A prospective study of endogenous serum hormone concentrations and breast cancer risk in post-menopausal women on the island of Guernsey

Thomas, H. V.; Key, TJ; Allen, D S; Moore, John W.; Dowsett, Mitchell; Fentiman, IS; Wang, D. Y.

doi:10.1038/bjc.1997.398

Cited by 202 publications

(68 citation statements)

References 22 publications

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“…The cohorts included were: EPIC-Norfolk, EPIC-Oxford, Guernsey Study, MRC National Survey of Health and Development (NSHD), Oxford Vegetarian Study, Whitehall II, UK Women's Cohort Study (UKWCS) ( Table 1). Participants in each cohort gave informed consent and each cohort study obtained ethics committee approval from the relevant agencies: the methods of recruitment, study design and relevant ethics committee approval have been described for these cohorts in detail elsewhere [8][9][10][11][12][13][14] . Each cohort collected dietary information using four-day (Guernsey, Oxford Vegetarian Study, UKWCS), five-day (NSHD) or seven-day diet diaries (EPIC-Norfolk, EPIC-Oxford, Whitehall II), either at recruitment or during a subsequent survey.…”

Section: Participantsmentioning

confidence: 99%

Meat, poultry and fish and risk of colorectal cancer: pooled analysis of data from the UK dietary cohort consortium

Spencer

Key

Appleby

et al. 2010

Cancer Causes Control

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A number of epidemiological studies using food frequency questionnaires report that high intakes of red and processed meat increase the risk of colorectal cancer. In the UK Dietary Cohort Consortium, we examined the associations of meat, poultry and fish intakes with colorectal cancer risk using standardised individual dietary data pooled from seven UK prospective studies. Four to seven-day diet diaries were analysed, disaggregating the weights of meat, poultry and fish from composite foods in order to investigate dose-response relationships in detail. 579 cases of colorectal cancer were identified and matched with 1,996 controls on age, sex and recruitment date. Conditional logistic regression models were used to estimate the odds ratios for colorectal cancer associated with meat, poultry and fish intakes, adjusting for age, height, weight, smoking, and intakes of alcohol, energy and dietary fibre. Disaggregated intakes were moderately low, e.g. mean red meat intakes were 38.2g/day among male and 16.0g/day among female controls. For red and processed meat combined, the odds ratio for highest (median 97.1g/day) compared with lowest (median 0.6g/day) intake was 0.88 (95% CI 0.65-1.20), P for trend=0.68. High (median 44.3g/day) compared with low (median 0g/day) intake of fatty fish was associated with reduced risk of colorectal cancer: OR 0.73 (95% CI 0.54-0.98) but there was no evidence of a linear trend (P=0.33). This study using pooled data from prospective diet diaries, among cohorts with low to moderate meat intakes, shows little evidence of association between consumption of red and processed meat and colorectal cancer risk.Keywords: prospective; diet diary; meat; fish; colorectal cancer. Abstract word count: 248Word count (excluding references and tables): 3,586Journal category: epidemiology.4

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Section: Participantsmentioning

confidence: 99%

Meat, poultry and fish and risk of colorectal cancer: pooled analysis of data from the UK dietary cohort consortium

Spencer

Key

Appleby

et al. 2010

Cancer Causes Control

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“…By the same token, increased and sustained physical activity can reduce the total lifetime ovulatory period and has been shown to confer a significant decrease in breast cancer risk [Bernstein et al, 1994]. Numerous epidemiological studies of breast cancer risk in postmenopausal women have shown higher mean serum estrogen concentrations than disease-free control subjects [Thomas et al, 1997]. These and additional risk factors share a common theme, i.e., increased lifetime tissue exposure to estrogens.…”

Section: Introductionmentioning

confidence: 99%

Increased proteasome‐dependent degradation of estrogen receptor‐alpha by TGF‐β1 in breast cancer cell lines

Petrel

Brueggemeier

2002

J of Cellular Biochemistry

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Normal mammary epithelial cells are rapidly induced to G 1 arrest by the widely expressed cytokine, transforming growth factor beta (TGF-β1). Studies in established breast cancer cell lines that express the estrogen receptor alpha (ERα) have demonstrated loss of this responsiveness. This inverse correlation suggests interpathway signaling important to cell growth and regulation. The adenocarcinoma breast cell line BT474, which was not growth arrested by TGF-β1, was used as a model of estrogen-inducible growth to explore interpathway crosstalk. Although BT474 cells were not growth-arrested by TGF-β1 as determined by flow cytometry analysis and 5′-bromo-3′-deoxyuridine incorporation into DNA, estrogen receptor protein levels were attenuated by 100 pM TGF-β1 after 6 h. This decrease in ERα reached 50% of untreated control levels by 24 h of treatment and was further supported by a 50% decrease in estrogen-inducible DNA synthesis. Inspection of ERα transcripts suggested that this decrease was primarily the result of altered ERα protein stability or availability. Use of the proteasome inhibitor, MG132, abolished all effects on ERα by TGF-β1. Collectively, this data supports a role for TGF-β1 in regulating the growth of otherwise insensitive breast cancer cells through modulation of ERα stability.Keywords breast cancer; estrogen receptor alpha; transforming growth factor beta; ubiquitin; proteasome; cell proliferation Breast cancer is a leading cause of death among women worldwide and an estimated 203,500 new cases will be diagnosed in the US alone in 2002 [American Cancer Society, 2001]. Systemic and locally produced estrogens are intimately associated with increased risk for breast cancer development. Early menarche and late menopause increase the lifetime exposure to estrogens and as much as a 20% decrease in breast cancer risk is observed for each year this exposure is shortened [Kelsey, 1979]. By the same token, increased and sustained physical activity can reduce the total lifetime ovulatory period and has been shown to confer a significant decrease in breast cancer risk [Bernstein et al., 1994]. Numerous epidemiological studies of breast cancer risk in postmenopausal women have shown higher mean serum estrogen concentrations than disease-free control subjects [Thomas et al., 1997]. These and additional risk factors share a common theme, i.e., increased lifetime tissue exposure to estrogens. Thus, estrogen exposure is a central and reoccurring phenomenon in breast cancer etiology.Although many risk factors have been identified, the molecular mechanisms underlying the initiation and progression of breast cancer are still elusive. Estrogens such as 17β-estradiol (E 2 ) play a key role in the development and maintenance of the mature mammary gland. The most well characterized cellular receptor for this steroid hormone is the estrogen receptor alpha (ERα) [Moggs and Orphanides, 2001]. This receptor is expressed in a tissue specific manner and regulates growth and differentiation in response to hormonal stimul...

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“…They also suggest that the contribution of androgens to risk is largely through their role as substrates for oestrogen production. Nine prospective studies have now reported on the association between endogenous sex hormone levels in postmenopausal women and subsequent breast cancer risk (Moore et al, 1986;Wysowski et al, 1987;Barrett-Connor et al, 1990;Gordon et al, 1990;Garland et al, 1992;Helzlsouer et al, 1994;Toniolo et al, 1995;Berrino et al, 1996;Dorgan et al, 1996;Thomas et al, 1997;Zeleniuch-Jacquotte et al, 1997;Hankinson et al, 1998;Cauley et al, 1999;Kabuto et al, 2000). The Endogenous Hormones and Breast Cancer Collaborative Group (TEHBCCG) conducted a pooled analysis of the original data of these studies and concluded that both oestrogen and androgen hormones were strongly associated with risk (TEHBCCG, 2002).…”

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confidence: 99%

Postmenopausal levels of oestrogen, androgen, and SHBG and breast cancer: long-term results of a prospective study

et al. 2004

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We assessed the association of sex hormone levels with breast cancer risk in a case -control study nested within the cohort of 7054 New York University (NYU) Women's Health Study participants who were postmenopausal at entry. The study includes 297 cases diagnosed between 6 months and 12.7 years after enrollment and 563 controls. Multivariate odds ratios (ORs) (95% confidence interval (CI)) for breast cancer for the highest quintile of each hormone and sex-hormone binding globulin (SHBG) relative to the lowest were as follows: 2.49 (1.47 -4.21), P trend ¼ 0.003 for oestradiol; 3.24 (1.87 -5.58), P trend o0.001 for oestrone; 2.37 (1.39 -4.04), P trend ¼ 0.002 for testosterone; 2.07 (1.28 -3.33), P trend o0.001 for androstenedione; 1.74 (1.05 -2.89), P trend o0.001 for dehydroepiandrosterone sulphate (DHEAS); and 0.51 (0.31 -0.82), P trend o0.001 for SHBG. Analyses limited to the 191 cases who had donated blood five to 12.7 years prior to diagnosis showed results in the same direction as overall analyses, although the tests for trend did not reach statistical significance for DHEAS and SHBG. The rates of change per year in hormone and SHBG levels, calculated for 95 cases and their matched controls who had given a second blood donation within 5 years of diagnosis, were of small magnitude and overall not different in cases and controls. The association of androgens with risk did not persist after adjustment for oestrone (1.08, 95% CI ¼ 0.92 -1.26 for testosterone; 1.15, 95% CI ¼ 0.95 -1.39 for androstenedione and 1.06, 95% CI ¼ 0.90 -1.26 for DHEAS), the oestrogen most strongly associated with risk in our study. Our results support the hypothesis that the associations of circulating oestrogens with breast cancer risk are more likely due to an effect of circulating hormones on the development of cancer than to elevations induced by the tumour. They also suggest that the contribution of androgens to risk is largely through their role as substrates for oestrogen production. Nine prospective studies have now reported on the association between endogenous sex hormone levels in postmenopausal women and subsequent breast cancer risk (Moore et al, 1986;Wysowski et al, 1987;Barrett-Connor et al, 1990;Gordon et al, 1990;Garland et al, 1992;Helzlsouer et al, 1994;Toniolo et al, 1995;Berrino et al, 1996;Dorgan et al, 1996;Thomas et al, 1997;Zeleniuch-Jacquotte et al, 1997;Hankinson et al, 1998;Cauley et al, 1999;Kabuto et al, 2000). The Endogenous Hormones and Breast Cancer Collaborative Group (TEHBCCG) conducted a pooled analysis of the original data of these studies and concluded that both oestrogen and androgen hormones were strongly associated with risk (TEHBCCG, 2002). Remaining questions include how long prior to diagnosis the associations between hormone levels and breast cancer are observed and whether androgens play a part independent of their role as substrates for oestrogen production. The New York University (NYU) Women's Health Study was one of the first prospective studies to report a positive association between ...

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A prospective study of endogenous serum hormone concentrations and breast cancer risk in post-menopausal women on the island of Guernsey

Cited by 202 publications

References 22 publications

Meat, poultry and fish and risk of colorectal cancer: pooled analysis of data from the UK dietary cohort consortium

Meat, poultry and fish and risk of colorectal cancer: pooled analysis of data from the UK dietary cohort consortium

Increased proteasome‐dependent degradation of estrogen receptor‐alpha by TGF‐β1 in breast cancer cell lines

Postmenopausal levels of oestrogen, androgen, and SHBG and breast cancer: long-term results of a prospective study

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