KEGG   DISEASE: Pancreatic cancerHelp
H00019                      Disease                                

Pancreatic cancer
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:br08402]
  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
     Malignant neoplasms of intestine
      Malignant neoplasms of large intestine
       2C10  Malignant neoplasm of pancreas
        H00019  Pancreatic cancer
Tumor markers [br08442.html]
Cancer-accociated carbohydrates [br08441.html]
BRITE hierarchy
hsa05212  Pancreatic cancer
nt06262  Pancreatic cancer
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
K-ras (mutation) [HSA:3845] [KO:K07827]
ERBB2 (overexpression) [HSA:2064] [KO:K05083]
p16/INK4A (mutation, deletion, promoter methylation) [HSA:1029] [KO:K06621]
p53 (mutation) [HSA:7157] [KO:K04451]
SMAD4 (mutation) [HSA:4089] [KO:K04501]
BRCA2 (germline mutation) [HSA:675] [KO:K08775]
STK11 (germline mutation) [HSA:6794] [KO:K07298]
Tobacco smoking and tobacco smoke
Gemcitabine hydrochloride [DR:D01155]
Floxuridine [DR:D04197]
Paclitaxel [DR:D00491]
Mitomycin [DR:D00208]
Erlotinib hydrochloride [DR:D04023]
Irinotecan hydrochloride [DR:D01061]
ICD-O: 8500/3, Tumor type: Ductal adenocarcinoma
Other DBs
ICD-11: 2C10.0
ICD-10: C25
MeSH: D010190
PMID:12459728 (gene, tumor type)
Bardeesy N, DePinho RA.
Pancreatic cancer biology and genetics.
Nat Rev Cancer 2:897-909 (2002)
PMID:16702400 (tumor type)
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)
PMID:15489140 (carcinogen)
Wogan GN, Hecht SS, Felton JS, Conney AH, Loeb LA.
Environmental and chemical carcinogenesis.
Semin Cancer Biol 14:473-86 (2004)
PMID:15552776 (carcinogen)
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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