Portal:CPTAC/Hallmark/Resisting

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Current revision (00:05, 4 December 2018) (view source)
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*[[Pathway:WP673]]
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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])
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*[[Pathway:WP585]]
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*[[Pathway:WP254]] Apoptosis
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*[[Pathway:WP3]]
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*[[Pathway:WP3982]] miRNA regulation of p53 pathway in prostate cancer
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*[[Pathway:WP4018]]
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*[[Pathway:WP1742]] TP53 Network
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*[[Pathway:WP581]]
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*[[Pathway:WP3844]] PI3K-AKT-mTOR signaling pathway and therapeutic opportunities
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*[[Pathway:WP2828]]
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*[[Pathway:WP1471]] Target Of Rapamycin (TOR) Signaling
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*[[Pathway:WP2868]]
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*[[Pathway:WP3972]]
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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)

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