Estrogen modification of 1,2-dimethylhydrazine carcinogenesis in C3HA mice

Turusov, V. S.; Морозова, О. В.; Samoilov, Dmitry

doi:10.1016/0304-3835(94)90298-4

Cited by 7 publications

(7 citation statements)

References 4 publications

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“…Persistent estrus produced by DES in C3HA mice inhibited the induction by DMH of clitoral gland tumors. The same effect was observed in the experiment referred to above [6] with the combined treatment of C3HA mice with DMH and EP. It appears that clitoral gland tumors induced by DMH in C3HA mice present a model rather sensitive to the modifying effect of estrogens-exogenous or endogenous.…”

Section: Discussionsupporting

confidence: 83%

“…), while the incidence of uterine sarcoma changed only at the DES dose of 1 mg/kg. Alteration by prenatal DES of the HOL incidence is similar on the whole to that produced in mice of the same strain receiving combined treatment with DMH and exogenous estrogen-estradiol dipropionate (EP): continuous administration of DMH and EP to adult C3HA females completely inhibited (from 59% to 0) the induction of HOL by DMH [6]. These lesions, particularly those reaching a large size, were not infrequently the immediate cause of animal death due to their rupture into the abdominal cavity.…”

Section: Discussionmentioning

confidence: 73%

“…In both of these studies, the effect of hyperestrogenization-exogenous or endogenous as in case of the neonatal androgenization-was much more pronounced (much higher uterine tumor incidence and much earlier appearance) than in the experiment presented here. Likewise, the effect of exogenous estrogen in the induction of uterine sarcomas in C3HA mice treated with DMH (from 0 to 28%) [6] was much stronger than the non-significant increase of these tumors in C3HA mice treated with DMH after prenatal DES. However, in the experiments referred to with the exogenous EP-either in C3HA or in CBA mice-the estrogen was applied at high doses for many weeks.…”

Section: Discussionmentioning

confidence: 86%

“…In CBA mice, on the contrary, a high incidence of uterine sarcomas and a very low incidence of hemorrhagic ovarian lesions are induced by DMH [4]. These mesenchymal lesions of the ovaries and of the uterus are strongly sex hormone dependent [5,6] and therefore seem to be a convenient model for studying the effect of perinatal hormone treatment. A previous study in CBA mice has shown that neonatal androgenization greatly altered the carcinogenesis induced by a subsequent DMH treatment [7].…”

Section: Introductionmentioning

confidence: 98%

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1,2-dimethylhydrazine carcinogenesis in C3HA and CBA female mice prenatally treated with diethylstilbestrol

Turusov

Trukhanova

Lanko

et al. 1997

Teratog. Carcinog. Mutagen.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 73%

Section: Discussionmentioning

confidence: 86%

Section: Introductionmentioning

confidence: 98%

See 2 more Smart Citations

1,2-dimethylhydrazine carcinogenesis in C3HA and CBA female mice prenatally treated with diethylstilbestrol

Turusov

Trukhanova

Lanko

et al. 1997

Teratog. Carcinog. Mutagen.

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“…lC, D) and in control uterine tissue, suggesting that there was a hormonal component to the pathogenesis of the uterine sarcomas (Tables I1 and 111). In some primary and transplanted tumors, the estrogen receptor was not detected, The stimulation of uterine sarcomas by estrogens has been repeatedly documented (37)(38)(39). The presence of the estrogen receptor was not correlated with a specific tumor type, stage, or p53 staining.…”

Section: Resultsmentioning

confidence: 99%

Predominant p53 G→A Transition Mutation and Enhanced Cell Proliferation in Uterine Sarcomas of CBA Mice Treated with 1,2-Dimethylhydrazine

et al. 1998

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A B S T R A~Mouse uterine tumors were examined for genetic alterations in the rus proto-oncogene and p53 tumor suppressor gene and for other biologically relevant immunohistochemical markers that may increase our understanding of the events that occur in uterine cancer. Fourteen dimethylhydrazine (DMH)-induced uterine sarcomas, including 3 primary malignant fibrous histiocytomas (MFH). 7 transplanted MFH, 3 stroinal sarcomas, and 1 undifferenthed sarcoma; were first screened by immunohistochemistry for p53 missense mutations, followed by single strand conformation polymorphism analysis and DNA sequencing for the identification of point mutations. There was 1 0 0 8 correlation between p53 protein immunopositivity and subsequent detection of p53 mutations in DMH-induced malignant fibrous histiocytomas. All M R I had a characteristic p53 G:C+A:T transition mutation. consistent with 06-methylguanine mispairing with thymine, the most common DNA lesion caused by alkylating agents. DMH-induced uterine MFH with p53 mutations also had a higher proliferative rate (qualitatively evaluated by immunohistochemical detection of proliferating cell nuclear antigen) when compared with other DMH-induced sarcomas. Uterine sarcomas were further evaluated for biological end points, such as estrogen receptor and desmin. Neoplastic cells from stromal sarcomas (SS), undifferentiated sarcomas (US), and MFH did not stain for desmin.The estrogen receptor was detected in normal uteri and a small portion of MFH, SS, and US. Our data suggest that DIMH-induced uterine sarcomas are not consistent with smooth muscle cell origin and that a subset of these tumors, specifically DIMH-induced malignant fibrous histiocytomas, have unique p53 G:C-tA:T transitions and a high proliferative rate.

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Carcinogenicity of intermediate frequency magnetic field in Tg.rasH2 mice

Nishimura

Doi²,

Imai³

et al. 2019

Bioelectromagnetics

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Although the likelihood of exposure to leaking intermediate frequency magnetic fields (MFs) from electronic devices, such as induction‐heating and wireless power transfer systems, has increased, biological data assessing the health risks associated with human exposure remain insufficient. We examined the carcinogenicity of a 20 kHz MF, a typical frequency produced by induction‐heating cookers, using a transgenic rasH2 mouse model. Twenty‐five male and female CByB6F1‐Tg(HRAS)2Jic mice were exposed to a 0.20 mT, 20 kHz MF (22 h/day) or sham‐exposed for 26 weeks. As a positive control, 10 male and female rasH2 mice from the same batch were administered a single intraperitoneal injection of 75 mg/kg N‐methyl‐N‐nitrosourea. A blinded histopathological evaluation was performed, and the same experiments were conducted twice, independently, to confirm the reproducibility of the results. Histopathological examination revealed that spontaneous neoplastic lesions, such as splenic hemangiosarcomas and gastric squamous cell papillomas, were less (1–3 per group) in the MF‐ and sham‐exposed groups. The frequency of the neoplastic lesions was not significantly different between the groups. Eight to ten mice in each positive‐control group exhibited malignant lymphoma. The outcomes were consistent between duplicated experiments, which indicates lack of carcinogenicity of 20 kHz MF in the rasH2 mouse model. Bioelectromagnetics. © 2019 The Authors. Bioelectromagnetics Published by Wiley Periodicals, Inc.

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Estrogen modification of 1,2-dimethylhydrazine carcinogenesis in C3HA mice

Cited by 7 publications

References 4 publications

1,2-dimethylhydrazine carcinogenesis in C3HA and CBA female mice prenatally treated with diethylstilbestrol

1,2-dimethylhydrazine carcinogenesis in C3HA and CBA female mice prenatally treated with diethylstilbestrol

Predominant p53 G→A Transition Mutation and Enhanced Cell Proliferation in Uterine Sarcomas of CBA Mice Treated with 1,2-Dimethylhydrazine

Carcinogenicity of intermediate frequency magnetic field in Tg.rasH2 mice

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