Histological studies and measurement of nucleic acid synthesis in rat mammary tumours induced by 9,10‐dimethyl‐1,2‐benzanthracene (DMBA)

Stevens, Lucas H.; Stevens, Evelyn; Currie, A. R.

doi:10.1002/path.1700890217

Cited by 19 publications

(3 citation statements)

References 15 publications

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“…The surviving rats were palpated twice a week from the fourth week after injection. Tumours were measured and charted as described previously (Stevens, Stevens and Currie, 1965). The experiment was terminated at 6 months and an assessment * Requests for reprints to Dr. D. N. Wheatley. was made of tumour types from their growth curves and histological appearances as described by Stevens et al, 1965.…”

Section: Methodsmentioning

confidence: 99%

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The effect of liver interference on mammary tumour induction by 7,12-dimethylbenz(a)anthracene in Sprague-Dawley rats.

Kernohan¹,

Inglis²,

Wheatley³

1967

Br J Cancer

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7,12-DIMETHYLBENz(a)ANTHRACENE (DMBA) given in a single dose (30 mg.). in oil by stomach tube or intravenously (5 mg.) in lipid emulsion induces mammary tumours in Sprague-Dawley rats within 2-3 months (Huggins, Briziarelli and Sutton, 1959;Huggins, Grand and Brillantes, 1961), and also causes severe adrenal necrosis within 2-3 days (Huggins and Morii, 1961). We have shown that DMBA itself is probably not responsible for adrenal necrosis (Wheatley, Kernohan and Currie, 1966;Wheatley, Hamilton, Currie, Boyland and Sims, 1966) but must first be metabolized by the liver. Boyland and Sims (1965) found that DMBA is metabolized by rat liver mainly by hydroxylation of the methyl groups; 7-hydroxymethyl-12-methylbenz(a)anthracene is probably the adrenocorticolytic metabolite (Boyland, Sims and Huggins, 1965;Wheatley, Hamilton, Currie, Boyland and Sims, 1966). Boyland et al. (1965) tested the carcinogenicity of DMBA and its hydroxymethyl derivatives in rats and mice. Briefly, the 7-hydroxymethyl derivative induced mammary tumours but with a longer mean induction time than DMBA whereas the 12-hydroxymethyl derivative was not carcinogenic in rats although it was in mice.It is also possible that a metabolite of DMBA, and not DMBA itself, is responsible for tumour induction. We have therefore tested the ability of DMBA ta produce tumours in rats with impaired liver function. MATERIALS AND METHODSSprague-Dawley female rats from an accredited stock were obtained from Oxford Laboratory Animal Colonies, Oxford, England. CC14 (AnalaR) was given to 60 rats at a dose of 0 3 ml. of a 50% solution in olive oil intraperitoneally.Forty-three rats were partially hepatectomized, two-thirds of the liver being removed by the method of Higgins and Anderson (1931). Forty rats were given olive oil intraperitoneally (013 ml.) as controls. Twenty-four hours later the rats received 5 mg. DMBA in 1V0 ml. 15 % cottonseed oil emulsion via a lateral tail vein. At the time of DMBA injection rats were 50 days old and weighed about 150 g.The severity of the combined treatments resulted in a high early mortality. The surviving rats were palpated twice a week from the fourth week after injection. Tumours were measured and charted as described previously (Stevens, Stevens and Currie, 1965). The experiment was terminated at 6 months and an assessment

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

The effect of liver interference on mammary tumour induction by 7,12-dimethylbenz(a)anthracene in Sprague-Dawley rats.

Kernohan¹,

Inglis²,

Wheatley³

1967

Br J Cancer

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“…DNA activity is greatest in least differentiated and most rapidly growing tumors. 39 We utilized these nucleic acid determinations in order to provide further measurable evidence of the morphological tissue changes caused by iodine deficiency in the breast. In addition, these data should reflect the cellular metabolic responses seen in breast tissues that have become dysplastic or neoplastic because of iodine inadequacy.…”

Section: R N a And D N A Determinationsmentioning

confidence: 99%

Section of Biological and Medical Sciences: IODINE METABOLISM AND BREAST CANCER*,†

Eskin

1970

Trans NY Acad Sci

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Combination of cyclophosphamide and estrogen therapy in dmba-induced rat mammary cancer

Kiang

Kennedy

1971

Cancer

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The effect of estrogen plus cyclophosphamide combination therapy was evaluated in DMBA‐induced mammary tumors in rats. These tumors were stimulated by estrogen therapy, especially when low doses were used. Well‐differentiated tumors were more vulnerable to this stimulation. A tumor, once stimulated by low‐ dose estrogen therapy, could progress or regress under the continuation of therapy and this outcome seemed to be related to its original growth pattern. Cyclophosphamide significantly inhibited the initial stimulatory effect induced by estrogen therapy. However, it also reduced the regression rate induced by high doses of estrogen. A corollary to human breast cancer may exist.

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Histological studies and measurement of nucleic acid synthesis in rat mammary tumours induced by 9,10‐dimethyl‐1,2‐benzanthracene (DMBA)

Cited by 19 publications

References 15 publications

The effect of liver interference on mammary tumour induction by 7,12-dimethylbenz(a)anthracene in Sprague-Dawley rats.

The effect of liver interference on mammary tumour induction by 7,12-dimethylbenz(a)anthracene in Sprague-Dawley rats.

Section of Biological and Medical Sciences: IODINE METABOLISM AND BREAST CANCER*,†

Combination of cyclophosphamide and estrogen therapy in dmba-induced rat mammary cancer

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