Record Display for the EPA National Library Catalog


Main Title Gap Junction Function and Cancer.
Author Holder, J. W. ; Elmore, E. ; Barrett, J. C. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. Genetic Toxicology Div. ;National Inst. for the Advancement of in Vitro Sciences, Irvine, CA. ;National Inst. of Environmental Health Sciences, Research Triangle Park, NC. Lab. of Molecular Carcinogenesis.
Publisher c1993
Year Published 1993
Report Number EPA/600/J-93/436 ;OHEA-R-403;
Stock Number PB94-146248
Additional Subjects Intercellular junctions ; Malignant neoplasms ; Cell communication ; Xenobiotics ; Homeostasis ; Liver neoplasms ; Precancerous conditions ; Metabolism ; Neoplasm metastasis ; Carcinogens ; Reprints ;
Library Call Number Additional Info Location Last
NTIS  PB94-146248 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 14p
Gap junctions (GJs) provide cell-to-cell communication of essential metabolites and ions. GJs allow tissues to average responses, clear waste products, and minimize the effects of xenobiotics by dilution and allowing steady-state catabolism. Many chemicals can adversely affect the membrane GJ assembly causing reversible alterations in GJ intercellular communication. During toxicity, essential metabolites, ions, and regulators are not shared homeostatically throughout a tissue community. Alterations in metabolic circuits are thought to interrupt organ integration. Persistent GJ perturbation can cause chronic effects (e.g., cancer), and many tumor promoters inhibit GJ intercellular communication. Liver precancerous foci intracommunicate (but at a reduced level) and intercommunicate improperly (or not at all) across the foci boundary to normal cells. In time, foci can become less regulated and more isolated within the tissue. GJs remain reduced quantitatively in the tumor progression stage and may be qualitatively altered in metastasis since connections are made between the primary tumor cells and foreign host cells at the secondary metastatic site.