Oestrogen and colonic epithelial cell growth.

Singh, Sukhdev; Langman, M. J. S.

doi:10.1136/gut.37.6.737

Cited by 32 publications

(21 citation statements)

References 33 publications

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“…Animal models showed that male rats had a higher risk developing colon cancer compared with their female counterparts when exposed to dimethylhydrazine, an experimental carcinogen. The results indicated that 17β-oestradiol (E 2 ) treatment could significantly reduce the frequency of dimethylhydrazine-induced large intestinal tumors in rats [1][2][3] . These evidences suggest that estrogen maybe involved in the growth of colonic tumors.…”

Section: Introductionmentioning

confidence: 87%

“…Some experimental results indicated that estrogen had a trophic effect on colon cancer [1,[11][12] . However, the effect of estrogen on colon cancer is controversial according to some reports.…”

Section: Discussionmentioning

confidence: 99%

“…Several epidemiologic studies have shown that colon cancer might be influenced by steroid hormones [1][2][3] , and estrogen use might be associated with a low risk of colon cancer [21][22][23][24][25][26][27] . Some experimental results indicated that estrogen had a trophic effect on colon cancer [1,[11][12] .…”

Section: Discussionmentioning

confidence: 99%

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Expression of estrogen receptor ® in human colorectal cancer

Xie¹,

Yu²,

Luo³

2004

WJG

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Section: Introductionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

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Expression of estrogen receptor ® in human colorectal cancer

Xie¹,

Yu²,

Luo³

2004

WJG

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“…Estrogens and androgens regulate growth, differentiation, and functioning of a variety of tissues, including that found in the gastrointestinal tract (33)(34)(35). Most of the action of estrogens and androgens seems to be exerted through the respective receptors of target cells (13,14).…”

Section: Discussionmentioning

confidence: 99%

Associations between ERα, ERβ, and AR Genotypes and Colon and Rectal Cancer

Slattery¹,

Sweeney²,

Murtaugh³

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Estrogen and androgens are thought to be involved in the etiology of colorectal cancer. We evaluate genetic variants of the estrogen receptor genes (ERa and ERb) and the androgen receptor gene (AR). We use data from two large case-control studies of colon (n = 1,580 cases and 1,968 controls) and rectal (n = 797 cases and 1,016 controls) cancer. We evaluated the 351A>G XbaI polymorphism of ERa, the 1,082 G>A and CA repeat polymorphisms of ERb, and the CAG repeat of AR. Having two 25 or more CA repeats in ERb was associated with an increased relative risk of colon cancer in women [odds ratio (OR), 2.13; 95% confidence interval (95% CI), 1.24-3.64] but not in men (P interaction relative excess risk from interaction < 0.01; multiplicative = 0.03). Increasing number of AR CAG repeats was directly associated with colon cancer among men (OR, 1.28; 95% CI, 1.06-1.54), but not women (OR, 0.83; 95% CI, 0.68-1.02); the interaction P value for AR gene Â sex was <0.01. Taking hormone replacement therapy (HRT) was associated with a reduced risk of colon cancer in the presence of the R allele of the ERb gene, whereas an R allele was associated with increased risk among postmenopausal women who did not take HRT. Postmenopausal women not using HRT who had z25 CA repeats of the ERb gene had over a 6-fold increased risk of colon cancer (OR, 6.71; 95% CI, 2.89-15.6). Our results suggest that the ERb gene is more important than ERA in the etiology of colorectal cancer. (Cancer Epidemiol Biomarkers Prev 2005;14(12):2936 -42)

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“…Both groups of hormones are involved in the control of cell proliferation and differentiation of several tissues, including those found in the gastrointestinal tract [2,3]. The effects of estrogens and androgens are mediated through specific receptors in the target cells where they exert their action [4,5].…”

Section: Introductionmentioning

confidence: 99%