eventually translate into aging as a pattern of cells and tissues acting increasingly out of tune. It is now possible to explore a wealth of ever-more sophisticated tools in both cell and molecular biology and the computational sciences to systematically study these cascades of stochastic variation in the various model systems for aging that are now available. This is likely to finally unlock the door to a full understanding of how we grow old.
Jan Vijg
- Published in print:
- 2007
- Published Online:
- April 2010
- ISBN:
- 9780198569237
- eISBN:
- 9780191728242
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780198569237.003.0008
- Subject:
- Biology, Evolutionary Biology / Genetics
A model, presented in Chapter 7, tentatively explains how random mutations can lead not only to cancer, but also to reduced function of the highly differentiated cells in vertebrates. Aging would ...
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A model, presented in Chapter 7, tentatively explains how random mutations can lead not only to cancer, but also to reduced function of the highly differentiated cells in vertebrates. Aging would then be the result of the ultimate failure of genome maintenance in preventing increased noise in the execution of various cellular programs due to accumulating errors in the information content of the genome. However, this model remains untested and could be wrong. Instead, aging could be partially or wholly due to a combination of other processes, most notably increased damage to cellular macromolecules, which may not be restricted to DNA, and the responses to their adverse effects. This chapter discusses the consequences of a scenario in which aging is predominantly a result of random, irreversible alterations in the somatic genome, and how that would impact our prospects to intervene and possibly retard or reverse aging-related cellular degeneration and organismal death.Less
A model, presented in Chapter 7, tentatively explains how random mutations can lead not only to cancer, but also to reduced function of the highly differentiated cells in vertebrates. Aging would then be the result of the ultimate failure of genome maintenance in preventing increased noise in the execution of various cellular programs due to accumulating errors in the information content of the genome. However, this model remains untested and could be wrong. Instead, aging could be partially or wholly due to a combination of other processes, most notably increased damage to cellular macromolecules, which may not be restricted to DNA, and the responses to their adverse effects. This chapter discusses the consequences of a scenario in which aging is predominantly a result of random, irreversible alterations in the somatic genome, and how that would impact our prospects to intervene and possibly retard or reverse aging-related cellular degeneration and organismal death.
