| Entry |
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| Name |
Pancreatic cancer |
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| Supergrp |
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| Description |
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.
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| Category |
Cancer
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| Brite |
Human diseases [BR:br08402]
Cancers
Cancers of the digestive system
H00019 Pancreatic cancer
Human diseases in ICD-11 classification [BR:br08403]
02 Neoplasms
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 [br08442.html]
H00019
Cancer-associated carbohydrates [br08441.html]
H00019
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| Pathway |
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| Network |
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| Element |
| N00012 | Mutation-activated KRAS/NRAS to ERK signaling pathway |
| N00032 | Mutation-activated KRAS/NRAS to PI3K signaling pathway |
| N00034 | ERBB2-overexpression to PI3K signaling pathway |
| N00070 | Mutation-inactivated p16(INK4a) to p16-cell cycle G1/S |
| N00071 | Deleted p16(INK4a) to p16-cell cycle G1/S |
| N00095 | ERBB2-overexpression to EGF-Jak-STAT signaling pathway |
| N00104 | Mutation-activated KRAS to RalGDS signaling pathway |
| N00115 | Mutation-inactivated TP53 to transcription |
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| Gene |
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| Carcinogen |
Tobacco smoking and tobacco smoke
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| Drug |
Gemcitabine hydrochloride [DR: D01155]
Floxuridine [DR: D04197]
Paclitaxel [DR: D00491]
Irinotecan hydrochloride [DR: D01061]
Mitomycin [DR: D00208]
Erlotinib hydrochloride [DR: D04023]
Olaparib [DR: D09730] (BRCA-mutated)
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| Comment |
ICD-O: 8500/3, Tumor type: Ductal adenocarcinoma
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| Other DBs |
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| Reference |
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| Authors |
Bardeesy N, DePinho RA. |
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| Title |
Pancreatic cancer biology and genetics. |
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| Journal |
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| Reference |
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| Authors |
Hezel AF, Kimmelman AC, Stanger BZ, Bardeesy N, Depinho RA. |
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| Title |
Genetics and biology of pancreatic ductal adenocarcinoma. |
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| Journal |
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| Reference |
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| Authors |
Bardeesy N, Sharpless NE, DePinho RA, Merlino G. |
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| Title |
The genetics of pancreatic adenocarcinoma: a roadmap for a mouse model. |
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| Journal |
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| Reference |
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| Authors |
Hruban RH, Goggins M, Parsons J, Kern SE. |
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| Title |
Progression model for pancreatic cancer. |
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| Journal |
Clin Cancer Res 6:2969-72 (2000) |
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| Reference |
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| Authors |
Wogan GN, Hecht SS, Felton JS, Conney AH, Loeb LA. |
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| Title |
Environmental and chemical carcinogenesis. |
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| Journal |
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| Reference |
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| Authors |
Sasco AJ, Secretan MB, Straif K. |
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| Title |
Tobacco smoking and cancer: a brief review of recent epidemiological evidence. |
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| Journal |
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| LinkDB |
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