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Molecular pathobiology of pancreatic adenocarcinoma.

Abstract

Pancreatic adenocarcinoma is a major cause of cancer death in the United States. Most cases are sporadic and are discovered at late stage when they are not curable by surgery. Information about the molecular biology of pancreatic adenocarcinoma has increased significantly in the last five years with the identification of alterations in the K-ras proto-oncogene and the p16INK4a, p53, FHIT, and DPC4 tumor suppressor genes in a high percentage of tumors. Pancreatic adenocarcinoma is not homogeneous genetically, however, and other genes are clearly involved in some sporadic and heritable tumors. This review summarizes recent data relating to the molecular biology of pancreatic adenocarcinoma with emphasis on features which may be of clinical significance for diagnosis and/or therapy. Molecular genetic alterations that disturb cell cycle regulation in tumor cells can affect their response to chemotherapeutic agents and radiation and many of these genes are targeted in pancreatic adenocarcinoma. Knowledge of these genetic alterations in individual tumors may allow selection of optimal therapeutic strategies for individual patients. Furthermore, molecular detection of oncogene and tumor suppressor gene mutations may find application as screening tests for pancreatic adenocarcinoma at least in high risk populations. Biological therapy aimed at specific oncogenes and tumor suppressor gene replacement therapy protocols for pancreatic adenocarcinoma are beginning and may offer promise in the future.

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  • Authors+Show Affiliations

    ,

    Department of Pathology and Laboratory Medicine, Brown University School of Medicine, Providence, RI 02906, USA.

    Source

    MeSH

    Acid Anhydride Hydrolases
    Adenocarcinoma
    Ataxia Telangiectasia
    BRCA2 Protein
    Chromosome Aberrations
    Chromosome Disorders
    Colorectal Neoplasms, Hereditary Nonpolyposis
    Cyclin-Dependent Kinase Inhibitor p16
    DNA-Binding Proteins
    Genes, erbB-2
    Genes, p53
    Genes, ras
    Humans
    Mass Screening
    Mutation
    Neoplasm Proteins
    Pancreatic Neoplasms
    Pancreatitis
    Peutz-Jeghers Syndrome
    Proteins
    Smad4 Protein
    Trans-Activators
    Transcription Factors

    Pub Type(s)

    Journal Article
    Review

    Language

    eng

    PubMed ID

    9820739

    Citation

    Mangray, S, and T C. King. "Molecular Pathobiology of Pancreatic Adenocarcinoma." Frontiers in Bioscience : a Journal and Virtual Library, vol. 3, 1998, pp. D1148-60.
    Mangray S, King TC. Molecular pathobiology of pancreatic adenocarcinoma. Front Biosci. 1998;3:D1148-60.
    Mangray, S., & King, T. C. (1998). Molecular pathobiology of pancreatic adenocarcinoma. Frontiers in Bioscience : a Journal and Virtual Library, 3, pp. D1148-60.
    Mangray S, King TC. Molecular Pathobiology of Pancreatic Adenocarcinoma. Front Biosci. 1998 Nov 15;3:D1148-60. PubMed PMID: 9820739.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Molecular pathobiology of pancreatic adenocarcinoma. AU - Mangray,S, AU - King,T C, Y1 - 1998/11/15/ PY - 1998/11/20/pubmed PY - 1998/11/20/medline PY - 1998/11/20/entrez SP - D1148 EP - 60 JF - Frontiers in bioscience : a journal and virtual library JO - Front. Biosci. VL - 3 N2 - Pancreatic adenocarcinoma is a major cause of cancer death in the United States. Most cases are sporadic and are discovered at late stage when they are not curable by surgery. Information about the molecular biology of pancreatic adenocarcinoma has increased significantly in the last five years with the identification of alterations in the K-ras proto-oncogene and the p16INK4a, p53, FHIT, and DPC4 tumor suppressor genes in a high percentage of tumors. Pancreatic adenocarcinoma is not homogeneous genetically, however, and other genes are clearly involved in some sporadic and heritable tumors. This review summarizes recent data relating to the molecular biology of pancreatic adenocarcinoma with emphasis on features which may be of clinical significance for diagnosis and/or therapy. Molecular genetic alterations that disturb cell cycle regulation in tumor cells can affect their response to chemotherapeutic agents and radiation and many of these genes are targeted in pancreatic adenocarcinoma. Knowledge of these genetic alterations in individual tumors may allow selection of optimal therapeutic strategies for individual patients. Furthermore, molecular detection of oncogene and tumor suppressor gene mutations may find application as screening tests for pancreatic adenocarcinoma at least in high risk populations. Biological therapy aimed at specific oncogenes and tumor suppressor gene replacement therapy protocols for pancreatic adenocarcinoma are beginning and may offer promise in the future. SN - 1093-9946 UR - https://www.unboundmedicine.com/medline/citation/9820739/Molecular_pathobiology_of_pancreatic_adenocarcinoma_ L2 - https://www.bioscience.org/1998/v3/d/mangray/list.htm DB - PRIME DP - Unbound Medicine ER -