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Results for “Semustine”

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At least 433 records · Page 24Linked to original sources
PubMed1981

Evaluation of vincristine, CCNU and methyl-CCNU at high level doses in an experimental murine renal adenocarcinoma model.

Balb/C mice were implanted with tumor cells from primary tumor in donor animals bearing renal cell adenocarcinoma. Survival time, tumor growth and metastatic occurrence in treated animals were not significantly improved by high dose Methyl-CCNU, CCNU or Vincristine. It was also concluded that the dose levels of Methyl-CCNU and CCNU used for this study were highly toxic causing early death in the animals. Such studies thus fail to support clinical hopes that these agents would be effective for chemotherapy regimens in human renal tumors.

Adenocarcinoma↗
PubMed1981

[Immunochemotherapeutic treatment of gastrointestinal neoplasms].

The results obtained with a three-fold association of drugs (VCR, 5Fu, MeCCNU) in the treatment of 68 patients suffering from advanced carcinoma of the gastroenteric system followed up over an approximately four year period at the Savona Oncology Centre are reported. The percentage of positive responses (CR + PR) was 75% for carcinoma of the colon-rectum and 44.4% for stomach cancer. The results obtained in intestinal carcinoma proved more satisfactory than those reported in the literature. This could be attributed to the contemporaneous use of Corynebacterium parvum which boosts the immunitary state and so enhances the defences of the host organism, making it more sensitive to polychemotherapy. In the light of this hypothesis, stress is laid on the need to use an immunochemotherapy approach for the treatment of advanced carcinoma of the gastroenteric apparatus.

Adjuvants, Immunologic↗
PubMed1981

Preferential action of liposome-entrapped 1-(2-chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea on lung metastasis of Lewis lung carcinoma as compared with the free drug.

Lipid vesicles entrapping a lipophilic antitumor agent, 1-(2-chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea (MeCCNU), within the membrane phase were prepared and their antimetastatic activity was compared with that of free MeCCNU using intravenously inoculated Lewis lung carcinoma. It was found that the liposome preparation exhibited more potent inhibitory activity than the free drug on colony formation in the lung, when administered intravenously as well as intraperitoneally. Superior life-prolongation effect was also observed with liposome preparations as compared with the free drug in this system. However, the two forms of MeCCNU showed almost the same activity against not only Lewis lung carcinoma but also P388 leukemia inoculated subcutaneously and intraperitoneally, respectively. These results suggest that the superior effect of liposome-entrapped MeCCNU on lung metastasis might be due, at least in part, to preferential distribution of liposomes to the lung as compared with the free drug.

Animals↗
PubMed1980

Lipophilic drugs and lipoproteins: partitioning effects on chloroethylnitrosourea reaction rates in serum.

Chloroethylnitrosoureas are anticancer agents that undergo chemical reactions in vitro and in vivo to form active alkylating agents. The rate at which lipophilic chloroethylnitrosourease decompose in serum is faster than in aqueous solution and comparable to in vivo clearance rates. The increase in reaction rate is known to be caused by a reaction catalyzed by protein. Addition of lipoproteins to serum stabilizes chloroethylnitrosoureas to degradation. A model is presented that correlates serum decomposition rates to lipoprotein concentrations. This model involves partitioning of lipophilic chloroethylnitrosoureas into the hydrophobic core region of the lipoproteins where the chloroethylnitrosourea is chemically stable and is not free to undergo protein binding nor aqueous chemical degradation reactions. Normal interindividual variations of serum lipoprotein concentrations and hence partitioning may be a significant factor affecting the tissue distribution and pharmacokinetics of lipophilic drugs.

Carmustine↗
PubMedDate not supplied

Baker's antifol in combination with 5-fluorouracil and methyl-CCNU in the treatment of metastatic colorectal cancer: a Southwest Oncology Group Study (Protocol 7764).

Fifty-one previously untreated patients with metastatic colorectal cancer were treated with a combination of 5-fluorouracil, methyl-CCNU, and Baker's antifol. Six of 34 fully evaluable patients achieved a response. There were no apparent benefits obtained with this combination compared to treatment with 5-fluorouracil alone.

Adult↗
PubMed1980

Studies of the effects of treatment with 5-flourouracil alone and in combination with either cyclophosphamide, methotrexate, or methyl-CCNU on hepatic drug-metabolizing enzymes in murine L1210 leukemia.

Studies have been conducted on liver microsomal enzymes of B6D2F(1) mice bearing a Day 4 L1210 ascites tumor after treatment with a single intraperitoneal injection of 5-fluorouracil (FUra) alone, and in combination with either cyclophosphamide (CP), methotrexate (MTX), or methyl-CCNU (MeCCNU). FUra (200 mg/kg) alone did not alter either ethylomorphine N-demethylase, aniline hydroxylase, or neotetrazolium reductase activities as compared to untreated nontumor-bearing mice on Days 2, 4 and 6 after treatment. FUra (50 mg/kg)d plus CP (200 mg/kg) decreased neotetrazolium reductase activity 17% on Days 4 and 6 after treatment and the enzyme activity then returned to control levels on Day 8. Ethyl morphine N-demethylase and aniline hydroxylase, or neotetrazolium reductase activities on Days 1, 2, 4 and 6 after treatment. FUra (50 mg/kg) plus MeCCNU (21 mg/kg) did not affect either ethylmorphine N-demethylase or aniline hydroxylase activities on Days 1, 2, 4, 6 and 8 after treatment. However, neotetrazolium reductase activity was decreased 15% on Day 2 and then returned to control levels on Day 4. These results indicate that treatment of mice bearing the L1210 ascites tumor with an optimal single does of FUdra alone and in combination with either CP, MTX or MeCCNU does not have marked or prolonged effects on liver microsomal drug-metabolizing enzyme activities.

Animals↗
PubMed1980

[Use of BCG as an immunoadjuvant in combination with antitumor agents in virus-induced leukemia].

The effect of administration of BCG in association with chemotherapy in histocompatible CD2F1 mice challenged ip with Moloney-virus-induced lymphoma LSTRA of Balb/c origin was studied. All untreated mice died with comparable median survival time (MST). Immunochemotherapy experiments were performed in histocompatible mice using BCG according to various treatment schedules with respect to tumor challenge and 3 nitrosureas of clinical interest (i.e. BCNU, MeCCNU and CCNU) administration. If recipients were subjected to ip treatment with drugs alone or in association with the non specific immunoadjuvant (IA) given after tumor challenge (on day +1); no significant antitumor effect was detected. Synergistic antitumor effects were evidenced when the antineoplastic agents were associated with IA administered on the "-14+1" regimen with respect to the tumor. The results pointed out that the antilymphoma effects of chemotherapy could be amplified by IA only when the treatment schedule included adjuvants administration prior to tumor challenge.

Animals↗
PubMedDate not supplied

Combination chemotherapy for advanced colorectal cancer with triazinate, ICRF-159, 5-FU, and methyl-CCNU.

Twenty-four patients with advanced metastatic colorectal cancer with measurable sites of disease were treated with a combination of 5-FU, methyl-CCNU, ICRF-159, and triazinate. Only two had objective regression of disease. Two patients died of complications from drug-induced myelosuppression. Toxic effects were moderate in the remaining patients. Attempts to escalate doses were limited by myelosuppression. The regimen used has no advantage over 5-FU alone. It is unlikely that triazinate and ICRF-159 will add substantially to the efficacy of chemotherapy for colorectal cancer.

Adult↗
PubMed1978

[Treatment of advanced digestive cancer with fluorouracil and methyl-CCNU].

We relate the experience obtained by treatment of 20 advanced digestive cancer patients, with the association of 5 fluorouracil and methyl-C.C.N.U. Objective response was found in 4 patients (20%). Toxicity consisted of leucopenia in 3 patients, allergic phenomena in 2 and diarrhea in 1 patient. Mean survival is increased in 3 months in responders, when compared with non-responders, although this difference has not statistical value.

Adult↗
PubMed1980

Enhancement of antitumor activity of alkylating agents by the radiation sensitizer misonidazole.

The influence of the radiosensitizer misonidazole on the effectiveness of several alkylating agents and cis-platinum against advanced solid murine tumors was investigated. Tumor regrowth delay, frequency of tumor regressions, and animal life span were used to evaluate misonidazole in combination with cyclophosphamide, L-phenylalanine mustard, 1-(2-chloroethyl)-3-trans-4-methylcyclohexyl)-1-nitrosourea, aziridinyl-benzoquinone, and cis-platinum. In the advanced M5076 ovarian carcinoma, misonidazole enhanced the activity of cyclophosphamide, L-phenylalanine mustard, 1-(2-chloroethyl)-3-trans-4-methylcyclohexyl)-1-nitrosourea, and aziridinyl benzoquinone, but not cis-platinum. In early B16 melanoma, misonidazole plus cyclophosphamide was no more effective than cyclophosphamide alone. In advanced Lewis lung carcinoma, misonidazole enhanced the antitumor activity of cyclophosphamide but not 1-(2-chloroethyl)-3-trans-4-methylcyclohexyl)-1-nitrosourea. Misonidazole, at 1000 mg/kg, increased the antitumor effectiveness of L-phenylalanine mustard and cyclophosphamide in M5076 tumors by factors of 2.2 and 1.8, but caused only a 1.2- and 1.3-fold increase in the myelotoxicity of these agents as determined by spleen colony assay of normal bone marrow. Misonidazole also increased the toxicity of cyclophosphamide and L-phenylalanine mustard in non-tumor-bearing mice but to a lesser degree than it enhanced antitumor activity. These results indicate that misonidazole is capable of enhancing the effects not only of ionizing radiation but of alkylating agents as well.

Alkylating Agents↗
PubMed1978

Differential sensitivities of five rat hepatoma cell lines to anticancer drugs.

Five permanent tumor cell lines derived originally from either a solid or an ascites biopsy of rat hepatoma exhibited differential sensitivities to bleomycin, Adriamycin, 1-beta-D-arabinofuranosylcytosine, hydroxyurea, 1-trans-(2)-chloroethyl)-3-(4-methoylcyclohexyl)-1-nitrosourea, and 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea. The cells were least sensitive to hydroxyurea and 1-beta-D-arabinofurano-sylcytosine, with some cell lines being almost totally resistant to these drugs. However, from 25- to 700-fold differences in survival were obtained between cell lines treated with either bleomycin or Adriamycin.

Animals↗
PubMed1978

Therapeutic potentiation of nitrosoureas using chlorpromazine and caffeine in the treatment of murine tumors.

The therapeutic usefulness of chlorpromazine (CPZ) and caffeine (CAF) in combination with selected nitrosoureas was investigated in mice bearing L1210 leukemia, Lewis lung carcinoma, and B16 melanoma. We found that using BCNU with either CAF or CPZ was therapeutically superior to using either agent alone to treat mice bearing L1210 leukemia. Administering all three drugs in combination did not improve upon the therapeutic responses obtained with the two-drug combinations. In mice implanted with Lewis lung carcinoma or B16 melanoma, responses to treatment with the triple combination of methyl-CCNU, CAF, and CPZ suggested, but did not clearly establish, superiority over each two-drug combination or methyl-CCNU alone.

Animals↗
PubMed1978

Phase I trial of ICRF-159 in combination with 1.3 bis-(2-chloroethyl)-1-nitrosourea (MeCCNU).

Both ICRF-159 and methyl-CCNU are agents with antitumor activity against gastrointestinal carcinoma; hence the exploration of this combination for possible synergism. Results of the study involving 19 patients show that bone marrow toxicity is the limiting factor for this combination of drugs. Moreover, a dose of 130 mg/mg of MeCCNU with 800 mg/m2/day of ICRF is well tolerated.

Bone Marrow↗