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"Oncogene signaling pathways" is not the name of a single molecule or receptor but rather refers to multiple interconnected molecular pathways that involve proteins and genes frequently mutated or dysregulated in cancer, mediating cell proliferation, survival, and other core processes[1][5]. This is a functional/process-oriented term, not a canonical target. Oncogene signaling pathways are collections of evolutionarily conserved cellular signaling cascades (such as PI3K/AKT/mTOR, Ras/MAPK, WNT/β-catenin, Notch, TGFβ, RTK-RAS, p53, MYC, and Hippo pathways) that, when dysregulated by genetic mutations or epigenetic events, drive hallmark cancer phenotypes like sustained proliferation, evasion of apoptosis, and metastasis[1][2][5]. These pathways involve multiple types of proteins (e.g., receptor tyrosine kinases, serine/threonine kinases, transcription factors) and interact through complex networks, often with co-occurrence or mutual exclusivity of alterations in individual tumors[1]. While many drugs and biomarkers are linked to discrete components within these pathways (e.g., BRAF, EGFR, ALK, PI3K), there is no single molecule called "Oncogene signaling pathway." The concept is central to contemporary oncology for classifying tumors, predicting prognosis, developing targeted therapies, and selecting patient-appropriate interventions, but is not a therapeutic target itself[1][2][5].
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