Effect of anticarcinogens on the transplacental carcinogenic effect of N-nitroso-N-ethylurea

Беспалов, В. Г.; Александров, В. А.

doi:10.1007/bf00839318

Cited by 9 publications

(11 citation statements)

References 3 publications

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“…Postnatal treatment with buformin started from age 2 months significantly inhibited the development of malignant neurogenic tumors in rats transplancentally exposed to NMU. Similar results have been observed in rats exposed transplacentally to N-nitrosoethylurea (NEU) and postnatally to phenformin [200]. The authors observed decreased development of nervous system and renal tumors induced transplacentally with NEU.…”

Section: Pharmacological Modulation Of Gh/insulin/igf-1 Signaling supporting

confidence: 79%

The key role of growth hormone–insulin–IGF-1 signaling in aging and cancer

Anisimov

Bartke

2013

Critical Reviews in Oncology/Hematology

173

123

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Studies in mammals have led to the suggestion that hyperglycemia and hyperinsulinemia are important factors in aging. GH/Insulin/insulin-like growth factor 1 (IGF-1) signaling molecules that have been linked to longevity include daf-2 and InR and their homologues in mammals, and inactivation of the corresponding genes increases lifespan in nematodes, fruit flies and mice. The life-prolonging effects of caloric restriction are likely related to decreasing IGF-1 levels. Evidence has emerged that antidiabetic drugs are promising candidates for both lifespan extension and prevention of cancer. Thus, antidiabetic drugs postpone spontaneous carcinogenesis in mice and rats, as well as chemical and radiation carcinogenesis in mice, rats and hamsters. Furthermore, metformin seems to decrease the risk for cancer in diabetic patients.

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Section: Pharmacological Modulation Of Gh/insulin/igf-1 Signaling supporting

confidence: 79%

The key role of growth hormone–insulin–IGF-1 signaling in aging and cancer

Anisimov

Bartke

2013

Critical Reviews in Oncology/Hematology

173

123

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“…Postnatal treatment with buformin started from the age of 2 months significantly inhibited the development of malignant neurogenic tumors in rats transplacentally exposed to NMU 97. Similar results have been observed in rats exposed transplacentally to N‐nitrosoethylurea (NEU) and postnatally to phenformin 98. The authors observed the decrease of development of nervous system and renal tumors induced transplacentally with NEU.…”

Section: Effect Of Antidiabetic Drugs On Carcinogenesissupporting

confidence: 65%

“…97 Similar results have been observed in rats exposed transplacentally to Nnitrosoethylurea (NEU) and postnatally to phenformin. 98 The authors observed the decrease of development of nervous system and renal tumors induced transplacentally with NEU. The treatment with phenformin also inhibited the carcinogenesis induced by a single total-body X-ray irradiation in rats.…”

Section: Effect Of Antidiabetic Drugs On Carcinogenesismentioning

confidence: 98%

Central and Peripheral Effects of Insulin/IGF‐1 Signaling in Aging and Cancer: Antidiabetic Drugs as Geroprotectors and Anticarcinogens

Anisimov

Berstein

Popovich

et al. 2005

Annals of the New York Academy of Sciences

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Studies in mammals have led to the suggestion that hyperglycemia and hyperinsulinemia are important factors both in aging and in the development of cancer. Insulin/insulin-like growth factor 1 (IGF-1) signaling molecules linked to longevity include DAF-2 and insulin receptor (InR) and their homologues in mammals and to inactivation of the corresponding genes followed by increased life span in nematodes, fruit flies, and mice. It is possible that the life-prolonging effect of caloric restriction are due to decreasing IGF-1 levels. A search of pharmacological modulators of life span-extending mutations in the insulin/IGF-1 signaling pathway and mimetics of effects of caloric restriction could be a direction in the regulation of longevity. Some literature and our own observations suggest that antidiabetic drugs could be promising candidates for both life span extension and prevention of cancer.

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“…More recently, abnormalities in these essential biological systems have been associated with an increased incidence of human cancer. [1][2][3][4][5][6][7] While the treatment of these important host factors is typically multifactorial and complex, there is some evidence that the anti-diabetic biguanide drug metformin (1,1-dimethylbiguanide hydrochloride) reduces the incidence of several types of cancers, including breast cancer. Like obesity and diabetes, breast cancer is both highly prevalent and morbid and there is significant overlap in the affected patient populations.…”

Section: Introductionmentioning

confidence: 99%

“…22,23 Metformin and related compounds, which include phenformin (1-phenylethylbiguanide), buformin (N-butylbiguanide), that counterbalance aberrant glucose metabolism have been shown to inhibit mammary tumorigenesis in rodent models (spontaneous or carcinogen induced) as well. [1][2][3][4][5][6][7]24 Metformin has most recently been shown…”

Section: Introductionmentioning

confidence: 99%

Metformin inhibits breast cancer cell growth, colony formation and induces cell cycle arrest in vitro

Alimova

Fan²,

Edgerton³

et al. 2009

Cell Cycle

464

348

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The anti-diabetic drug metformin reduces human cancer incidence and improves the survival of cancer patients, including those with breast cancer. We studied the activity of metformin against diverse molecular subtypes of breast cancer cell lines in vitro. Metformin showed biological activity against all estrogen receptor (ER) positive and negative, erbB2 normal and abnormal breast cancer cell lines tested. It inhibited cellular proliferation, reduced colony formation and caused partial cell cycle arrest at the G(1) checkpoint. Metformin did not induce apoptosis (as measured by DNA fragmentation and PARP cleavage) in luminal A, B or erbB2 subtype breast cancer cell lines. At the molecular level, metformin treatment was associated with a reduction of cyclin D1 and E2F1 expression with no changes in p27(kip1) or p21(waf1). It inhibited mitogen activated protein kinase (MAPK) and Akt activity, as well as the mammalian target of rapamycin (mTOR) in both ER positive and negative, erbB2-overexpressing and erbB2-normal expressing breast cancer cells. In erbB2-overexpressing breast cancer cell lines, metformin reduced erbB2 expression at higher concentrations, and at lower concentrations within the therapeutic range, it inhibited erbB2 tyrosine kinase activity evidenced by a reduction of phosphorylated erbB2 (P-erbB2) at both auto- and Src- phosphorylation sites. These data suggest that metformin may have potential therapeutic utility against ER positive and negative, erbB2-overexpressing and erbB2-normal expressing breast cancer cells.

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Effect of anticarcinogens on the transplacental carcinogenic effect of N-nitroso-N-ethylurea

Cited by 9 publications

References 3 publications

The key role of growth hormone–insulin–IGF-1 signaling in aging and cancer

The key role of growth hormone–insulin–IGF-1 signaling in aging and cancer

Central and Peripheral Effects of Insulin/IGF‐1 Signaling in Aging and Cancer: Antidiabetic Drugs as Geroprotectors and Anticarcinogens

Metformin inhibits breast cancer cell growth, colony formation and induces cell cycle arrest in vitro

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