AKT1, AKT2, AKT3, ARHGEF7, BCL2, BCL2L1, BIRC5, BRAF, BRCA2, CCNA2, CCNB1, CCND1, CCND2, CCNE1, CCNE2, CDC42, CDK2, CDK4, CDKN1A, CDKN1B, CDKN2A, CDKN2B, CDKN2C, CDKN2D, CYP2E1, E2F1, E2F3, E2F4, EGF, EGFR, ELK1, ERBB2, FIGF, GRB2, HBEGF, HSP90AA1, IGF1, IL6, JAK1, JAK2, JAK3, KDR, KIT, KRAS, MAP2K1, MAP2K2, MAPK1, MAP...K3, MDM2, MMP1, MMP2, MMP3, MMP7, MMP9, NFKB1, NFKB2, NOTCH1, PIK3CA, PIK3CB, PIK3CD, PIK3R1, PIK3R2, PTGS2, RAC1, RAC2, RAF1, RB1, REL, RELA, RELB, RHOA, RHOB, SMAD2, SMAD3, SMAD4, SOS1, SRC, STAT1, STAT2, STAT3, STAT5B, STAT6, TGFA, TGFB1, TGFB2, TGFB3, TGFBR1, TGFBR2, TP53, VEGFA, VEGFB, VEGFC
View More... View Less...

Pancreatic carcinoma is one of the most enigmatic and aggressive malignant diseases. Neoplasms of the pancreas encompass a wide spectrum of benign and malignant tumors. Pancreatic adenocarcinoma, the malignant neoplasm of the exocrine duct cells, accounts ... for more than ninety percent of all pancreatic tumors. Pancreatic ductal adenocarcinoma evolves from a progressive cascade of cellular, morphological and architectural changes from normal ductal epithelium through pre-neoplastic lesions termed PanIN (Pancreatic Intraepithelial Neoplasia). These PanIN lesions are in turn associated with somatic alterations in canonical oncogenes and tumor suppressor genes. Pancreatic cancer like many other tumors over-expresses the RTKs (Receptor Tyrosine Kinases), EGFR (Epidermal Growth Factor Receptor) and/or its family members (like Her2), and TGF-BetaRs (Transforming Growth Factor-Beta Receptors). The expression of RTKs and their ligands, basically growth factors, is an early event in the development of pancreatic cancer (PanIN-1A and PanIN-1B stages). After ligand binding, these receptors both homo- and heterodimerize and become active. Activation involves trans-phosphorylation of Tyrosine residues by their intrinsic Tyrosine kinase activity. Phosphotyrosine residues generate docking sites for other signaling molecules harboring either Src Homology-2 or Phosphotyrosine-interacting domains. The activation of RTKs triggers a signaling cascade, which involves SOS (Son of Sevenless), Src (v-Src Avian Sacroma (Schmidt-Ruppin A-2) Viral Oncogene), GRB2 (Growth Factor Receptor-Bound Protein-2), and MAPKs (Mitogen-Activated Protein Kinases) activation, ultimately resulting in a cellular proliferative response. Activation of these pathways regulates proliferation thereby contributing to cellular transformation.
View More... View Less...