Record Display for the EPA National Library Catalog


Main Title Effect of Chemotherapy on the In vivo Frequency of Glycophorin A 'Null' Variant Erythrocytes (Revised).
Author Bigbee, W. L. ; Wyrobek, A. J. ; Langlois, R. G. ; Jensen, R. H. ; Everson, R. B. ;
CORP Author Lawrence Livermore National Lab., CA. Biomedical Sciences Div. ;National Inst. of Environmental Health Sciences, Research Triangle Park, NC. Epidemiology Branch.;Health Effects Research Lab., Research Triangle Park, NC.;Department of Energy, Washington, DC.
Publisher c1990
Year Published 1990
Report Number EPA-R-808642-01 ;EPA-R-811819-02-0; EPA/600/J-90/286;
Stock Number PB91-145029
Additional Subjects Combined antineoplastic agents ; Toxicity ; Mutagenicity tests ; Erythrocytes ; 8Glycophorin ; Alleles ; Breast neoplasms ; Cross-sectional studies ; Reprints ;
Library Call Number Additional Info Location Last
NTIS  PB91-145029 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 14p
A human in vivo somatic cell assay based on the enumeration of variant erythrocytes lacking expression of an allelic form of the cell-surface sialoglycoprotein, glycophorin A, was applied to the study of blood samples from patients obtained prior to, during, and following chemotherapy for malignant disease in order to determine the effect of mutagenic chemical agents on the frequency of variant cells. Significant elevations in the mean frequency of variant cells over pre-therapy and normal levels were observed in samples obtained during and after therapy. In a time-series study; 14 breast cancer patients treated with CAF (cyclophosphamide, adriamycin, 5-fluorouracil), CMF (cyclophosphamide, methotrexate, 5-fluorouracil), or VMF (vinblastine, methotrexate, 5-fluorouacil) adjuvant chemotherapy were sampled repeatedly during and after therapy. For the CAF and CMF patients an increase in the frequency of variant cells was observed with a lag in the appearance of induced variants after initiation of therapy; variant frequencies gradually increased during therapy reaching a maximum at or shortly after the end of therapy, then declined to near pre-therapy levels within 6 months. The maximum level of induced variants ranged from 2- to 7-fold over pre-therapy or normal levels depending on the combination of agents used.