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Tumor-suppressing pathways in cystic pancreatic tumors.

Abstract

INTRODUCTION AND AIMS

Serous and mucinous cystic pancreatic tumors have different clinical behavior. We evaluated whether they also have genotypic differences by analyses of the tumor suppressor genes, p16INK4a, p53, and DPC4.

METHODOLOGY

Seven serous cystadenomas (SCA) and seven malignant mucinous cystadenocarcinomas (MCC) were analyzed for alterations in the tumor suppressor genes p16INK4a, p53, and DPC4 by single-strand conformational variant analysis, direct sequencing, and immunohistochemical analysis. Methylation-specific polymerase chain reaction analysis was performed to identify p16INK4a promoter hypermethylation. Clinical data were compared with genetic data.

RESULTS

None of the seven patients with SCAs but five of the seven patients with MCCs died of the tumor after a median follow-up of 44.5 months (range, 4-169 months). All seven MCCs had alterations in at least one tumor suppressor gene compared with none of the seven SCAs. Of the seven MCCs, three had inactivating p16INK4a promoter hypermethylation, five had p53 alterations, and three had DPC4 mutations.

CONCLUSIONS

The tumor suppressor genes p16INK4a, p53, and appear to play an important role in the tumorigenesis of MCCs but not SCAs. These molecular data underscore the clinical and histologic differences of serous and mucinous cystic pancreatic tumors.

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  • Authors+Show Affiliations

    ,

    Department of General Surgery, Philipps University of Marburg, Germany.

    , , , , , , ,

    Source

    Pancreas 26:1 2003 Jan pg 42-8

    MeSH

    Cyclin-Dependent Kinase Inhibitor p16
    Cystadenocarcinoma, Mucinous
    Cystadenocarcinoma, Serous
    DNA Methylation
    DNA Mutational Analysis
    DNA, Neoplasm
    DNA-Binding Proteins
    Genes, Tumor Suppressor
    Genes, p16
    Genes, p53
    Humans
    Immunohistochemistry
    Pancreatic Neoplasms
    Polymorphism, Single-Stranded Conformational
    Smad4 Protein
    Trans-Activators
    Tumor Suppressor Protein p53

    Pub Type(s)

    Comparative Study
    Journal Article

    Language

    eng

    PubMed ID

    12499916

    Citation

    Gerdes, Berthold, et al. "Tumor-suppressing Pathways in Cystic Pancreatic Tumors." Pancreas, vol. 26, no. 1, 2003, pp. 42-8.
    Gerdes B, Wild A, Wittenberg J, et al. Tumor-suppressing pathways in cystic pancreatic tumors. Pancreas. 2003;26(1):42-8.
    Gerdes, B., Wild, A., Wittenberg, J., Barth, P., Ramaswamy, A., Kersting, M., ... Bartsch, D. K. (2003). Tumor-suppressing pathways in cystic pancreatic tumors. Pancreas, 26(1), pp. 42-8.
    Gerdes B, et al. Tumor-suppressing Pathways in Cystic Pancreatic Tumors. Pancreas. 2003;26(1):42-8. PubMed PMID: 12499916.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Tumor-suppressing pathways in cystic pancreatic tumors. AU - Gerdes,Berthold, AU - Wild,Anja, AU - Wittenberg,Judith, AU - Barth,Peter, AU - Ramaswamy,Annette, AU - Kersting,Michael, AU - Lüttges,Jutta, AU - Klöppel,Günter, AU - Bartsch,Detlef K, PY - 2002/12/25/pubmed PY - 2003/1/9/medline PY - 2002/12/25/entrez SP - 42 EP - 8 JF - Pancreas JO - Pancreas VL - 26 IS - 1 N2 - INTRODUCTION AND AIMS: Serous and mucinous cystic pancreatic tumors have different clinical behavior. We evaluated whether they also have genotypic differences by analyses of the tumor suppressor genes, p16INK4a, p53, and DPC4. METHODOLOGY: Seven serous cystadenomas (SCA) and seven malignant mucinous cystadenocarcinomas (MCC) were analyzed for alterations in the tumor suppressor genes p16INK4a, p53, and DPC4 by single-strand conformational variant analysis, direct sequencing, and immunohistochemical analysis. Methylation-specific polymerase chain reaction analysis was performed to identify p16INK4a promoter hypermethylation. Clinical data were compared with genetic data. RESULTS: None of the seven patients with SCAs but five of the seven patients with MCCs died of the tumor after a median follow-up of 44.5 months (range, 4-169 months). All seven MCCs had alterations in at least one tumor suppressor gene compared with none of the seven SCAs. Of the seven MCCs, three had inactivating p16INK4a promoter hypermethylation, five had p53 alterations, and three had DPC4 mutations. CONCLUSIONS: The tumor suppressor genes p16INK4a, p53, and appear to play an important role in the tumorigenesis of MCCs but not SCAs. These molecular data underscore the clinical and histologic differences of serous and mucinous cystic pancreatic tumors. SN - 1536-4828 UR - https://www.unboundmedicine.com/medline/citation/12499916/Tumor_suppressing_pathways_in_cystic_pancreatic_tumors_ L2 - http://Insights.ovid.com/pubmed?pmid=12499916 DB - PRIME DP - Unbound Medicine ER -