Catherine M. White
National Institutes of Health
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Featured researches published by Catherine M. White.
Mammalian Genome | 1994
Theodora R. Devereux; Roger W. Wiseman; N. Kaplan; S. Garren; Julie F. Foley; Catherine M. White; Colleen H. Anna; M. A. Watson; Arti C. Patel; S. Jarchow; Robert R. Maronpot; Marshall W. Anderson
Previous studies have hypothesized that at least three genetic loci contribute to differences in pulmonary adenoma susceptibility between mouse strains A/J and C57BL/6J. One gene that may confer susceptibility to lung tumorigenesis is the Kras protooncogene. To identify other relevant loci involved in this polygenic trait, we determined tumor multiplicity in 56 randomly chosen N-ethyl-N-nitrosourea-treated (A/J×C57BL/6J) N1×C57BL/6 backcross (AB6N2) progeny and correlated it with genotypes at 77 microsatellite markers spanning the genome. A correlation of lung tumor multiplicity phenotypes with genotypes of microsatellite markers on distal Chromosome (Chr) 6 in the Kras region (Pas1) was confirmed, and a new region on Chr 19 (designated Pas3) was identified that also contributes to susceptibility. Linkage analysis on Chr 19 with 270 AB6N2 mice localized the region flanked by D19Mit42 and D19Mit19 that is most closely associated with lung tumor susceptibility. The Pas3 locus may be an enhancer of the susceptibility locus on Chr 6.
Experimental Lung Research | 1991
Steven A. Belinsky; Theodora R. Devereux; Catherine M. White; Julie F. Foley; Robert R. Maronpot; Marshall W. Anderson
The role of the Clara and type II cell in the development of pulmonary tumors in the A/J mouse and Fischer rat was investigated by determining the relationship of DNA methylation and repair in pulmonary cells to oncogene activation and by characterizing the morphology of pulmonary tumors induced by treatment with 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). Marked differences in the formation of the promutagenic adduct O6-methylguanine (O6MG) were observed in pulmonary cells following treatment of rats with NNK. Concentrations of this adduct in Clara cells greatly exceeded (3- to 30-fold) those detected in type II cells and whole lung with doses of NNK ranging from 0.1 to 50 mg/kg. In addition, very low rates of repair of this adduct were detected in Clara cells, whereas efficient adduct removal occurred in type II cells. The importance of this adduct and the role of cell specificity was suggested by the fact that a strong correlation was observed between the concentration of O6MG in Clara cells and tumor incidence in the Fischer rat with doses of NNK ranging from 0.03-50 mg/kg. In contrast, no differences in adduct concentration between type II and Clara cells from A/J mice were observed under conditions resulting in pulmonary tumor formation. Activation of the K-ras gene was detected in lung tumors from A/J mice. This gene was activated by a mutation in codon 12 involving a GC to AT transition (GGT to GAT) and is consistent with base mispairing produced by the formation of O6MG. Activation of this gene was not associated with lung tumor formation in the Fischer rat. DNA from rat lung tumors did induce tumors in the nude mouse carcinogenicity assay. In addition, rat repetitive sequences were detected in DNA isolated from these nude mouse tumors. In spite of the cell selectivity for DNA methylation in Clara cells from rat and the relationship between O6MG formation and tumorigenicity, early proliferative lesions observed in both mice and rats involved the alveolar areas. Ultrastructural examination of these lesions and adenomas revealed morphologic features characteristic of the type II cell. Thus the lack of agreement between biochemical and morphological findings makes it difficult to hypothesize a cell of origin for the pulmonary neoplasms induced by NNK. However, these studies indicate that the concentration of O6MG in Clara cells is an excellent indicator of the carcinogenic potency of NNK in the rat.(ABSTRACT TRUNCATED AT 400 WORDS)
Life Sciences | 1979
Wayne A. Colburn; Catherine M. White
Abstract Antisera prepared in rabbits against 4-Monochlorobiphenyl and 3,4,3′,4′-Tetrachlorobiphenyl were used to alter the tissue distribution of these environmental pollutants in the mouse. Mice were passively immunized with rabbit antisera following the absorption and distribution of the substituted biphenyls. Immunization caused in vivo redistribution of the compounds into the vascular space. Tissue/blood concentration ratios were greater in the control than in the antiserum treated animals. Changes intissue/blood ratios were similar to the serum/ antiserum ratios as determined by equilibrium dialysis experiments. These results indicate that it is possible to remove chlorinated biphenyls from tissue stores using specific antisera. Second, the partition of compounds between control serum and specific antiserum may be useful as a prospective screen to detect antisera with sufficient antigen affinity for tissue redistribution studies.
Cancer Research | 1990
Steven A. Belinsky; Julie F. Foley; Catherine M. White; Marshall W. Anderson; Robert R. Maronpot
Cancer Research | 1986
Steven A. Belinsky; Catherine M. White; Joyce A. Boucheron; Frank C. Richardson; James A. Swenberg; Marshall W. Anderson
Molecular Carcinogenesis | 1993
Theodora R. Devereux; Catherine M. White; Monika E. Hegi; Arti C. Patel; Marshall W. Anderson; Robert R. Maronpot; Julie F. Foley; Arnold Greenwell; Steven A. Belinsky
Cancer Research | 1987
Steven A. Belinsky; Catherine M. White; Theodora R. Devereux; James A. Swenberg; Marshall W. Anderson
Carcinogenesis | 1988
Steven A. Belinsky; Dolan Me; Catherine M. White; Robert R. Maronpot; Anthony E. Pegg; Marshall W. Anderson
Molecular Carcinogenesis | 1995
Joan P. Packenham; Jack A. Taylor; Colleen H. Anna; Catherine M. White; Theodora R. Devereux
Carcinogenesis | 1994
Theodora R. Devereux; Catherine M. White; Robert C. Sills; John R. Bucher; Robert R. Maronpot; Marshall W. Anderson