Case--Control Study of Endogenous Steroid Hormones and Endometrial Cancer

Potischman, Nancy; Hoover, Robert N.; Brinton, Louise A.; Siiteri, Pentti K.; Dorgan, Joanne F.; Swanson, Christine A.; Berman, Michael L.; Mortel, Rodrigue; Twiggs, Leo B.; Barrett, Rolland J.; Wilbanks, George D.; Persky, Victoria; Lurain, John R.

doi:10.1093/jnci/88.16.1127

Cited by 274 publications

(186 citation statements)

References 38 publications

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“…Three additional manuscripts were excluded for not presenting risk estimates [9,18,19]. We also excluded three publications from the same case-control study [20][21][22], as these included a subset of the study population in the manuscript by Potischman et al [23]. One additional study [24] was excluded for having the same dietary data as in Littman et al, 2001 [25].…”

Section: Manuscript Selection and Data Extractionmentioning

confidence: 99%

Dietary lipids and endometrial cancer: the current epidemiologic evidence

Bandera

Kushi

Moore

et al. 2007

Cancer Causes Control

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Section: Manuscript Selection and Data Extractionmentioning

confidence: 99%

Dietary lipids and endometrial cancer: the current epidemiologic evidence

Bandera

Kushi

Moore

et al. 2007

Cancer Causes Control

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“…Many questions regarding endometrial cancer risk factors persist (10). For example, what changes occur at the cellular level to explain why exposures early in life (e.g., oral contraceptive use) reduce cancer risk decades after the exposure has ended?…”

Section: Epidemiologic Evidence For Two Pathways Of Endometrial Carcimentioning

confidence: 99%

“…Systemic estrogenism may be assessed by evaluating risk factor data and serum hormone levels, but interpretation of these data has been confusing, suggesting that simultaneous assessment of local tissue levels might be informative (10). Measurement of tissue hormone levels is a new, technically challenging area that suffers from some of the same limitations as single serum measurements obtained in case-control studies; it reflects only a single point in time when a tumor is already present.…”

Section: Classic Pathway Of Endometrial Carcinogenesis (Genesis Of Tymentioning

confidence: 99%

Theories of Endometrial Carcinogenesis: A Multidisciplinary Approach

2000

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Historical observations have suggested that endometrial carcinomas vary in histopathologic appearance and clinical features. More recent, systematic studies have provided epidemiologic, clinicopathologic, and molecular support for these observations. Specifically, studies suggest that the most common type of endometrial carcinoma, endometrioid adenocarcinoma, develops from endometrial hyperplasia in the setting of excess estrogen exposure and usually pursues an indolent clinical course. In contrast, a minority of endometrial carcinomas, best represented by serous carcinoma, do not seem to be related to estrogenic risk factors or elevated serum hormone levels, and these tumors seem to develop from atrophic rather than hyperplastic epithelium. We have proposed that serous carcinomas develop from "endometrial intraepithelial carcinoma," a lesion representing malignant transformation of the endometrial surface epithelium. Whereas endometrioid carcinoma and endometrial hyperplasia are associated with microsatellite instability and ras and PTEN mutations, serous carcinoma and endometrial intraepithelial carcinoma are associated with p53 mutations and abnormal accumulation of p53 protein. Based on these data regarding the pathogenesis of endometrioid and serous carcinoma, we have proposed a dualistic model of endometrial carcinogenesis incorporating a "classic" estrogen-driven pathway and an "alternative" pathway seemingly unrelated to hormones. It is hoped that further studies may permit the extension and modification of this model and that these advances will lead to improved diagnosis, management, and prevention.

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“…In women with polycystic ovary syndrome (PCOS), levels of SHBG are frequently low and may contribute to the hyperandrogenic phenotype of the syndrome (Kajaia et al, 2007). Changes in SHBG levels are also implicated in the pathogenesis of osteoporosis and hormone-dependent cancers (Goderie-Plomp et al, 2004;Lorentzon et al, 2005;The Endogenous Hormones and Breast Cancer Collaborative Group, 2002;Potischman et al, 1996;Weiss et al, 2008)). Thus, it is important to understand the factors that modulate SHBG levels.…”

Section: Introductionmentioning

confidence: 99%

Genetic variants of sex hormone-binding globulin and their biological consequences

Xita¹,

Tsatsoulis²

2010

Molecular and Cellular Endocrinology

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To cite this version:Nectaria Xita, Agathocles Tsatsoulis. Genetic variants of sex hormone-binding globulin and their biological consequences. Molecular and Cellular Endocrinology, Elsevier, 2009, 316 (1) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. ABSTRACTSeveral hormonal and metabolic factors have been found to influence the production of sex hormone-binding globulin (SHBG). In addition, twin studies have suggested that genetic factors may also contribute to variation in SHBG levels. Given the clinical significance of SHBG in regulating bioavailable sex steroid hormones, a number of studies examined the potential association between polymorphisms of SHBG gene and serum SHBG levels as well as their possible contribution in the pathogenesis of common diseases. Thus, polymorphisms of SHBG, altering either the production or the metabolism of the protein, may represent part of the genetic background of sex steroid hormone activity in humans. There is considerable heterogeneity in the results of these studies indicating the multiplicity of the factors influencing SHBG variation. However, the weight of evidence suggests that some common genetic variants of SHBG may influence SHBG levels and in part contribute to the phenotypic expression of human diseases.

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Case--Control Study of Endogenous Steroid Hormones and Endometrial Cancer

Abstract: Further research should focus on alternative endocrinologic mechanisms for risk associated with obesity and body fat distribution and for the biologic relevance of the increased risk associated with androstenedione in both premenopausal and postmenopausal disease.

Cited by 274 publications

References 38 publications

Dietary lipids and endometrial cancer: the current epidemiologic evidence

Dietary lipids and endometrial cancer: the current epidemiologic evidence

Theories of Endometrial Carcinogenesis: A Multidisciplinary Approach

Genetic variants of sex hormone-binding globulin and their biological consequences

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