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Biomedical subjects

W F Benedict

Publications and source records attributed to W F Benedict.

At least 145 records · Page 8Linked to original sources
PubMed1975

1-beta-D-arabinofuranosylcytosine-induced malignant transformation of hamster and rat cells in culture.

The potent antileukemic chemotherapeutic drug, 1-beta-D-arabinofuranosylcytosine (ara-C), was observed to transform malignantly secondary hamster fetal cells as well as established rat cells in vitro. Results indicated that: (a) hamster cells altered by treatment with ara-C are morphologically indistinguishable from cells transformed with benzo(a)pyrene; (b) the ara-C-induced transformation can be observed under conditions of little or no inhibition of DNA synthesis and little or no cytotoxicity; (c) the transformation can occur with only a 6-hr exposure to ara-C; and (d) the transformation of hamster cells seems to require cellular DNA synthesis for cells in S phase are much more sensitive to ara-C-induced transformation than are G1-arrested cells. Representative transformed colonies of hamster and rat cells produced rapidly growing fibrosarcomas in inoculated newborn hamsters and rats, respectively. Control cells remained nontumorigenic.

Animals↗
PubMed1972

Chromatid breakage: differential effect of inhibitors of DNA synthesis during G 2 phase.

The cell cycle specificity of chromatid breakage induced by inhibitors of DNA synthesis depends on the mechanism of drug action. 5-Hydroxy-2-formylpyridine thiosemicarbazone, hydroxyurea, and guanazole, compounds that inhibit ribonucleotide reductase, do not cause chromatid breakage during G(2) phase. In contrast, two active antitumor agents, arabinosylcytosine and 5-azacytidine, which are either incorporated into polynucleotides or affect DNA polymerase, produce chromatid breakage during G(2) phase. All of these agents except guanazole also induce breakage in S phase.

Animals↗
PubMed1972

Expression of aryl hydrocarbon hydroxylase induction and suppression of tyrosine aminotransferase induction in somatic-cell hybrids.

Aryl hydrocarbon hydroxylase activity is inducible in mouse 3T3 fibroblasts by benz[alpha]anthracene, whereas no detectable basal or inducible levels of this enzyme occur in rat-hepatoma tissue culture cells. Conversely, tyrosine aminotransferase activity is inducible in hepatoma cells by dexamethasone, whereas only low noninducible levels of this enzyme exist in 3T3 cells. In hybrids formed by fusion of these two parent lines, levels of inducible hydroxylase activity range from the same as, to more than 20-fold greater than, that in the 3T3 parent; aminotransferase levels remain very low and noninducible in all of these same hybrids. A majority of the 1S-chromosomal complement from each parent is retained in most of these hybrids. The kinetics of hydroxylase induction and degradation, responses of hydroxylase induction to actinomycin D and cycloheximide, and the relative thermolability of the control and induced activities are similar in the 3T3 parent and in the hybrids. Failure to inactivate any of the aminotransferase activity in the hybrids with antibody specific for the rat enzyme indicates that all of the basal noninducible aminotransferase activity is derived from the mouse 3T3 parent.

Animals↗
PubMed1971

Chromatid breakage: cytosine arabinoside-induced lesions inhibited by ultraviolet irradiation.

Exposure to ultraviolet light can reduce the frequency of chromatid breaks induced by cytosine arabinoside in the DNA synthetic and post-DNA synthetic phases of the cell cycle. This effect can be correlated temporally with a decrease in the uptake of tritiated thymidine after ultraviolet treatment, implying that the genesis of such breakage is intimately related to DNA synthesis and that such synthesis is not confined to the DNA synthetic phase.

Animals↗