Seeing the Forest through the Phylogenetic Tree
Tumors arise as a result of cumulative genetic alterations (gene mutations, copy-number changes, gene fusions, or RNA overexpression or underexpression) that affect the properties of single cells and endow them with a growth advantage. Early on, this stepwise path was depicted as a linear model of sequential acquisition of mutations leading to tumor progression.1 It has now become clear that evolution to increasingly malignant phenotypes is a complex, multilayered process, in which various competing subclones that arise from the stochastic accumulation of genomic alterations are selected for fitness by environmental pressures, such as those imposed by the therapeutic approaches used to treat the patient.2 Although this model of tumor progression is indirectly supported by tumor surveys conducted at a single time point (such as the Cancer Genome Atlas), no single research protocol to date has directly tackled the issue of tumor heterogeneity, evolution, and treatment resistance..
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Artikel |
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Erscheinungsjahr: |
2017 |
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Erschienen: |
2017 |
Enthalten in: |
Zur Gesamtaufnahme - volume:376 |
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Enthalten in: |
The New England journal of medicine - 376(2017), 22, Seite 2190 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Ana I Robles [VerfasserIn] |
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520 | |a Tumors arise as a result of cumulative genetic alterations (gene mutations, copy-number changes, gene fusions, or RNA overexpression or underexpression) that affect the properties of single cells and endow them with a growth advantage. Early on, this stepwise path was depicted as a linear model of sequential acquisition of mutations leading to tumor progression.1 It has now become clear that evolution to increasingly malignant phenotypes is a complex, multilayered process, in which various competing subclones that arise from the stochastic accumulation of genomic alterations are selected for fitness by environmental pressures, such as those imposed by the therapeutic approaches used to treat the patient.2 Although this model of tumor progression is indirectly supported by tumor surveys conducted at a single time point (such as the Cancer Genome Atlas), no single research protocol to date has directly tackled the issue of tumor heterogeneity, evolution, and treatment resistance. | ||
650 | 4 | |a Phylogeny | |
650 | 4 | |a Genes | |
650 | 4 | |a Medical research | |
650 | 4 | |a Oncology | |
650 | 4 | |a Tumors | |
650 | 4 | |a Mutation | |
650 | 4 | |a Phylogenetics | |
650 | 4 | |a Lung cancer | |
700 | 0 | |a Jean C Zenklusen |4 oth | |
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