Record Display for the EPA National Library Catalog


Main Title Quantification and Molecular Characterization of 'hprt' Mutants of Human T-Lymphocytes.
Author Moore, M. M. ; Harrington-Brock, K. ; Zimmerman, L. J. ; Burnette, L. P. ; Smith., T. W. ;
CORP Author Environmental Health Research and Testing, Inc., Research Triangle Park, NC. ;Vermont Univ., Burlington. Genetics Lab.;Health Effects Research Lab., Research Triangle Park, NC. Environmental Toxicology Div.
Publisher c1993
Year Published 1993
Report Number EPA-68-D10148, EPA-R-83565; EPA/600/J-94/207;
Stock Number PB94-163862
Additional Subjects T-Lymphocytes ; Point mutation ; Hypoxanthine phosphoribosyltransferase ; Humans ; Clone cells ; Phenotype ; Deoxyribonucleic acids ; Polymerase chain reaction ; Translocation(Genetics) ; Gene deletion ; Reprint ;
Library Call Number Additional Info Location Last
NTIS  PB94-163862 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 8p
Somatic mutations have been implicated as critical early events in carcinogenesis. Point mutations, deletions, and translocation events have been shown to activate oncogenes or inactivate suppressor oncogenes. In human population monitoring, quantitative analysis of mutation events that affect gene function is limited to those genes whose cellular phenotypes can be identified by selection procedures and to those tissues (like blood) that are accessible for analysis. In an effort to determine the frequency and types of mutations that can be detected at the hypoxanthine guanine phosphoribosyltransferase (hprt) gene, we have used the T-cell cloning assay and have developed a strategy to propagate mutants and screen for point mutations and breakage events. To date we have found presumed point mutations, intragenic deletions, and deletions that extend outside of the hprt gene. By analyzing mutations in selectable, nonessential gene markers, it should be possible to understand mechanisms of both spontaneous and induced genetic damage. An association of these specific genetic events with human diseases and the evaluation of the ability of environmental chemicals to induce these specific types of mutations will lead to a rational basis for evaluating risks from various chemical exposures.