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All rights reserved. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAhHwJ4IkbdGXbJX7qhiesvjKMxPMYhgN38S-730TmTaI#_5 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RAhHwJ4IkbdGXbJX7qhiesvjKMxPMYhgN38S-730TmTaI#_4 http://www.w3.org/ns/prov#value Several anticancer therapies target, albeit indirectly, the PI3K/ Akt1 axis and cause inhibition of Akt1 phosphorylation and induction of apoptosis. Examples include herceptin, which inhibits ErbB2 in breast cancer cells; cyclooxygenase-2 (COX-2) inhibitors, which inhibit COX-2 and PDK1 in colon and prostate cancer; gefitnib (Iressa), which targets mutant epidermal growth factor receptor in lung cancer cells; and imatinib mesylate (Gleevec, STI- 571), which targets bcr-abl in leukemia. Conversely, inhibition of anoikis, which contributes to metastasis by trkB or TWIST, involves Akt activation. 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