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- NCIT_C91446 NCIT_NHC0 "C91446" @default.
- NCIT_C91446 NCIT_P106 "Functional Concept" @default.
- NCIT_C91446 NCIT_P108 "Pancreatic Cancer Pathway" @default.
- NCIT_C91446 NCIT_P207 "C2984259" @default.
- NCIT_C91446 NCIT_P215 "hsa05212" @default.
- NCIT_C91446 NCIT_P325 "Normal duct epithelium progresses to infiltrating cancer through a series of histologically defined precursors (PanINs). The overexpression of HER-2/neu and activating point mutations in the K-ras gene occur early, inactivation of the p16 gene at an intermediate stage, and the inactivation of p53, SMAD4, and BRCA2 occur relatively late. Activated K-ras engages multiple effector pathways. Although EGF receptors are conventionally regarded as upstream activators of RAS proteins, they can also act as RAS signal transducers via RAS-induced autocrine activation of the EGFR family ligands. Pancreatic ductal adenocarcinoma (PDA) show elevated expression of EGF receptors (e.g. HER2/neu) and their ligands (e.g. TGF-alpha) consistent with the presence of this autocrine loop. Moreover, PDA shows extensive genomic instability and aneuploidy. Telomere attrition and mutations in p53 and BRCA2 are likely to contribute to these phenotypes. Inactivation of the SMAD4 tumour suppressor gene leads to loss of the inhibitory influence of the transforming growth factor-beta signaling pathway." @default.
- NCIT_C91446 normalizedInformationContent "68.836275093488439" @default.
- NCIT_C91446 referenceCount "111" @default.
- NCIT_C91446 hasExactSynonym "Pancreatic Cancer Pathway" @default.
- NCIT_C91446 hasExactSynonym "Pancreatic cancer" @default.
- NCIT_C91446 type Class @default.
- NCIT_C91446 isDefinedBy ncit.owl @default.
- NCIT_C91446 label "Pancreatic Cancer Pathway" @default.
- NCIT_C91446 subClassOf NCIT_C20633 @default.
- NCIT_C91446 subClassOf NCIT_C39701 @default.
- NCIT_C91446 subClassOf NCIT_C91436 @default.
- NCIT_C91446 subClassOf NCIT_C91446 @default.