Portal:CPTAC/Hallmark/Resisting
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| + | Tumor cells use a variety of strategies to limit or circumvent apoptosis. Most common is the loss of TP53 tumor suppressor function, which eliminates this critical damage sensor from the apoptosis-inducing circuitry. Alternatively, tumors may achieve similar ends by increasing expression of antiapoptotic regulators (Bcl-2, Bcl-xL) or of survival signals (Igf1/2), by downregulating proapoptotic factors (Bax, Bim, Puma), or by short-circuiting the extrinsic ligand-induced death pathway. (Adapted from [https://www.ncbi.nlm.nih.gov/pubmed/21376230 Hallmarks of cancer: the next generation, Hanahan and Weinberg, Cell 2011]) | ||
*[[Pathway:WP254]] Apoptosis | *[[Pathway:WP254]] Apoptosis | ||
*[[Pathway:WP3982]] miRNA regulation of p53 pathway in prostate cancer | *[[Pathway:WP3982]] miRNA regulation of p53 pathway in prostate cancer | ||
*[[Pathway:WP1742]] TP53 Network | *[[Pathway:WP1742]] TP53 Network | ||
*[[Pathway:WP3844]] PI3K-AKT-mTOR signaling pathway and therapeutic opportunities | *[[Pathway:WP3844]] PI3K-AKT-mTOR signaling pathway and therapeutic opportunities | ||
| - | *[[Pathway: | + | *[[Pathway:WP1471]] Target Of Rapamycin (TOR) Signaling |
Current revision
Tumor cells use a variety of strategies to limit or circumvent apoptosis. Most common is the loss of TP53 tumor suppressor function, which eliminates this critical damage sensor from the apoptosis-inducing circuitry. Alternatively, tumors may achieve similar ends by increasing expression of antiapoptotic regulators (Bcl-2, Bcl-xL) or of survival signals (Igf1/2), by downregulating proapoptotic factors (Bax, Bim, Puma), or by short-circuiting the extrinsic ligand-induced death pathway. (Adapted from Hallmarks of cancer: the next generation, Hanahan and Weinberg, Cell 2011)
- Pathway:WP254 Apoptosis
- Pathway:WP3982 miRNA regulation of p53 pathway in prostate cancer
- Pathway:WP1742 TP53 Network
- Pathway:WP3844 PI3K-AKT-mTOR signaling pathway and therapeutic opportunities
- Pathway:WP1471 Target Of Rapamycin (TOR) Signaling
