N-Nitrosomethylurea-Induced Rat Mammary Tumours as Models of Human Breast cancer

Gusterson, B A; Williams, J C

doi:10.1177/014107688107400111

Cited by 7 publications

(9 citation statements)

References 5 publications

(4 reference statements)

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“…All experimental procedures and protocols were approved by the Animal Care and Use Committee of the Airlangga University (ethical clearance no. 062-KE), and complied with the guidelines of `Guide for the Care and Use of Laboratory Animals` [8].…”

Section: Experimental Animal Modelmentioning

confidence: 99%

Apoptotic effect of Physalis minima Linn ethanol extract on breast cancer cells via p53 wild-type and Apaf-1 protein

Handayani¹,

Handajani²,

Susilo³

et al. 2020

Trop. J. Pharm Res

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Purpose: To produce an anti-cancer agent from Physalis minima ethanol extract as well as prevent the growth of NMU-induced breast cancer and MCF-7 cell line.Methods: This research used an animal model (Wistar-Furth rats), and cell line used in this study was normal breast-cell line MCF-7. The rats were administered with the ethanol extract of Physalis minima Linn (100, 250 and 400 mg/kg/day) by gavage, once a day for 4 weeks. Meanwhile, MCF-7 cell lines were cultured in medium and incubated in 100 μg/mL of ethanol extract of Physalis minima for 48 h. The samples were analyzed using histology and immunohistochemistry techniques for expression of p53 antibody DO-1 and APAF-1.Results: The results of immunohistological analysis in the breast organ showed that Physalis minima Linn extract significantly (p < 0.05) increased the tumor suppressor protein p53 at doses of 100, 250 and 400 mg/kg/day. In addition, the extract also significantly (p < 0.05) increased APAF-1, which is a gene determining cell death, at doses of 100, 200 and 400 mg/day.Conclusion: Ethanol extract of Physalis minima Linn inhibits the cytotoxic activity of NMU-induced breast cancer by increasing the tumor suppressor protein p53 and APAF-1. Thus, Physalis minima Linn extract can potentially be used as a complementary treatment for inhibiting the growth of breast cancer cells in patients. Keywords: Apoptosis protease-activating factor-1, Breast cancer, MCF-7 cell line, Physalis minima, p53

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Section: Experimental Animal Modelmentioning

confidence: 99%

Apoptotic effect of Physalis minima Linn ethanol extract on breast cancer cells via p53 wild-type and Apaf-1 protein

Handayani¹,

Handajani²,

Susilo³

et al. 2020

Trop. J. Pharm Res

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“…The MNU induction model is a standard paradigm for studying breast tumors in rats. (9)(10)(11)(12) Tumors are induced at rates exceeding 50%…”

Section: Experimental Modelmentioning

confidence: 99%

“…In contrast, 10 weeks after injection of MNU, we observed a 1% to 5% detriment to BMD, a 14% to 21% detriment to strength, and a 6% to 14% detriment to structure at the epiphysis and a 22% to 27% detriment to structure at the metaphysis. MNU induction is a well-accepted rodent breast cancer model, (12,14,35) but it is not without limitations. (11,12) Thompson and Singh (9) describe a course of MNU-induced tumors that is analogous to human breast cancer, although markedly more rapid.…”

Section: Mnu-induced Breast Tumors On Bone Health In Rats (Figs 2 Thmentioning

confidence: 99%

“…MNU induction is a well-accepted rodent breast cancer model, (12,14,35) but it is not without limitations. (11,12) Thompson and Singh (9) describe a course of MNU-induced tumors that is analogous to human breast cancer, although markedly more rapid. They also note, however, that the cellular processes underlying chemically induced cancer models are not well understood at this time.…”

Section: Mnu-induced Breast Tumors On Bone Health In Rats (Figs 2 Thmentioning

confidence: 99%

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Breast tumors induced by N-methyl-N-nitrosourea are damaging to bone strength, structure, and mineralization in the absence of metastasis in rats

Thorpe

Valentine

Moulton

et al. 2010

Journal of Bone and Mineral Research

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Current theory on the influence of breast cancer on bone describes metastasis of tumor cells to bone tissue, followed by induction of osteoclasts and bone degradation. Tumor influences on bone health in pre-or nonmetastatic models are unknown. Female rats (n ¼ 48, 52 days old) were injected with N-methyl-N-nitrosourea (MNU) to induce breast cancer. Animals were euthanized 10 weeks later, and tumors were weighed and classified histologically. Right femurs were extracted for testing of bone mineral density (BMD) by dual X-ray absorptiometry (DXA), bone mechanical strength by three-point bending and femoral neck bending tests, and structure by microcomputed tomography (mCT). Of 48 rats, 22 developed one or more tumors in response to MNU injection by 10 weeks. Presence of any tumor predicted significantly poorer bone health in 17 of 28 measures. In tumored versus nontumored animals, BMD was adversely affected by 3%, force at failure of the femoral midshaft by 4%, force at failure of the femoral neck by 12%, and various trabecular structural parameters by 6% to 27% (all p < .05). Similarly, greater tumor burden, represented by total tumor weight, adversely correlated with bone outcomes: r ¼ À0.51 for BMD, À0.42 and À0.35 for femur midshaft force and work at failure, and between 0.36 and 0.59 (absolute values) for trabecular architecture (all p < .05). Presence of MNU-induced tumors and total tumor burden showed a negative association with bone health of the femur in rats in the absence of metastasis. Further study is required to elucidate mechanisms for this association. ß

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“…This model has previously been used to develop tamoxifen therapy in women with breast cancer [7], and is considered to be appropriate for studies of novel compounds potentially useful for the treatment of breast cancer. Substantial evidence suggests that this rodent model system mimics human breast cancer: the initiation of cancer occurs primarily at the same site in both humans and rats, the majority of the tumors express estrogen and progesterone receptors, and tumor development is dependent on the reproductive history, diet, and hormonal milieu [8]. Thus the model provides an opportunity to examine cause-and-effect relationships of the in situ environment fully impacted by systemic factors [9].…”

Section: Introductionmentioning

confidence: 99%

17α-Ethynyl-5α-androstane-3α, 17β-diol Treatment of MNU-Induced Mammary Cancer in Rats

Ahlem¹,

Frincke²,

White³

et al. 2011

International Journal of Breast Cancer

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N-methyl-N-nitrosourea (MNU) induces estrogen-dependent mammary tumors in female Lewis rats. We explored the antineoplastic activity of a synthetic androstane derivative, 17α-ethynyl-5α-androstane-3α, 17β-diol (HE3235), as a single agent or in combination with docetaxel compared to tamoxifen, anastrazole, and docetaxel monotherapies against MNU-induced mammary tumors in female Lewis rats. Treatment with HE3235 alone rapidly reduced tumor burden, similar in effect to tamoxifen and anastrozole. The combination of HE3235 with docetaxel was more effective than any single agent, although without apparent toxicity. Only HE3235 or HE3235 plus docetaxel continued to suppress tumor growth after cessation of treatment. HE3235 treatment increased immunohistochemical markers of apoptosis and expression of proapoptotic genes and estrogen receptor beta and decreased expression of antiapoptotic genes, androgen receptor, and estrogen receptor alpha. These data warrant clinical investigation of HE3235 for breast cancer treatment.

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N-Nitrosomethylurea-Induced Rat Mammary Tumours as Models of Human Breast cancer

Cited by 7 publications

References 5 publications

Apoptotic effect of Physalis minima Linn ethanol extract on breast cancer cells via p53 wild-type and Apaf-1 protein

Apoptotic effect of Physalis minima Linn ethanol extract on breast cancer cells via p53 wild-type and Apaf-1 protein

Breast tumors induced by N-methyl-N-nitrosourea are damaging to bone strength, structure, and mineralization in the absence of metastasis in rats

17α-Ethynyl-5α-androstane-3α, 17β-diol Treatment of MNU-Induced Mammary Cancer in Rats

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