MARC details
000 -LEADER |
fixed length control field |
04635nam a22004815i 4500 |
001 - CONTROL NUMBER |
control field |
978-3-031-32573-1 |
003 - CONTROL NUMBER IDENTIFIER |
control field |
DE-He213 |
005 - DATE AND TIME OF LATEST TRANSACTION |
control field |
20240729140103.0 |
007 - PHYSICAL DESCRIPTION FIXED FIELD--GENERAL INFORMATION |
fixed length control field |
cr nn 008mamaa |
008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION |
fixed length control field |
230624s2023 sz | s |||| 0|eng d |
020 ## - INTERNATIONAL STANDARD BOOK NUMBER |
ISBN |
9783031325731 |
-- |
978-3-031-32573-1 |
072 #7 - SUBJECT CATEGORY CODE |
Subject category code |
MJCL |
Source |
bicssc |
072 #7 - SUBJECT CATEGORY CODE |
Subject category code |
MED062000 |
Source |
bisacsh |
072 #7 - SUBJECT CATEGORY CODE |
Subject category code |
MJCL |
Source |
thema |
100 1# - MAIN ENTRY--PERSONAL NAME |
Personal author |
Jackson, Robert C. |
Relator term |
author. |
Relator code |
aut |
-- |
http://id.loc.gov/vocabulary/relators/aut |
245 10 - TITLE STATEMENT |
Title |
Evolutionary Dynamics of Malignancy |
Subtitle |
: The Genetic and Environmental Causes of Cancer / |
250 ## - EDITION |
Edition statement |
1st ed. 2023. |
264 #1 - PRODUCTION, PUBLICATION, DISTRIBUTION, MANUFACTURE, AND COPYRIGHT NOTICE |
Place of production, publication, distribution, manufacture |
Cham : |
Name of producer, publisher, distributor, manufacturer |
Springer International Publishing : |
-- |
Imprint: Springer, |
Date of production, publication, distribution, manufacture, or copyright notice |
2023. |
300 ## - PHYSICAL DESCRIPTION |
Physical description |
XIV, 269 p. 96 illus., 58 illus. in color. |
Other physical details |
online resource. |
336 ## - CONTENT TYPE |
Content type term |
text |
Content type code |
txt |
Source |
rdacontent |
337 ## - MEDIA TYPE |
Media type term |
computer |
Media type code |
c |
Source |
rdamedia |
338 ## - CARRIER TYPE |
Carrier type term |
online resource |
Carrier type code |
cr |
Source |
rdacarrier |
505 0# - CONTENTS |
Contents |
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 ## - ABSTRACT |
Abstract |
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 - SUBJECT HEADINGS |
Subject term |
Cancer. |
650 #0 - SUBJECT HEADINGS |
Subject term |
Cancer |
General subdivision |
Animal models. |
650 #0 - SUBJECT HEADINGS |
Subject term |
Cancer |
General subdivision |
Treatment. |
650 #0 - SUBJECT HEADINGS |
Subject term |
Cancer |
General subdivision |
Genetic aspects. |
650 14 - SUBJECT HEADINGS |
Subject term |
Cancer Biology. |
650 24 - SUBJECT HEADINGS |
Subject term |
Cancer Models. |
650 24 - SUBJECT HEADINGS |
Subject term |
Cancer Therapy. |
650 24 - SUBJECT HEADINGS |
Subject term |
Cancer Genetics and Genomics. |
650 24 - SUBJECT HEADINGS |
Subject term |
Cancer Microenvironment. |
710 2# - ADDED CORPORATE NAME |
Added corporate author |
SpringerLink (Online service) |
856 ## - ONLINE RESOURCE |
Uniform Resource Identifier |
<a href="#gotoholdings">#gotoholdings</a> |
Link text |
Access resource |
245 ## - TITLE STATEMENT |
Medium |
[E-Book] |
347 ## - DIGITAL FILE CHARACTERISTICS |
File type |
text file |
Encoding format |
PDF |
Source |
rda |
912 ## - |
-- |
ZDB-2-SBL |
912 ## - |
-- |
ZDB-2-SXB |