Rapid development of hepatic tumors in transforming growth factor alpha transgenic mice associated with increased cell proliferation in precancerous hepatocellular lesions initiated by N-nitrosodiethylamine and promoted by phenobarbital

Carcinogenesis. 1994 Sep;15(9):1791-8. doi: 10.1093/carcin/15.9.1791.

Abstract

The carcinogenic and tumor-promoting effects of human transforming growth factor alpha (TGF-alpha) overexpression were examined in a two-stage chemical carcinogenesis protocol using TGF-alpha transgenic mouse line MT42. Male MT42 and CD-1 mice received a single i.p. injection of 5 mg N-nitrosodiethylamine (DEN)/kg body wt at 15 days of age, and were placed on a diet containing 0.05% of phenobarbital (PB) from 4 weeks of age for 35 weeks. DEN-, PB-treated and saline-injected animals in each strain were used as controls. A total of three sequential sacrifices (at 10, 23 and 37 experimental weeks) was performed. Hepatocellular carcinomas (HCCs) developed earlier at high incidence (100%) after 23 experimental weeks in MT42 mice receiving DEN/PB, while CD-1 mice had a 40% incidence of HCCs only after week 37. HCCs also developed in the DEN-initiated MT42 mice at 80% incidence after week 23, but no HCCs were observed in the DEN-initiated CD-1 mice. PB induced preneoplastic foci (67%), adenomas (33%) and HCCs (33%) after 37 weeks in MT42 mice, but no lesions were found in CD-1 mice. Thus, the carcinogenic response to DEN and/or PB was accelerated in the MT42 transgenic mice. Furthermore, PB promotion was observed from week 10 in MT42 mice and week 23 in CD-1 mice. Thus, the promoting effect of PB was also accelerated in the MT42 transgenic mice. Proliferating cell nuclear antigen (PCNA) labeling indices of hepatocellular foci and adenomas in DEN- or DEN/PB-treated MT42 mice were significantly higher than those of CD-1 mice. TGF-alpha expression determined by immunohistochemistry revealed higher levels in these lesions than in hepatocytes of surrounding parenchyma of MT42 transgenic mice. In conclusion, TGF-alpha transgenic mice clearly demonstrated enhanced sensitivity to the development of hepatocellular carcinoma in the DEN initiation and PB promotion regime, possibly through a mechanism of increased hepatocyte proliferation in precancerous lesions (foci and adenomas), driven by high expression of the mitogen TGF-alpha in these lesions.

Publication types

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

MeSH terms

  • Animals
  • Body Weight / drug effects
  • Cell Division / drug effects
  • Cocarcinogenesis*
  • Diethylnitrosamine / toxicity*
  • Gene Expression / drug effects
  • Immunohistochemistry
  • Liver Neoplasms, Experimental / chemically induced*
  • Liver Neoplasms, Experimental / genetics*
  • Liver Neoplasms, Experimental / pathology
  • Male
  • Mice
  • Mice, Transgenic
  • Phenobarbital / toxicity*
  • Precancerous Conditions / chemically induced*
  • Precancerous Conditions / genetics*
  • Precancerous Conditions / pathology
  • Proliferating Cell Nuclear Antigen / analysis
  • Transforming Growth Factor alpha / analysis
  • Transforming Growth Factor alpha / genetics*
  • Transforming Growth Factor alpha / physiology*

Substances

  • Proliferating Cell Nuclear Antigen
  • Transforming Growth Factor alpha
  • Diethylnitrosamine
  • Phenobarbital