Pregnancy, progesterone and progestins in relation to breast cancer risk

Campagnoli, C; Abbà, Chiara; Ambroggio, Simona; Peris, Clementina

doi:10.1016/j.jsbmb.2005.08.015

Cited by 35 publications

(20 citation statements)

References 104 publications

(142 reference statements)

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“…The association of estrogen-dydrogesterone combinations with a nonsignificantly elevated relative risk in our study reinforces the plausibility of our finding since the retroprogesterone dydrogesterone is the progestin with the chemical structure and pharmacological effects closest to those of progesterone. The high degree of androgenicity of progestins used in certain HRTs has been hypothesized to play a role in the increased risk of breast cancer [5]. Our results do not support this hypothesis, as, when combined with an estrogen, neither promegestone, nomegestrol acetate, chlormadinone acetate or medrogestone (all nonandrogenic progestagens) nor cyproterone acetate (an antiandrogenic progestagen) had effects that differed significantly from that of norethisterone acetate (the most androgenic progestagen cited).…”

Section: Discussioncontrasting

confidence: 86%

“…However, small structural changes in progestagens may considerably alter their effects [2,3]. Until now, most studies have evaluated estrogen associated with medroxyprogesterone acetate or 19-nortestosterone derivatives [4,5], but other combined estrogen-progestagen therapies are used around the world and it is still unclear whether some are more hazardous than others. The relationship between estrogen-only therapy and breast cancer risk is also the subject of intense debate: unopposed estrogen use was associated with a decreased risk of breast cancer in the Women's Health Initiative (WHI) trial [6], but not in some observational studies [7][8][9][10][11][12][13][14].…”

Section: Introductionmentioning

confidence: 99%

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Unequal risks for breast cancer associated with different hormone replacement therapies: results from the E3N cohort study

Fournier

Berrino

Clavel‐Chapelon

2007

Breast Cancer Res Treat

555

156

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Large numbers of hormone replacement therapies (HRTs) are available for the treatment of menopausal symptoms. It is still unclear whether some are more deleterious than others regarding breast cancer risk. The goal of this study was to assess and compare the association between different HRTs and breast cancer risk, using data from the French E3N cohort study. Invasive breast cancer cases were identified through biennial self-administered questionnaires completed from 1990 to 2002. During follow-up (mean duration 8.1 postmenopausal years), 2,354 cases of invasive breast cancer occurred among 80,377 postmenopausal women. Compared with HRT never-use, use of estrogen alone was associated with a significant 1.29-fold increased risk (95% confidence interval 1.02-1.65). The association of estrogen-progestagen combinations with breast cancer risk varied significantly according to the type of progestagen: the relative risk was 1.00 (0.83-1.22) for estrogen-progesterone, 1.16 (0.94-1.43) for estrogen-dydrogesterone, and 1.69 (1.50-1.91) for estrogen combined with other progestagens. This latter category involves progestins with different physiologic activities (androgenic, nonandrogenic, antiandrogenic), but their associations with breast cancer risk did not differ significantly from one another. This study found no evidence of an association with risk according to the route of estrogen administration (oral or transdermal/percutaneous). These findings suggest that the choice of the progestagen component in combined HRT is of importance regarding breast cancer risk; it could be preferable to use progesterone or dydrogesterone.

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Section: Discussioncontrasting

confidence: 86%

Section: Introductionmentioning

confidence: 99%

Unequal risks for breast cancer associated with different hormone replacement therapies: results from the E3N cohort study

Fournier

Berrino

Clavel‐Chapelon

2007

Breast Cancer Res Treat

555

156

View full text Add to dashboard Cite

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“…While the nature of the differential functions of progestational agents during pregnancy are incompletely understood, current understanding clearly supports dramatic differences between these agents with respect to tissue specificity, receptor binding affinity, and potency. [21][22][23] Work in this arena is needed, particularly in light of published reports of benefit of vaginal P vis-a-vis prematurity prevention. 24 Table I Genes in the Toll-like receptor signaling pathway, grouped by functional category.…”

Section: Commentmentioning

confidence: 99%

Human decidual cell Toll-like receptor signaling in response to endotoxin: The effect of progestins

Simhan

Chiao

Mattison

et al. 2008

American Journal of Obstetrics and Gynecology

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Objective-To determine if progesterone (P), 17-α-hydroxyprogesterone (17OHP) and 17-α hydroxyprogesterone caproate (17OHPC) modulate the Toll-like receptor (TLR) pathway in the response of decidua to lipopolysaccharide.Study Design-Cultured human decidual cells were incubated under control conditions, lipopolysaccharide alone, or pretreatment with each of the three progestins. Relative expression of 113 genes in the TLR pathway was determined using microarray.Results-We failed to demonstrate a suppression of TLR gene pathway expression in human decidual cells in response to lipopolysaccharide when pretreated with progestins. Pretreatment with each progestin prior to lipopolysaccharide resulted in a relative increase in the expression of the proapoptotic molecule, CASP8. There were no differences among the progestins.Conclusions-Our data do not support suppression of TLR pathways as a mechanism for the benefit of 17OHPC. Increased CASP8 gene expression raises the possibility that progestins "prime" the decidual cell to respond with a NFκB-mediated inflammatory response.

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“…shorter duration of dominant progesterone effect) is associated with an increased risk of developing breast cancer [6]. The risk of colon cancer is increased in breast cancer patients, most likely also on the basis of a relative lack of progesterone [5].…”

Section: Progestogens and Estrogens In Colon Cancermentioning

confidence: 99%

Long-term use of progestogens: Colon adenoma and colon carcinoma

Schindler¹

2007

Gynecological Endocrinology

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Colon cancer is the second most common cancer in women in the Western world and there is a trend towards an increasing risk. Colon adenoma is a potential precursor for colon cancer. Adenoma and carcinoma of the colon seem to be influenced by estrogens and progesterone/progestins. This is related to the presence of estrogen and progesterone receptors, with apparently higher concentrations in colon cancers than in adenomas. Epidemiological data and the finding of a significant reduction in colon cancer risk related to hormone replacement therapy (HRT), and in particular the length of HRT intake, indicate that progesterone/progestins have a preventive effect. This has not been shown with postmenopausal estrogen replacement therapy (ERT) alone. Furthermore, the recurrence rate of adenoma appears to be reduced, and the survival of colon cancer patients improved, with HRT; such effects have not been documented with ERT.

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Pregnancy, progesterone and progestins in relation to breast cancer risk

Cited by 35 publications

References 104 publications

Unequal risks for breast cancer associated with different hormone replacement therapies: results from the E3N cohort study

Unequal risks for breast cancer associated with different hormone replacement therapies: results from the E3N cohort study

Human decidual cell Toll-like receptor signaling in response to endotoxin: The effect of progestins

Long-term use of progestogens: Colon adenoma and colon carcinoma

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