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The molecular genetics of pancreatic cancer.

Abstract

Pancreatic cancer is the fifth leading cause of cancer death in the United States, and despite improvements in the results of surgical treatment for this disease, little impact has been made upon overall mortality. New advances in treatment will depend upon improved adjuvant therapy, early diagnosis, and a better understanding of tumor biology. This article summarizes the results of molecular genetic studies in pancreatic cancer and their potential clinical significance. Familial predisposition to pancreatic cancer, cytogenic studies, DNA ploidy analysis, and examination of specific oncogenes and tumor suppressor genes are reviewed. The most frequent mutations detected have been in the K-ras oncogene, which occur in 80% of pancreatic cancers. These mutations do not correlate with tumor stage or survival, but can be useful in differentiating pancreatic exocrine from endocrine tumors and chronic pancreatitis. Mutations in the p53 gene occur in approximately 50% of tumors, and appear to be an independent prognostic factor for patient survival. Mutations in the CDKN2 gene are frequently seen in sporadic pancreatic cancers, and have been implicated in cases of familial pancreatic cancer. The significance of mutations in APC, MCC, DCC, c-erbB-2, RB-1, and mismatch repair genes in the genesis of pancreatic cancer is less clear.

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  • Publisher Full Text
  • Authors+Show Affiliations

    ,

    Department of Surgery, University of Iowa Hospitals and Clinics, Iowa City, USA.

    Source

    Surgical oncology 6:1 1997 pg 1-18

    MeSH

    Genes, p53
    Genes, ras
    Humans
    Molecular Biology
    Mutation
    Pancreatic Neoplasms
    Sensitivity and Specificity

    Pub Type(s)

    Journal Article
    Review

    Language

    eng

    PubMed ID

    9364657

    Citation

    Howe, J R., and K C. Conlon. "The Molecular Genetics of Pancreatic Cancer." Surgical Oncology, vol. 6, no. 1, 1997, pp. 1-18.
    Howe JR, Conlon KC. The molecular genetics of pancreatic cancer. Surg Oncol. 1997;6(1):1-18.
    Howe, J. R., & Conlon, K. C. (1997). The molecular genetics of pancreatic cancer. Surgical Oncology, 6(1), pp. 1-18.
    Howe JR, Conlon KC. The Molecular Genetics of Pancreatic Cancer. Surg Oncol. 1997;6(1):1-18. PubMed PMID: 9364657.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - The molecular genetics of pancreatic cancer. AU - Howe,J R, AU - Conlon,K C, PY - 1997/1/1/pubmed PY - 1997/11/19/medline PY - 1997/1/1/entrez SP - 1 EP - 18 JF - Surgical oncology JO - Surg Oncol VL - 6 IS - 1 N2 - Pancreatic cancer is the fifth leading cause of cancer death in the United States, and despite improvements in the results of surgical treatment for this disease, little impact has been made upon overall mortality. New advances in treatment will depend upon improved adjuvant therapy, early diagnosis, and a better understanding of tumor biology. This article summarizes the results of molecular genetic studies in pancreatic cancer and their potential clinical significance. Familial predisposition to pancreatic cancer, cytogenic studies, DNA ploidy analysis, and examination of specific oncogenes and tumor suppressor genes are reviewed. The most frequent mutations detected have been in the K-ras oncogene, which occur in 80% of pancreatic cancers. These mutations do not correlate with tumor stage or survival, but can be useful in differentiating pancreatic exocrine from endocrine tumors and chronic pancreatitis. Mutations in the p53 gene occur in approximately 50% of tumors, and appear to be an independent prognostic factor for patient survival. Mutations in the CDKN2 gene are frequently seen in sporadic pancreatic cancers, and have been implicated in cases of familial pancreatic cancer. The significance of mutations in APC, MCC, DCC, c-erbB-2, RB-1, and mismatch repair genes in the genesis of pancreatic cancer is less clear. SN - 0960-7404 UR - https://www.unboundmedicine.com/medline/citation/9364657/The_molecular_genetics_of_pancreatic_cancer_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0960-7404(97)00001-7 DB - PRIME DP - Unbound Medicine ER -