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Pancreatic tumours: molecular pathways implicated in ductal cancer are involved in ampullary but not in exocrine nonductal or endocrine tumorigenesis.

Abstract

Alterations of K- ras, p53, p16 and DPC4/Smad4 characterize pancreatic ductal cancer (PDC). Reports of inactivation of these latter two genes in pancreatic endocrine tumours (PET) suggest that common molecular pathways are involved in the tumorigenesis of pancreatic exocrine and endocrine epithelia. We characterized 112 primary pancreatic tumours for alterations in p16 and DPC4 and immunohistochemical expression of DPC4. The cases included 34 PDC, 10 intraductal papillary-mucinous tumours (IPMT), 6 acinar carcinomas (PAC), 5 solid-pseudopapillary tumours (SPT), 16 ampulla of Vater cancers (AVC) and 41 PET. All tumours were also presently or previously analysed for K- ras and p53 mutations and allelic loss at 9p, 17p and 18q. Alterations in K- ras, p53, p16 and DPC4 were found in 82%, 53%, 38% and 9% of PDC, respectively and in 47%, 60%, 25% and 6% of AVC. Alterations in these genes were virtually absent in PET, PAC or SPT, while in IPMT only K- ras mutations were present (30%). Positive immunostaining confirmed the absence of DPC4 alterations in all IPMT, SPT, PAC and PET, while 47% of PDC and 38% of AVC were immunonegative. These data suggest that pancreatic exocrine and endocrine tumourigenesis involves different genetic targets and that among exocrine pancreatic neoplasms, only ductal and ampullary cancers share common molecular events.

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  • Authors+Show Affiliations

    ,

    Department of Pathology, Università di Verona, Italy.

    , , , , , , ,

    Source

    British journal of cancer 84:2 2001 Jan pg 253-62

    MeSH

    Adenocarcinoma, Mucinous
    Ampulla of Vater
    Base Sequence
    Carcinoma, Acinar Cell
    Carcinoma, Ductal, Breast
    Carcinoma, Pancreatic Ductal
    Carcinoma, Papillary
    Common Bile Duct Neoplasms
    Cyclin-Dependent Kinase Inhibitor p16
    DNA
    DNA Mutational Analysis
    DNA-Binding Proteins
    Endocrine Gland Neoplasms
    Endocrine Glands
    Exocrine Glands
    Humans
    Immunohistochemistry
    Loss of Heterozygosity
    Mutation
    Pancreatic Neoplasms
    Polymorphism, Single-Stranded Conformational
    Smad4 Protein
    Trans-Activators
    Tumor Suppressor Protein p53
    ras Proteins

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    11161385

    Citation

    Moore, P S., et al. "Pancreatic Tumours: Molecular Pathways Implicated in Ductal Cancer Are Involved in Ampullary but Not in Exocrine Nonductal or Endocrine Tumorigenesis." British Journal of Cancer, vol. 84, no. 2, 2001, pp. 253-62.
    Moore PS, Orlandini S, Zamboni G, et al. Pancreatic tumours: molecular pathways implicated in ductal cancer are involved in ampullary but not in exocrine nonductal or endocrine tumorigenesis. Br J Cancer. 2001;84(2):253-62.
    Moore, P. S., Orlandini, S., Zamboni, G., Capelli, P., Rigaud, G., Falconi, M., ... Scarpa, A. (2001). Pancreatic tumours: molecular pathways implicated in ductal cancer are involved in ampullary but not in exocrine nonductal or endocrine tumorigenesis. British Journal of Cancer, 84(2), pp. 253-62.
    Moore PS, et al. Pancreatic Tumours: Molecular Pathways Implicated in Ductal Cancer Are Involved in Ampullary but Not in Exocrine Nonductal or Endocrine Tumorigenesis. Br J Cancer. 2001;84(2):253-62. PubMed PMID: 11161385.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Pancreatic tumours: molecular pathways implicated in ductal cancer are involved in ampullary but not in exocrine nonductal or endocrine tumorigenesis. AU - Moore,P S, AU - Orlandini,S, AU - Zamboni,G, AU - Capelli,P, AU - Rigaud,G, AU - Falconi,M, AU - Bassi,C, AU - Lemoine,N R, AU - Scarpa,A, PY - 2001/2/13/pubmed PY - 2001/3/10/medline PY - 2001/2/13/entrez SP - 253 EP - 62 JF - British journal of cancer JO - Br. J. Cancer VL - 84 IS - 2 N2 - Alterations of K- ras, p53, p16 and DPC4/Smad4 characterize pancreatic ductal cancer (PDC). Reports of inactivation of these latter two genes in pancreatic endocrine tumours (PET) suggest that common molecular pathways are involved in the tumorigenesis of pancreatic exocrine and endocrine epithelia. We characterized 112 primary pancreatic tumours for alterations in p16 and DPC4 and immunohistochemical expression of DPC4. The cases included 34 PDC, 10 intraductal papillary-mucinous tumours (IPMT), 6 acinar carcinomas (PAC), 5 solid-pseudopapillary tumours (SPT), 16 ampulla of Vater cancers (AVC) and 41 PET. All tumours were also presently or previously analysed for K- ras and p53 mutations and allelic loss at 9p, 17p and 18q. Alterations in K- ras, p53, p16 and DPC4 were found in 82%, 53%, 38% and 9% of PDC, respectively and in 47%, 60%, 25% and 6% of AVC. Alterations in these genes were virtually absent in PET, PAC or SPT, while in IPMT only K- ras mutations were present (30%). Positive immunostaining confirmed the absence of DPC4 alterations in all IPMT, SPT, PAC and PET, while 47% of PDC and 38% of AVC were immunonegative. These data suggest that pancreatic exocrine and endocrine tumourigenesis involves different genetic targets and that among exocrine pancreatic neoplasms, only ductal and ampullary cancers share common molecular events. SN - 0007-0920 UR - https://www.unboundmedicine.com/medline/citation/11161385/Pancreatic_tumours:_molecular_pathways_implicated_in_ductal_cancer_are_involved_in_ampullary_but_not_in_exocrine_nonductal_or_endocrine_tumorigenesis_ L2 - http://dx.doi.org/10.1054/bjoc.2000.1567 DB - PRIME DP - Unbound Medicine ER -