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At least 19 recordsLinked to original sources
PubMed1992

An application of 3D-QSAR to the analysis of the sequence specificity of DNA alkylation by uracil mustard.

The sequence specificity of DNA alkylation by uracil mustard was examined using a novel three-dimensional QSAR method known as HASL, or the hypothetical active site lattice. The structures of a variety of 4-mer sequences obtained from pBR322 and SV40 were related to their degree of guanine-N7 alkylation by uracil mustard. The resulting correlations were found to point to a significant contribution from bases on the 3' side of the target guanine nucleotide. The HASL models derived from the analysis of 52 guanine-containing 4-mer sequences were used to highlight those atomic features in the favored TGCC sequence that were found most important in determining specificity. It was found that the NH2-O systems present in the two GC base pairs on the 3' side of the target guanine were significantly correlated to the degree of alkylation by uracil mustard. This finding is consistent with a prealkylation binding event occurring between these sites along the major groove and the uracil mustard O2/O4 system.

Alkylation↗
PubMed1965

URACIL MUSTARD: A POTENT INDUCER OF LUNG TUMORS IN MICE.

Uracil mustard, injected intraperitoneally, increased the incidence and average number of pulmonary tumors in A/J mice. In comparison to a typical alkylating agent, nitrogen mustard, or to urethan, uracil mustard (on a molar basis) was considerably more carcinogenic.

DNA↗
PubMed1980

Uracil mustard in the treatment of thrombocytosis.

Uracil mustard was used for the treatment of thrombocytosis in 14 patients, eight who had polycythemia vera and six who had essential thrombocytosis. Intermittent treatment with 1 to 2 mg/day for 14 days was used for most patients, and continuous treatment was used for three patients. The nadir of the platelet count occurred during a mean period of five to seven weeks, and the mean duration between courses was seven months. The drug selectively depressed the platelet count, with a minimal effect on leukocytes and erythrocytes. Uracil mustard is an effective drug for the control of thrombocytosis.

Administration, Oral↗
PubMed1999

Uracil mustard revisited.

BACKGROUND: A patient with diffuse large cell lymphoma who had a complete response lasting 35 years following a 3-day course of uracil mustard stimulated a recall review of patients treated with this oral alkylating agent. METHODS: Records of patients treated with uracil mustard between 1958 and 1970 were reviewed. A current histologic review according to the International Formulation was performed when possible. Total doses of uracil mustard were similar to those of mechlorethamine, although there were variations in the dose schedule. RESULTS: Employing criteria used over 25 years ago to evaluate patients' responses, the overall regression rate for 94 non-Hodgkin lymphoma patients was 69.2% (complete response [CR] 23.4%). Of 62 patients with Hodgkin disease, 69.4% responded (CR 9.7%). For 39 patients with chronic lymphatic leukemia, the combined complete and partial response rate was 74% (CR 7.7%). Thrombocytopenia was the primary toxicity. CONCLUSIONS: Uracil mustard is an unmarketed, inexpensive oral alkylating agent that has been effective in the treatment of patients with lymphoma, chronic lymphatic leukemia, and thrombocythemia. Perhaps it should be reevaluated.

Adolescent↗
PubMed1962

Sarcoma 180 inhibition by combinations of 6-thioguanine and uracil mustard.

Combinations of 6-thioguanine and uracil mustard produced greater inhibition of the growth of sarcoma 180 than that equivalent to the sum of the inhibitory effects caused by the optimum levels of the individual drugs. This potentiation was accomplished without marked weight loss by the host. Some possible biochemical mechanisms responsible for the drug synergy are discussed.

Animals↗
PubMed1988

Acute leukemia following treatment of polycythemia vera and essential thrombocythemia with uracil mustard.

Transformation to acute leukemia (AL) is known to occur in polycythemia vera (PV) and essential thrombocythemia (ET). Myelosuppressive therapy with agents such as 32P and alkylating agents increase this risk in both disorders. The alkylating agent, uracil mustard (UM), which is an effective agent for controlling thrombocytosis, has not been reported to be leukemogenic. We have treated 29 patients with UM (9 treated continuously and 20 treated intermittently): II with PV, 16 with ET, and 2 with myelofibrosis (MF). Three patients developed AL, two after continuous therapy. These two patients with PV had received the fourth highest and highest total dose of UM, and their duration of treatment was the third and fourth longest among the nine patients treated continuously, respectively. One out of 20 patients treated intermittently with UM developed AL. This patient (3) with ET had received the highest total dose of UM, and her duration of treatment was the longest among the 20 patients treated intermittently.

Acute Disease↗
PubMed1978

Pulmonary toxicity recurring after a six week course of busulfan therapy and after subsequent therapy with uracil mustard.

A growing number of drugs, including a number of alkylating agents, have been implicated as the cause of pulmonary diseases. A patient with chronic myelogenous leukemia presented with typical cytology, biopsy, and roentgenologic findings of lung toxicity after only six weeks of therapy with busulfan. There was subsequent clearing. A similar roentgenologic change also occurred after administration of uracil mustard. This has not been reported previously.

Busulfan↗
PubMed1986

Inhibitory effects of 5-(2-pyrazinyl)-4-methyl-1,2-dithiol-3-thione (Oltipraz) on carcinogenesis induced by benzo[a]pyrene, diethylnitrosamine and uracil mustard.

5-(2-Pyrazinyl)-4-methyl-1,2-dithiol-3-thione (Oltipraz) was studied for its capacity to inhibit carcinogen-induced neoplasia in female ICR/Ha mice. When administered by oral intubation 48 h prior to benzo[a]pyrene (BP), also given by oral intubation, Oltipraz inhibited the occurrence of pulmonary adenomas and tumors of the forestomach. The ratio of the number of tumors occurring in the mice receiving Oltipraz to that of the corresponding controls was: lung, 0.36 and forestomach 0.38. Inhibition also occurred when Oltipraz was given p.o. 24 h prior to BP. In other experiments, oral administration of Oltipraz 48 h prior to p.o. administration of diethylnitrosamine or uracil mustard inhibited pulmonary adenoma formation but to a lesser extent than with BP as the carcinogen. The low toxicity of Oltipraz found previously, coupled with evidence of protective effects against chemically diverse carcinogens, suggests that this compound should be studied further for its possible use as an agent for the chemoprevention of neoplasia.

Animals↗