Overexpression of cyclin D1 occurs frequently in human pancreatic endocrine tumors

J Clin Endocrinol Metab. 2000 Nov;85(11):4373-8. doi: 10.1210/jcem.85.11.6937.


The molecular pathogenesis of human pancreatic endocrine tumors (PETs) is poorly understood. Three independent animal models have pointed to the pivotal role of the G1/S cell cycle transition in pancreatic endocrine cell proliferation. We thus hypothesized that the cell cycle regulator cyclin D1 may contribute to the pathogenesis of human PETs. Overexpression of cyclin D1 was identified in 43% of cases, and no correlation was observed with clinical phenotype. The novel observation of frequent overexpression of cyclin D1 suggests that this established oncogene may be implicated in the pathogenesis of human PETs. The absence of detectable alterations in cyclin D1 genomic structure suggests that the mechanism for its oncogenic activation in PETs may be transcriptional or posttranscriptional.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Aged, 80 and over
  • Child
  • Cyclin D1 / analysis
  • Cyclin D1 / genetics*
  • Female
  • Humans
  • Immunohistochemistry
  • Male
  • Middle Aged
  • Multiple Endocrine Neoplasia / genetics
  • Multiple Endocrine Neoplasia Type 1 / genetics
  • Multiple Endocrine Neoplasia Type 1 / pathology
  • Pancreatic Neoplasms / classification
  • Pancreatic Neoplasms / genetics*
  • Pancreatic Neoplasms / pathology
  • Pancreatic Neoplasms / surgery


  • Cyclin D1