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- NCIT_C91479 NCIT_NHC0 "C91479" @default.
- NCIT_C91479 NCIT_P106 "Functional Concept" @default.
- NCIT_C91479 NCIT_P108 "Glioblastoma Multiforme Pathway" @default.
- NCIT_C91479 NCIT_P207 "C2984291" @default.
- NCIT_C91479 NCIT_P215 "hsa05214" @default.
- NCIT_C91479 NCIT_P325 "Glioblastoma multiforme (GBM) formation is either de novo (primary GBMs) or due to the progression of a lower grade glioma to a higher grade one through the acquisition of additional mutations (secondary GBMs). In primary GBM, disruption of the p53 pathway often occurs through loss of ARF, or less frequently through amplification of MDM2. Disruption of the RB pathway occurs through loss of INK4A. Amplification and/or mutation of the epidermal growth factor receptor (EGFR) is the most frequently detected genetic defect that is associated with primary GBM. In secondary GBM, loss of p53 and activation of the growth-factor-receptor-tyrosine-kinase signaling pathway (such as through overexpression of PDGF/PDGFR) initiates tumour formation, whereas disruption of the retinoblastoma (RB) pathway contributes to the progression of tumour development. Loss of PTEN has been implicated in both pathways, although it is much more common in the pathogenesis of primary GBM." @default.
- NCIT_C91479 normalizedInformationContent "70.007054275464455" @default.
- NCIT_C91479 referenceCount "93" @default.
- NCIT_C91479 hasExactSynonym "GBM Pathway" @default.
- NCIT_C91479 hasExactSynonym "Glioblastoma Multiforme Pathway" @default.
- NCIT_C91479 hasExactSynonym "Glioma Pathway" @default.
- NCIT_C91479 hasExactSynonym "Glioma" @default.
- NCIT_C91479 type Class @default.
- NCIT_C91479 isDefinedBy ncit.owl @default.
- NCIT_C91479 label "Glioblastoma Multiforme Pathway" @default.
- NCIT_C91479 subClassOf NCIT_C20633 @default.
- NCIT_C91479 subClassOf NCIT_C39701 @default.
- NCIT_C91479 subClassOf NCIT_C91436 @default.
- NCIT_C91479 subClassOf NCIT_C91479 @default.