Publications by authors named "M McManaway"

To quantify the toxicity of low-LET radiation from incorporated radionuclides, we have determined the toxicity of decays of [3H]dThd pulse-incorporated into CHO cells in early S phase, with the cells frozen for decay accumulation at 30, 120 or 360 min after the pulse. D37 values of 1500, 2000 and 2100 decays were found by colony formation assay, corresponding to average nuclear doses of 4.6 and 2.

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We have explored the factors which influence tumorigenicity of Burkitt's lymphoma (BL) cell lines in athymic nude mice. Four cell lines, Namalwa, CA46, JD38, and ST486 revealed tumor incidence of 63.5, 69.

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[3H]Cyclofoxy (CF: 17-cyclopropylmethyl-3,14-dihydroxy-4,5-alpha-epoxy-6-beta-fluoromorp hinan) is an opioid antagonist with affinity to both mu and kappa subtypes that was synthesized for quantitative evaluation of opioid receptor binding in vivo. Two sets of experiments in rats were analyzed. The first involved determining the metabolite-corrected blood concentration and tissue distribution of CF in brain 1 to 60 min after i.

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In a high proportion of Burkitt lymphomas, transcription of the c-myc gene is initiated from a cryptic promoter in the first intron, creating abnormal messenger RNA molecules in which intron sequences, normally spliced out of the nascent transcripts, persist. An antisense oligodeoxynucleotide directed against these intron sequences greatly inhibited the proliferation of Burkitt lymphoma cell lines containing the abnormal transcripts (ST486 and JD38), but not that of cell lines containing normal c-myc transcripts (KK124). Flow cytometry showed a pronounced reduction in intracellular c-myc protein levels in cell lines containing aberrant myc transcripts, but no change in other cellular proteins.

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Neoplasms have been shown to be associated with specific non-random chromosomal abnormalities. The present paper summarizes molecular consequences of chromosomal translocations in lymphoid malignancies, especially in Burkitt's lymphoma. Among such consequences are derangements of the regulation of oncogene transcription.

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