Inhibition by nomegestrol acetate and other synthetic progestins on proliferation and progesterone receptor content of T47-D human breast cancer cells

Botella, J.; Duranti, E; Duc, I.; A, Cognet; Delansorne, Remi; Pâris, J.

doi:10.1016/0960-0760(94)90170-8

Cited by 45 publications

(28 citation statements)

References 17 publications

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“…The PR content of T47D, measured by the affinity method, has been shown to be strongly down-regulated by NOMAC after 6 days of continuous treatment. 15 However, Western blotting (Fig. 1) showed persisting expression of PR protein after 3 days of continuous NOMAC treatment, and in higher amounts than in HMEC cultured in the same conditions.…”

Section: Discussionmentioning

confidence: 99%

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Effects of a progestogen on normal human breast epithelial cell apoptosis in vitro and in vivo

et al. 2003

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SUMMARYMany investigators have reported cyclic proliferation of normal human breast epithelial cells. A delicate balance between proliferation and apoptosis (programmed cell death) ensures breast homeostasis. Both the follicular and luteal phases of the menstrual cycle are characterized by proliferation, whereas apoptosis occurs only at the end of the latter phase. In this study, we observed that the withdrawal of a synthetic progestin (nomegestrol acetate or NOMAC), but not continuous treatment with it, induced apoptosis of normal human breast epithelial cells in vitro and in women who applied NOMAC gel to their breasts. Furthermore, this apoptotic response was specific to normal breast cells, since withdrawal of NOMAC did not induce apoptosis of tumoral T47D cells in vitro or of fibroadenoma cells in women. These observations open up new perspectives in the prevention of hyperplasia and breast cancer.

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Section: Discussionmentioning

confidence: 99%

“…14 Its half-life, which is longer than 3 days in the culture medium of T47-D cells, 15 affords highly steady-state concentrations if the medium is renewed daily.…”

Section: Introductionmentioning

confidence: 99%

Effects of a progestogen on normal human breast epithelial cell apoptosis in vitro and in vivo

et al. 2003

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“…First, it is well-known that progestagens induce PR downregulation in breast cancer cells in vitro (26), but this down-regulation is transient and disappears 48 hours after progestagen withdrawal (27). Second, the phenotype ER+/PRÀ may be due to overexpression of human epidermal growth factor receptor 2 (28).…”

Section: Discussionmentioning

confidence: 99%

Progestagens Use Before Menopause and Breast Cancer Risk According to Histology and Hormone Receptors

Fabre

Fournier

Mesrine

et al. 2008

Cancer Epidemiology, Biomarkers &Amp; Prevention

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In a previous study, we found a positive association between premenopausal use of progestagens and breast cancer risk. We conducted the present study to assess the risk of breast cancers defined by their histology and hormone receptors status. We evaluated the association between progestagen-only intake (except for mini pills) before menopause and after the age of 40 years and invasive breast cancer risk in 67,057 women participating in the French E3N cohort study. Histologically confirmed invasive breast cancers (2,264) were identified through biennial self-administered questionnaires completed from 1992 to 2002. Risk estimates were calculated using the Cox proportional hazard model. We found an increased risk of lobular carcinoma associated with premenopausal use of progestagens among both current and past users [hazard raatio (HR), 1.51; 95% confidence interval (95% CI), 1.02-2.24 and HR, 1.38; 95% CI, 1.08-1.75, respectively]. Among current users, the use of progestagens for 4.5 years or more was associated with an increased risk of estrogen receptor -positive/progesterone receptor -positive carcinomas (HR, 1.68; 95% CI, 1.05-2.68), whereas current use of progestagens for <4.5 years was associated with an increase in the estrogen receptor -positive/progesterone receptornegative carcinoma risk (HR, 1.61; 95% CI, 1.05-2.46). The premenopausal use of progestagens after the age of 40 years may be preferentially associated with the risk of lobular breast cancer and differentially affect the risk of breast cancer according to the hormone receptor status. (Cancer Epidemiol Biomarkers Prev 2008;17(10):2723 -8)

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“…As a 19-norP derivative, nomegestrol acetate (NOMAC, 17␣-acetoxy-6-methyl-19-nor-4,6-pregnadiene-3,20-dione) is a potent and clinically useful progestin devoid of androgenic, mineralocorticoid and estrogenic effects [25][26][27][28][29][30] that is used alone in France and some countries (Lutenyl ® ), or in combination with 17␤-estradiol (E 2 ) for HRT (Naemis ® ); It is under current development for OC. The main objective of the present review is to gather data already available and to concentrate on interaction with sex steroid receptors and the lack of estrogenic effects on breast cancer cells in vitro.…”

Section: Introductionmentioning

confidence: 99%

“…The effect is less clear-cut when the progestomimetic potency is considered ( Table 2). [27]. b Progestagenic activity measured as described in Paris et al [30] according to the method used by Clauberg [33] and modified by McPhail [34].…”

Section: Introductionmentioning

confidence: 99%

An overview of nomegestrol acetate selective receptor binding and lack of estrogenic action on hormone-dependent cancer cells

Shields-Botella¹,

Duc²,

Duranti³

et al. 2003

The Journal of Steroid Biochemistry and Molecular Biology

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Inhibition by nomegestrol acetate and other synthetic progestins on proliferation and progesterone receptor content of T47-D human breast cancer cells

Cited by 45 publications

References 17 publications

Effects of a progestogen on normal human breast epithelial cell apoptosis in vitro and in vivo

Effects of a progestogen on normal human breast epithelial cell apoptosis in vitro and in vivo

Progestagens Use Before Menopause and Breast Cancer Risk According to Histology and Hormone Receptors

An overview of nomegestrol acetate selective receptor binding and lack of estrogenic action on hormone-dependent cancer cells

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