Oestrogen and the colon: potential mechanisms for cancer prevention

Kennelly, Rory; Kavanagh, Dara; Hogan, Aisling; Winter, Desmond C.

doi:10.1016/s1470-2045(08)70100-1

Cited by 138 publications

(138 citation statements)

References 65 publications

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“…Estrogen receptors influence cellular growth by regulating gene transcription (Ascenzi et al 2006). In the colon, ERa is expressed at low levels, and ERb is thought to be the primary mediator of sex steroid effects on colonic tissue (Kennelly et al 2008). ERa and ERb differ in their transcriptional functions, although they are highly homologous in their structural and functional domains and show similar DNA-binding properties and estrogen-binding affinities (McInerney et al 1998, Delaunay et al 2000, Ascenzi et al 2006.…”

Section: Discussionmentioning

confidence: 99%

“…Both estrogen receptor a (ERa) and ERb can be detected in colon tissue, while ERb is found to be more prevalent than ERa (Foley et al 2000, Konstantinopoulos et al 2003, Jassam et al 2005. Loss of ERb has been related to advanced tumor progression (Kennelly et al 2008) and recent cell line studies support the assumption that estrogen acts via ERb as an inhibitor of malignant cell growth (Hartman et al 2009, Wilkins et al 2010.…”

Section: Introductionmentioning

confidence: 92%

“…An increasing body of evidence points to the involvement of sex steroids in development and progression of colorectal cancer (CRC; Kennelly et al 2008, Koo & Leong 2010. Inverse associations between CRC risk and menopausal hormone therapy (MHT) observed in both, clinical and observational studies support this hypothesis (Chlebowski et al 2004, La Vecchia et al 2005.…”

Section: Introductionmentioning

confidence: 99%

“…The effect of estrogen on tumor development may be mediated through its receptors (Slattery et al 2005, Kennelly et al 2008. Both estrogen receptor a (ERa) and ERb can be detected in colon tissue, while ERb is found to be more prevalent than ERa (Foley et al 2000, Konstantinopoulos et al 2003, Jassam et al 2005.…”

Section: Introductionmentioning

confidence: 99%

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Modification of menopausal hormone therapy-associated colorectal cancer risk by polymorphisms in sex steroid signaling, metabolism and transport related genes

Rudolph

Sainz

Hein

et al. 2011

Endocrine Related Cancer

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The mechanisms underlying the association of menopausal hormone therapy (MHT) with reduced colorectal cancer (CRC) risk are unknown and the identification of genetic modifiers may yield further insight. We explored the effect modification of MHT-associated CRC risk in postmenopausal women by 47 polymorphisms with known or putative functional relevance in 16 candidate genes related to hormone metabolism (COMT, CYP1A1, CYP1A2, CYP1B1, CYP2C9, CYP2C19, CYP3A4, CYP17A1, GSTP, and HSD17B1), transport (ABCB1), and signaling (ESR1, ESR2, SHBG, PGR, and NR1I2). A total of 685 CRC patients and 684 healthy controls from a German population-based case-control study (DACHS) were genotyped. Multiplicative statistical interaction between polymorphisms and ever MHT use as well as duration of use was assessed using multivariate logistic regression. CRC risk associated with ever MHT use as well as with duration was significantly modified by rs1202168 in the transporter gene ABCB1 (P interactionZ0.04). The MHT-associated risk reduction was not significant in homozygous non-carriers (odds ratio (OR) ever useZ0.84, 95% confidence interval (CI) 0.53-1.34; OR per 5 year durationZ0.94, 95% CI 0.83-1.08), while homozygous carriers of the minor T allele had a 57% lower risk with ever use of MHT (95% CI 0.21-0.88) and a 22% lower risk per 5 years of MHT use (95% CI 0.62-0.97). Significant effect modification was also observed for the ESR1_rs910416 polymorphism (P interactionZ0.03 for ever use and 0.07 for duration of use), whereby the decreased risk was attenuated in homozygous carriers of the minor C allele (OR ever useZ0.87, 95% CI 0.48-1.60, OR per 5 year durationZ0.99, 95% CI 0.83-1.18). Results of this exploratory study provide first evidence that polymorphisms in genes related to estrogen transport and signaling may modify MHT-associated CRC risk but warrant replication in an independent population.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Modification of menopausal hormone therapy-associated colorectal cancer risk by polymorphisms in sex steroid signaling, metabolism and transport related genes

Rudolph

Sainz

Hein

et al. 2011

Endocrine Related Cancer

View full text Add to dashboard Cite

show abstract

“…Therefore, progestin might be a key factor for preventing and suppressing ovarian cancer cell growth. In contrast to ovarian cancer, estrogen appears to have protective effects against colon cancer (Kennelly et al, 2008). However, the role of hormone replacement therapy with estrogen for the treatment of colon cancer is poorly understood, and further analyses are needed.…”

Section: The Role Of Sex Steroid Hormone Receptors In Cancer Therapymentioning

confidence: 99%

Hormone Therapy for the Treatment of Patients with Malignant Salivary Gland Tumor (MSGT)

Sumida¹,

Ishikawa²

2012

Sex Steroids

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Differences in Colon Adenomas and Carcinomas Among Women and Men

Roy¹,

Bianchi²

2009

JAMA

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Oestrogen and the colon: potential mechanisms for cancer prevention

Cited by 138 publications

References 65 publications

Modification of menopausal hormone therapy-associated colorectal cancer risk by polymorphisms in sex steroid signaling, metabolism and transport related genes

Modification of menopausal hormone therapy-associated colorectal cancer risk by polymorphisms in sex steroid signaling, metabolism and transport related genes

Hormone Therapy for the Treatment of Patients with Malignant Salivary Gland Tumor (MSGT)

Differences in Colon Adenomas and Carcinomas Among Women and Men

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