DISEASE: Pancreatic cancer
Solid tumor [DS:
Infiltrating ductal adenocarcinoma is the most common malignancy of the pancreas. When most investigators use the term 'pancreatic cancer' they are referring to pancreatic ductal adenocarcinoma (PDA). 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. 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 signalling pathway.
Human diseases [BR:
Cancers of the digestive system
H00019 Pancreatic cancer
Human diseases in ICD-11 classification [BR:
Malignant neoplasms, except of lymphoid, haematopoietic, central nervous system or related tissues
Malignant neoplasms, stated or presumed to be primary, of specified sites, except of lymphoid, haematopoietic, central nervous system or related tissues
Malignant neoplasms of digestive organs
2C10 Malignant neoplasm of pancreas
H00019 Pancreatic cancer
Tumor markers [
Cancer-associated carbohydrates [
Pathways in cancer
Central carbon metabolism in cancer
Proteoglycans in cancer
Mutation-activated KRAS/NRAS to ERK signaling pathway
Mutation-activated KRAS/NRAS to PI3K signaling pathway
ERBB2-overexpression to PI3K signaling pathway
Mutation-inactivated p16(INK4a) to p16-cell cycle G1/S
Deleted p16(INK4a) to p16-cell cycle G1/S
ERBB2-overexpression to EGF-Jak-STAT signaling pathway
Mutation-activated KRAS to RalGDS signaling pathway
Mutation-inactivated TP53 to transcription
K-ras (mutation) [HSA:
ERBB2 (overexpression) [HSA:
p16/INK4A (mutation, deletion, promoter methylation) [HSA:
p53 (mutation) [HSA:
SMAD4 (mutation) [HSA:
BRCA2 (germline mutation) [HSA:
STK11 (germline mutation) [HSA:
Tobacco smoking and tobacco smoke
Gemcitabine hydrochloride [DR:
Irinotecan hydrochloride [DR:
Erlotinib hydrochloride [DR:
ICD-O: 8500/3, Tumor type: Ductal adenocarcinoma
(gene, tumor type)
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Pancreatic cancer biology and genetics.
Nat Rev Cancer 2:897-909 (2002)
Hezel AF, Kimmelman AC, Stanger BZ, Bardeesy N, Depinho RA.
Genetics and biology of pancreatic ductal adenocarcinoma.
Genes Dev 20:1218-49 (2006)
Bardeesy N, Sharpless NE, DePinho RA, Merlino G.
The genetics of pancreatic adenocarcinoma: a roadmap for a mouse model.
Semin Cancer Biol 11:201-18 (2001)
Hruban RH, Goggins M, Parsons J, Kern SE.
Progression model for pancreatic cancer.
Clin Cancer Res 6:2969-72 (2000)
Wogan GN, Hecht SS, Felton JS, Conney AH, Loeb LA.
Environmental and chemical carcinogenesis.
Semin Cancer Biol 14:473-86 (2004)
Sasco AJ, Secretan MB, Straif K.
Tobacco smoking and cancer: a brief review of recent epidemiological evidence.
Lung Cancer 45 Suppl 2:S3-9 (2004)
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