Portal:CPTAC/Hallmark/Instability
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Current revision (21:50, 26 May 2020) (view source) (Adding new pathways) |
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| - | *[[Pathway:WP707]] | + | 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:WP3878]] | + | *[[Pathway:WP707]] DNA Damage Response |
| - | *[[Pathway: | + | *[[Pathway:WP3878]] ATM Signaling Network in Development and Disease |
| - | *[[Pathway:WP3875]] | + | *[[Pathway:WP710]] DNA Damage Response (only ATM dependent) |
| - | *[[Pathway:WP438]] | + | *[[Pathway:WP3875]] ATR Signaling |
| - | *[[Pathway:WP531]] | + | *[[Pathway:WP438]] Non-homologous end joining |
| - | *[[Pathway:WP704]] | + | *[[Pathway:WP531]] Mismatch repair |
| - | *[[Pathway:WP4016]] | + | *[[Pathway:WP704]] Methylation pathways |
| - | *[[Pathway:WP3959]] | + | *[[Pathway:WP4016]] DNA IR-damage and cellular response via ATR |
| - | *[[Pathway:WP2516]] | + | *[[Pathway:WP3959]] DNA IR-Double Strand Breaks (DSBs) and cellular response via ATM |
| + | *[[Pathway:WP2516]] ATM Signaling Pathway | ||
| + | *[[Pathway:WP241]] One Carbon Metabolism | ||
| + | *[[Pathway:WP4216]] Chromosomal and microsatellite instability in colorectal cancer | ||
| + | *[[Pathway:WP4240]] Regulation of sister chromatid separation at the metaphase-anaphase transition | ||
| + | *[[Pathway:WP4931]] Direct reversal repair | ||
| + | *[[Pathway:WP4752]] Base Excision Repair | ||
| + | *[[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)
- Pathway:WP707 DNA Damage Response
- Pathway:WP3878 ATM Signaling Network in Development and Disease
- Pathway:WP710 DNA Damage Response (only ATM dependent)
- Pathway:WP3875 ATR Signaling
- Pathway:WP438 Non-homologous end joining
- Pathway:WP531 Mismatch repair
- Pathway:WP704 Methylation pathways
- Pathway:WP4016 DNA IR-damage and cellular response via ATR
- Pathway:WP3959 DNA IR-Double Strand Breaks (DSBs) and cellular response via ATM
- Pathway:WP2516 ATM Signaling Pathway
- Pathway:WP241 One Carbon Metabolism
- Pathway:WP4216 Chromosomal and microsatellite instability in colorectal cancer
- Pathway:WP4240 Regulation of sister chromatid separation at the metaphase-anaphase transition
- Pathway:WP4931 Direct reversal repair
- Pathway:WP4752 Base Excision Repair
- Pathway:WP4753 Nucleotide Excision Repair
