Cimetidine Reduction of Tumour Formation in Mice

Gifford, RobertR.M.; Ferguson, RonaldM.; Voss, B

doi:10.1016/s0140-6736(81)91555-5

Cited by 110 publications

(53 citation statements)

References 7 publications

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“…In contrast to the data presented by Osband et al (1981) and Gifford et al (1981) cimetidine had no direct anti-neoplastic effect in our tumour model but amplified the parasite-induced anti-tumour effect. These observations further support the potential of cimetidine in regulating immune responses, including its role in cancer immunotherapy.…”

Section: Minecontrasting

confidence: 99%

“…In two recent papers (Osband et al, 1981;Gifford et al, 1981) cimetidine, an H2-receptor antagonist, was shown to possess anti-neoplastic properties in mice. In the experimental tumour models used, the specific immunity, based on the presence of cytotoxic T cells, was probably enhanced by the pharmacological blocking effect of cimetidine on H2-receptor-bearing suppressor cells.…”

Section: Minementioning

confidence: 99%

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Cimetidine amplifies the anti-neoplastic effect of Trichinella spiralis in mice

Ruitenberg¹,

Kruizinga²,

Steerenberg³

et al. 1982

Br J Cancer

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Section: Minecontrasting

confidence: 99%

Section: Minementioning

confidence: 99%

Cimetidine amplifies the anti-neoplastic effect of Trichinella spiralis in mice

Ruitenberg¹,

Kruizinga²,

Steerenberg³

et al. 1982

Br J Cancer

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“…injections of metiamide, a histamine type 2-receptor antagonist did not influence tumour growth, but significantly lengthened the survival of tumour-bearing C57BL/6 mice. Longer survival has also been found with oral cimetidine (another histamine type 2-receptor antagonist) in C57BL/6 mice injected with 3 LL tumour cells (Osband et al, 1981) and in the C57BL/6-EL4 and C3H-Mc43 tumour models (Gifford et al, 1981). The inhibiting effect of cimetidine on tumour growth was attributed to the inhibition of suppressor cells.…”

Section: Discussionmentioning

confidence: 96%

Decrease in tumour growth by injections of histamine or serotonin in fibrosarcoma-bearing mice: Influence of H1 and H2 histamine receptors

Burtin¹,

Scheinmann²,

Salomon³

et al. 1982

Br J Cancer

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Summary.-C3H and C57 BL/6 mice carrying methylcholanthrene-induced fibrosarcomas were injected i.p. daily with histamine, metiamide (anti-histamine type-2 receptor), histamine + metiamide, mepyramine (anti-histamine type-i receptor), serotonin and methysergide (anti-serotonin). Inhibition of tumour growth and lengthened survival were observed with histamine and histamine+ metiamide. The best results (both on tumour growth and survival) were obtained with serotonin. Survival was increased by metiamide and decreased by mepyramine and methysergide. In histamine-treated and in serotonin-treated mice, histological studies of the tumours showed large and numerous foci of haemorrhagic necrosis.Stimulation of histamine type-I or serotonin receptors and inhibition of histamine type-2 receptors play a beneficial role in the host's defence against tumours.

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“…dose used in the present report. While this dose is much larger than CMT doses clinically recommended in man (up to 20 mg/ kg/day), peak murine plasma levels from this dose are comparable to levels obtained in man following standard doses (Gifford et al, 1981). Thus, the CMT dose used in the current study should be of biological significance in man.…”

Section: Resultsmentioning

confidence: 81%

“…Inactivation of suppressor cells by CMT indicated a direct immunological tumoricidal role for the drug. Simultaneously Gifford et al (1981) showed that CMT significantly reduces tumour formation and increases the survival of mice given the EL4 ascites lymphoma or the Mc43 fibrosarcoma. No direct in vitro cytoxicity of CMT was seen.…”

Section: Resultsmentioning

confidence: 96%

Cimetidine enhancement of cyclophosphamide antitumour activity

Dorr¹,

Alberts²

1982

Br J Cancer

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Summary.-Male DBA2 mice were given 106 P-388 leukaemic cells i.p. and cimetidine (CMT) at 100 mg/kg 1 day for 10 days, or as a single 100mg/kg injection 30 min before cyclophosphamide (CTX). CMT significantly prolonged the survival of groups of mice receiving 50, 100 and 200 mg/kg of CTX 3 days after tumour inoculation.Median survival increased by 5-5 days (P <0-05), 10 days (P <0.05) and 13 days (P < 0.05) respectively. The addition of CMT had the effect of roughly doubling the CTX dose, without increasing the lethality. CMT produced the only long-term survival seen in the study (1-2/10) CMT alone had no apparent antitumour activity. CMT significantly prolonged mean pentobarbital sleep to 28-6-60 min vs only 10 min for phenobarbital treated mice. Both CMT regimens increased the plasma concentration time products for CTX-induced metabolites (NBP) by about 1-3 fold (in contrast to a 33% reduction with phenobarbital). On average the single-dose CMT regimen produced the greatest effect on survival, on pentobarbital sleep duration and on total NBP reactive species. Probable mechanisms for the CMT-CTX interaction include competitive microsomal enzyme inhibition and/or acutely depressed hepatic blood flow. Caution should be used in combining CMT with full doses of CTX and any other highly metabolized antineoplastic agents in man.

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Cimetidine Reduction of Tumour Formation in Mice

Cited by 110 publications

References 7 publications

Cimetidine amplifies the anti-neoplastic effect of Trichinella spiralis in mice

Cimetidine amplifies the anti-neoplastic effect of Trichinella spiralis in mice

Decrease in tumour growth by injections of histamine or serotonin in fibrosarcoma-bearing mice: Influence of H1 and H2 histamine receptors

Cimetidine enhancement of cyclophosphamide antitumour activity

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