Portal:CPTAC/Hallmark/Instability

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(Added WP4240)
Current revision (21:50, 26 May 2020) (view source)
(Adding new pathways)
 
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The ability of genome maintenance systems to detect and resolve defects in the DNA ensures that rates of spontaneous mutation are usually very low during each cell generation. In the course of acquiring the mutations needed for tumorigenesis, cancer cells often increase the rates of mutation. This is achieved through increased sensitivity to mutagenic agents, through a breakdown in one or several components of the genomic maintenance machinery, or both. (Adapted from [https://www.ncbi.nlm.nih.gov/pubmed/21376230 Hallmarks of cancer: the next generation, Hanahan and Weinberg, Cell 2011])
*[[Pathway:WP707]] DNA Damage Response
*[[Pathway:WP707]] DNA Damage Response
*[[Pathway:WP3878]] ATM Signaling Network in Development and Disease
*[[Pathway:WP3878]] ATM Signaling Network in Development and Disease
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*[[Pathway:WP4216]] Chromosomal and microsatellite instability in colorectal cancer
*[[Pathway:WP4216]] Chromosomal and microsatellite instability in colorectal cancer
*[[Pathway:WP4240]] Regulation of sister chromatid separation at the metaphase-anaphase transition
*[[Pathway:WP4240]] Regulation of sister chromatid separation at the metaphase-anaphase transition
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*[[Pathway:WP4931]] Direct reversal repair
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*[[Pathway:WP4752]] Base Excision Repair
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*[[Pathway:WP4753]] Nucleotide Excision Repair

Current revision

The ability of genome maintenance systems to detect and resolve defects in the DNA ensures that rates of spontaneous mutation are usually very low during each cell generation. In the course of acquiring the mutations needed for tumorigenesis, cancer cells often increase the rates of mutation. This is achieved through increased sensitivity to mutagenic agents, through a breakdown in one or several components of the genomic maintenance machinery, or both. (Adapted from Hallmarks of cancer: the next generation, Hanahan and Weinberg, Cell 2011)

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