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Titlebook: Evolutionary Dynamics of Malignancy; The Genetic and Envi Robert C. Jackson Book 2023 The Editor(s) (if applicable) and The Author(s), unde

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發(fā)表于 2025-3-21 16:24:47 | 只看該作者 |倒序?yàn)g覽 |閱讀模式
書目名稱Evolutionary Dynamics of Malignancy
副標(biāo)題The Genetic and Envi
編輯Robert C. Jackson
視頻videohttp://file.papertrans.cn/318/317934/317934.mp4
概述Discusses changes in pathways that drive malignant transformation.Chapters are enriched with computational models in an electronic supplement.Targeted to tumour biologists, clinicians and drug develop
圖書封面Titlebook: Evolutionary Dynamics of Malignancy; The Genetic and Envi Robert C. Jackson Book 2023 The Editor(s) (if applicable) and The Author(s), unde
描述.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
出版日期Book 2023
關(guān)鍵詞cancer evolution; evolutionary dynamics; mathematical modeling of cancer; computational models; cancer t
版次1
doihttps://doi.org/10.1007/978-3-031-32573-1
isbn_softcover978-3-031-32575-5
isbn_ebook978-3-031-32573-1
copyrightThe Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerl
The information of publication is updating

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發(fā)表于 2025-3-21 22:23:17 | 只看該作者
Genetic and Chromosomal Instability,etic damage. Tumours are genetically unstable, such that the number of mutations and chromosomal abnormalities increases with time. Genetic and/or chromosomal instability is now regarded as the defining characteristic of cancer..Cancer genome projects, based upon whole genome sequencing, have identi
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Cancer as a Disease of Defective Cell Cycle Checkpoint Function,factors. The normal cell division cycle contains checkpoints that prevent a cell from progressing to the next phase if abnormalities (e.g. DNA damage) are present; the cell will not progress until the problem is corrected. If the damage cannot be corrected in a few hours, the damaged cell will under
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The DNA Damage Checkpoint,DNA damage that can trigger the checkpoint include single-strand breaks, double-strand breaks, stalled replication forks, and premature chain termination. Many tumours have mutations or deletions of one or more components of the DDR. For this reason, tumours are often repair-deficient, so that DNA-d
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Dynamics of the Spindle Assembly Checkpoint,ergoing cytokinesis and completing cell division. In normal cells, prolonged cell cycle arrest by the SAC results in apoptosis. Most cancer cells have mutations or expression changes in components of the SAC that allow cells with abnormal chromosomes to escape the checkpoint, and because of over-rid
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Chronic Myelomonocytic Leukaemia: A Three-Hit Malignancy,ined. Those epigenetic changes may in turn be a result of genetic or chromosomal instability. Malignant progression caused by epigenetic silencing of function of tumour suppressor genes will often require inactivation of both alleles, though in some cases loss of a single allele may result in alleli
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Evading the Antitumour Immune Response,r immune response. As tumour progression proceeds, genetic instability results in the developing tumour becoming increasingly immunogenic. Immune surveillance may result in early-stage tumours being eliminated without developing into clinically evident disease. Less immunogenic tumours may be held i
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