國立虎尾科技大學 |

Evolutionary dynamics of malignancy = the genetic and environmental causes of cancer /

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Evolutionary dynamics of malignancy/ by Robert C. Jackson.
Reminder of title:	the genetic and environmental causes of cancer /
Author:	Jackson, Robert C.
Published:	Cham :Springer International Publishing : : 2023.,
Description:	xiv, 269 p. :ill., digital ; : 24 cm.;
Contained By:	Springer Nature eBook
Subject:	Cancer - Genetic aspects. -
Online resource:	https://doi.org/10.1007/978-3-031-32573-1
ISBN:	9783031325731

Evolutionary dynamics of malignancy = the genetic and environmental causes of cancer /
Jackson, Robert C.

Evolutionary dynamics of malignancythe genetic and environmental causes of cancer /[electronic resource] :by Robert C. Jackson. - Cham :Springer International Publishing :2023. - xiv, 269 p. :ill., digital ;24 cm.

Chapter 1: Cancer as a Disease of Cell Proliferation -- Chapter 2: Genetic and Chromosomal Instability -- Chapter 3: Cancer as a Disease of Defective Cell Cycle Checkpoint Function -- Chapter 4: The DNA Damage Checkpoint -- Chapter 5: Dynamics of the Spindle Assembly Checkpoint -- Chapter 6: Cancer as a Disease of Complexity: The Dynamics of Drug Resistance -- Chapter 7: Chronic Myeloid Leukaemia: a One-Hit Malignancy -- Chapter 8: Chronic Myelomonocytic Leukaemia: a Three-Hit Malignancy -- Chapter 9: The Cancer Stem Cell and Tumour Progression -- Chapter 10: Evading the antitumour immune response -- Chapter 11: Implications of Evolutionary Dynamics for Cancer Treatment and Prevention -- Chapter 12: In science, all conclusions are provisional.

Advances in cancer genomics are transforming our understanding of cancer, and have profound implications for its prevention, diagnosis, and treatment. Evolutionary dynamics suggests that as few as two mutations can cause transformation of normal cells into cancer stem cells. A process of Darwinian selection, involving a further three or more mutations, taking place over a period of years, can then result in progression to a life-threatening tumour. In many cases the immune response can recognise and eliminate the mutant cells, but most advanced tumours have mutations that activate immune checkpoints and enable the tumour to hide from the immune system. For the most hard-to-treat tumours, future progress will require molecular diagnostics to detect cancer-causing mutations in healthy subjects, and new drugs or vaccines that prevent the progression process. Chapters of this book deal with the signalling pathways that control cell division, and changes in these pathways in cancer cells. Three cell cycle checkpoints that are often mutated in cancer are analysed in detail. A discussion of chronic myeloid leukaemia illustrates the role of reactive oxygen species in driving progression from a chronic to an acute condition. A single drug that suppresses reactive oxygen can prevent disease progression and turn an otherwise deadly disease into a condition that can be managed to enable many years of normal life. Another chapter discusses chronic myelomonocytic leukaemia, a disease that involves both genetic and epigenetic change. Tumour progression is discussed as a multi-stage process in which cancer stem cells evolve into genetically unstable, invasive, metastatic, drug-resistant growths. Each of these stages can act as targets for drugs or immunomodulators, but the future of cancer treatment lies in understanding tumour dynamics, and arresting malignancy at the earliest possible stage. Evolutionary dynamics is a primarily mathematical technique, but the target readership will be tumour biologists, clinicians, and drug developers. Computational detail is provided in an online supplement, but the main text emphasises the implications of the dynamics for an understanding of tumour biology and does not require mathematical expertise.

ISBN: 9783031325731

Standard No.: 10.1007/978-3-031-32573-1doiSubjects--Topical Terms:

782504
Cancer
--Genetic aspects.

LC Class. No.: RC268.4

Dewey Class. No.: 616.994042

Evolutionary dynamics of malignancy = the genetic and environmental causes of cancer /
LDR:04027nam a2200325 a 4500 001 1105581
003 DE-He213
005 20230624134237.0
006 m d
007 cr nn 008maaau
008 231013s2023 sz s 0 eng d
020 $a 9783031325731 $q (electronic bk.)
020 $a 9783031325724 $q (paper)
024 7 $a 10.1007/978-3-031-32573-1 $2 doi
035 $a 978-3-031-32573-1
040 $a GP $c GP
041 0 $a eng
050 4 $a RC268.4
072 7 $a MJCL $2 bicssc
072 7 $a MED062000 $2 bisacsh
072 7 $a MJCL $2 thema
082 0 4 $a 616.994042 $2 23
090 $a RC268.4 $b .J13 2023
100 1 $a Jackson, Robert C. $3 1414680
245 1 0 $a Evolutionary dynamics of malignancy $h [electronic resource] : $b the genetic and environmental causes of cancer / $c by Robert C. Jackson.
260 $a Cham : $c 2023. $b Springer International Publishing : $b Imprint: Springer,
300 $a xiv, 269 p. : $b ill., digital ; $c 24 cm.
505 0 $a Chapter 1: Cancer as a Disease of Cell Proliferation -- Chapter 2: Genetic and Chromosomal Instability -- Chapter 3: Cancer as a Disease of Defective Cell Cycle Checkpoint Function -- Chapter 4: The DNA Damage Checkpoint -- Chapter 5: Dynamics of the Spindle Assembly Checkpoint -- Chapter 6: Cancer as a Disease of Complexity: The Dynamics of Drug Resistance -- Chapter 7: Chronic Myeloid Leukaemia: a One-Hit Malignancy -- Chapter 8: Chronic Myelomonocytic Leukaemia: a Three-Hit Malignancy -- Chapter 9: The Cancer Stem Cell and Tumour Progression -- Chapter 10: Evading the antitumour immune response -- Chapter 11: Implications of Evolutionary Dynamics for Cancer Treatment and Prevention -- Chapter 12: In science, all conclusions are provisional.
520 $a Advances in cancer genomics are transforming our understanding of cancer, and have profound implications for its prevention, diagnosis, and treatment. Evolutionary dynamics suggests that as few as two mutations can cause transformation of normal cells into cancer stem cells. A process of Darwinian selection, involving a further three or more mutations, taking place over a period of years, can then result in progression to a life-threatening tumour. In many cases the immune response can recognise and eliminate the mutant cells, but most advanced tumours have mutations that activate immune checkpoints and enable the tumour to hide from the immune system. For the most hard-to-treat tumours, future progress will require molecular diagnostics to detect cancer-causing mutations in healthy subjects, and new drugs or vaccines that prevent the progression process. Chapters of this book deal with the signalling pathways that control cell division, and changes in these pathways in cancer cells. Three cell cycle checkpoints that are often mutated in cancer are analysed in detail. A discussion of chronic myeloid leukaemia illustrates the role of reactive oxygen species in driving progression from a chronic to an acute condition. A single drug that suppresses reactive oxygen can prevent disease progression and turn an otherwise deadly disease into a condition that can be managed to enable many years of normal life. Another chapter discusses chronic myelomonocytic leukaemia, a disease that involves both genetic and epigenetic change. Tumour progression is discussed as a multi-stage process in which cancer stem cells evolve into genetically unstable, invasive, metastatic, drug-resistant growths. Each of these stages can act as targets for drugs or immunomodulators, but the future of cancer treatment lies in understanding tumour dynamics, and arresting malignancy at the earliest possible stage. Evolutionary dynamics is a primarily mathematical technique, but the target readership will be tumour biologists, clinicians, and drug developers. Computational detail is provided in an online supplement, but the main text emphasises the implications of the dynamics for an understanding of tumour biology and does not require mathematical expertise.
650 0 $a Cancer $x Genetic aspects. $3 782504
650 0 $a Cancer $x Environmental aspects. $3 1414681
650 1 4 $a Cancer Biology. $3 1388882
650 2 4 $a Cancer Models. $3 1396927
650 2 4 $a Cancer Therapy. $3 1389305
650 2 4 $a Cancer Genetics and Genomics. $3 1391074
650 2 4 $a Cancer Microenvironment. $3 1389809
710 2 $a SpringerLink (Online service) $3 593884
773 0 $t Springer Nature eBook
856 4 0 $u https://doi.org/10.1007/978-3-031-32573-1
950 $a Biomedical and Life Sciences (SpringerNature-11642)