Record Display for the EPA National Library Catalog


Main Title Role of Hyperplastic Nodules in Dichloroacetic Acid-Induced Hepatocarcinogenesis in B6C3F1 Male Mice.
Author Richmond, R. E. ; DeAngelo, A. B. ; Potter, C. L. ; Daniel, F. B. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. ;Northern Kentucky Univ., Highland Heights. Dept. of Biological Sciences.
Publisher c1991
Year Published 1991
Report Number EPA/600/J-91/202;
Stock Number PB91-242610
Additional Subjects Dichloroacetate ; Liver neoplasms ; Hyperplasia ; Mice ; Biological tumor markers ; Adenoma ; Carcinoma ; Aldehyde dehydrogenase ; Alpha fetoproteins ; Oncogene proteins ; Reprints ;
Library Call Number Additional Info Location Last
NTIS  PB91-242610 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 7p
Dichloracetic acid (DCA) is a hepatocarcinogen in the male B6C3F1 mouse. It induces primarily hyperplastic nodules (HN) prior to the appearance of hepatocellular adenoma (HA) or carcinoma (HC). The study was undertaken to determine the role of HN in the progression of DCA-induced hepatocarcinogenesis. Five tumor markers were assessed: P21 ras, P39 c-jun, phosphotyrosine (PT), aldehyde dehydrogenase (ALD), and a-fetoprotein (AFP). All were known to be expressed in neoplastic lesions. The results demonstrated: (1) Except for c-jun, HN expressed markers significantly less often than either HA or HC. Equal expression of c-jun occurred in any of the 3 lesion types. (2) HN that were marker positive contained small nests of marker positive hepatocytes among a field of normal appearing unstained hepatocytes. No marker-positive cells were detected in normal appearing liver outside of HN. Altered foci were few and did not express these markers. These results support the idea that the nests within HN are areas of transformed or neoplastic hepatocytes. The absence of marker expression in normal liver and in the AF indicates that HN may be the only significant preneoplastic lesion in DCA-induced carcinogenesis.