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008			230624s2023 sz | o |||| 0|eng d
020			_a9783031325731
024	7		_a10.1007/978-3-031-32573-1 _2doi
040			_aES-MaUEC _bspa _cES-MaUEC _dES-MaUEC
050		4	_aRC268.4 _b2023 EB
100	1		_aJackson, Robert C. _eautor _4aut _4http://id.loc.gov/vocabulary/relators/aut _9690277
245	1	0	_aEvolutionary Dynamics of Malignancy : _bThe Genetic and Environmental Causes of Cancer _cby Robert C Jackson
250			_a1st ed. 2023
264		1	_aCham _bSpringer International Publishing _c2023
300			_a1 recurso en línea
336			_atexto _btxt _2rdacontent
337			_aelectrónico _bc _2rdamedia
338			_arecurso electrónico _bcr _2rdacarrier
505	0		_aChapter 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			_aAdvances 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.
988			_aSpringer_BiomedLife_2023
650		7	_2embne _9273952 _aCáncer _xAspectos genéticos
856	4	0	_uhttps://go.openathens.net/redirector/universidadeuropea.es?url=https://doi.org/10.1007/978-3-031-32573-1 _zAcceso a este recurso digital (usuarios Universidad Europea de Madrid)
942			_2lcc _cLE
998			_b05/2024 _dz _eIG _zSI