Proliferation, senescence, and neoplastic progression of beta cells in hyperplasic pancreatic islets

Cell. 1988 Jan 15;52(1):97-105. doi: 10.1016/0092-8674(88)90534-x.

Abstract

Three different cases of pancreatic beta cell hyperplasia in mice are accompanied by an increase in a subclass of cells expressing tyrosine hydroxylase (TH), a neuronal enzyme. In the nontumorigenic cases of islet growth during normal pregnancy and in the obese mutant mouse, the TH-insulin cells do not divide, in contrast to the "insulin-only" cells. In later stages the number of proliferating insulin-only cells decreases concomitant with an increase in the number of nondividing TH-insulin cells, suggesting that the TH-insulin cells are on a pathway to senescence. In the presence of an oncoprotein the TH-insulin cells are able to proliferate. The proliferation of this cell type may represent an escape from the senescence pathway and progression to immortal tumor cells.

Publication types

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

MeSH terms

  • Animals
  • Cell Division
  • Cell Survival
  • Cell Transformation, Neoplastic / pathology*
  • Female
  • Hyperplasia
  • Immunohistochemistry
  • Insulin / biosynthesis
  • Insulinoma / pathology
  • Islets of Langerhans / enzymology
  • Islets of Langerhans / pathology*
  • Mice
  • Mice, Obese
  • Mice, Transgenic
  • Mitosis
  • Obesity / enzymology
  • Oncogenes
  • Pancreatic Neoplasms / pathology
  • Pregnancy / metabolism
  • Tyrosine 3-Monooxygenase / biosynthesis
  • Tyrosine 3-Monooxygenase / metabolism

Substances

  • Insulin
  • Tyrosine 3-Monooxygenase