Endogenous Circulating Sex Hormone Concentrations and Colon Cancer Risk in Postmenopausal Women: A Prospective Study and Meta-Analysis

Abstract Background Observational studies have consistently reported that postmenopausal hormone therapy use is associated with lower colon cancer risk. However, epidemiological studies examining the associations between circulating concentrations of endogenous estrogens and colorectal cancer have reported inconsistent results. Methods We investigated the associations between circulating concentrations of estrone, estradiol, free estradiol, testosterone, free testosterone, androstenedione, dehydroepiandrosterone (DHEA), progesterone, and sex hormone binding globulin (SHBG) with colon cancer risk in a nested case–control study of 1,028 postmenopausal European women (512 colon cancer cases, 516 matched controls) who were non-current users of exogenous hormones at blood collection. Multivariable conditional logistic regression models were used to compute odds ratios (ORs) and 95% confidence intervals (CIs) to evaluate the association between circulating sex hormones and colon cancer risk. We also conducted a dose-response meta-analysis of prospective studies of circulating estrone and estradiol with colorectal, colon, and rectal cancer risk in postmenopausal women. All statistical tests were 2-sided. Results In the multivariable model, a non-statistically significant positive relationship was found between circulating estrone and colon cancer risk (OR per log2-1 unit increment = 1.17, 95%CI = 1.00–1.38; ORquartile4-quartile1 = 1.33, 95%CI = 0.89–1.97, Ptrend = 0.20). Circulating concentrations of estradiol, free estradiol, testosterone, free testosterone, androstenedione, DHEA, progesterone, and SHBG were not associated with colon cancer risk. In the dose-response meta-analysis, no clear evidence of associations were found between circulating estradiol, and estrone concentrations with colorectal, colon, and rectal cancer risk. Conclusion Our observational and meta-analysis results do not support an association between circulating concentrations of endogenous sex hormones and colon or rectal cancer in postmenopausal women.

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Serum Lipids and the Risk of Gastrointestinal Malignancies in the Swedish AMORIS Study

Journal of Cancer Epidemiology ◽

10.1155/2012/792034 ◽

2012 ◽

Vol 2012 ◽

pp. 1-10 ◽

Cited By ~ 30

Author(s):

Wahyu Wulaningsih ◽

Hans Garmo ◽

Lars Holmberg ◽

Niklas Hammar ◽

Ingmar Jungner ◽

...

Keyword(s):

Rectal Cancer ◽

Colon Cancer ◽

Cancer Risk ◽

Proportional Hazards ◽

Cox Proportional Hazards ◽

Gastrointestinal Malignancies ◽

Colon Cancer Risk ◽

Colon And Rectal Cancer ◽

Increased Risk ◽

Lipid Components

Background. Metabolic syndrome has been linked to an increased cancer risk, but the role of dyslipidaemia in gastrointestinal malignancies is unclear. We aimed to assess the risk of oesophageal, stomach, colon, and rectal cancers using serum levels of lipid components.Methods. From the Swedish Apolipoprotein Mortality Risk (AMORIS) study, we selected 540,309 participants (> 20 years old) with baseline measurements of total cholesterol (TC), triglycerides (TG), and glucose of whom 84,774 had baseline LDL cholesterol (LDL), HDL cholesterol (HDL), apolipoprotein B (apoB), and apolipoprotein A-I (apoA-I). Multivariate Cox proportional hazards regression was used to assess glucose and lipid components in relation to oesophageal, stomach, colon, and rectal cancer risk.Results. An increased risk of oesophageal cancer was observed in persons with high TG (e.g. HR: 2.29 (95% CI: 1.42–3.68) for the 4th quartile compared to the 1st) and low LDL, LDL/HDL ratio, TC/HDL ratio, log (TG/HDL), and apoB/apoA-I ratio. High glucose and TG were linked with an increased colon cancer risk, while high TC levels were associated with an increased rectal cancer risk.Conclusion. The persistent link between TC and rectal cancer risk as well as between TG and oesophageal and colon cancer risk in normoglycaemic individuals may imply their substantiality in gastrointestinal carcinogenesis.

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Dietary Flavonoids and the Risk of Colorectal Cancer: An Updated Meta-Analysis of Epidemiological Studies

Nutrients ◽

10.3390/nu10070950 ◽

2018 ◽

Vol 10 (7) ◽

pp. 950 ◽

Cited By ~ 22

Author(s):

Hui Chang ◽

Lin Lei ◽

Yun Zhou ◽

Fayin Ye ◽

Guohua Zhao

Keyword(s):

Colorectal Cancer ◽

Rectal Cancer ◽

Colon Cancer ◽

Cancer Risk ◽

Meta Analysis ◽

Epidemiological Studies ◽

Case Control Studies ◽

High Intake ◽

Colon Cancer Risk ◽

Dietary Flavonoids

Aim: The aim of this study was to perform an up-to-date meta-analysis of the association between the intake of dietary flavonoids and the risk of colorectal cancer. Methods: The PubMed and EMBASE databases were searched to identify eligible studies. The risk of colorectal cancer for the highest versus the lowest categories of flavonoids intake were assessed. Results: A total of 12 studies (5 cohort and 7 case-control studies) involving 17,481 cases and 740,859 controls were eligible for meta-analysis. High intake of dietary flavonols, flavones and anthocyanidins may decrease the risk of colorectal cancer; the pooled odds ratio (OR) for the highest intake compared with the lowest was 0.70 (0.54–0.90), 0.79 (0.83–0.99) and 0.78 (0.64–0.95), respectively. No association between the intake of total flavonoids, flavanones or flavan-3-ols and the risk of colorectal cancer was observed. Furthermore, the data showed that high intake of flavonols may decrease the risk of colon cancer [0.80 (0.68–0.94)] but not rectal cancer [0.93 (0.74–1.18)], while on the contrary, the intake of flavones may decrease rectal cancer risk [0.82 (0.70–0.97)] but not colon cancer risk [0.88 (0.69–1.13)]. Conclusions: The present study suggested that high intake of flavonols (such as quercetin) may reduce the risk of colon cancer, and high intake of flavones (such as apigenin) may reduce the risk of rectal cancer.

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Alcohol Consumption by Beverage Type and Risk of Breast Cancer: A Dose-Response Meta-Analysis of Prospective Cohort Studies

Alcohol and Alcoholism ◽

10.1093/alcalc/agaa012 ◽

2020 ◽

Vol 55 (3) ◽

pp. 246-253 ◽

Cited By ~ 1

Author(s):

Qiuyu Sun ◽

Weihong Xie ◽

Yanli Wang ◽

Feifei Chong ◽

Mengmeng Song ◽

...

Keyword(s):

Breast Cancer ◽

Breast Cancer Risk ◽

Cancer Risk ◽

Cohort Studies ◽

Postmenopausal Women ◽

Dose Response ◽

Alcohol Intake ◽

Meta Analysis ◽

Response Analysis ◽

Total Alcohol

Abstract Aims Alcohol intake has been shown to increase the risk of breast cancer. However, the dose-response analysis of different alcoholic beverages (spirits, wine and beer) is not clear. Our meta-analysis aims to provide a dose-response estimation between different alcohols and breast cancer risk. Methods Search of PubMed and Web of Science and manual searches were conducted up to 1 December 2018, and summary relative risks (RRs) and attributable risk percentage (ARP) for alcohol intake on the development of breast cancer were calculated. Dose-response meta-analysis modeled relationships between drinking type and breast cancer risk. Sources of heterogeneity were explored, and sensitivity analyses were conducted to test the robustness of findings. Results In total, 22 cohort studies and 45,350 breast cancer cases were included. Current drinkers for ER+ had an increased risk compared with never drinkers. In dose-response analysis, there was a statistically significant linear trend with breast cancer risk increasing gradually by total alcohol and wine dose: when adding 10 g per day, the risk increased by 10.5% (RR = 1.10, 95%CI = 1.08–1.13) in total alcohol and 8.9% (RR = 1.08, 95%CI = 1.04–1.14) in wine. For postmenopausal women, the risk increases by 11.1% (RR = 1.11, 95%CI = 1.09–1.13) with every 10 g of total alcohol increase. Furthermore, the breast cancer alcohol-attributed percentage is higher in Europe than in North America and Asia. Conclusions The effect of drinking on the incidence of breast cancer is mainly manifested in ER+ breast cancer. Quantitative analysis showed total drinking had a significant risk for breast cancer, especially for postmenopausal women. However, for different alcohols, just wine intake has the similar results.

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Adult BMI Change and Risk of Colon Cancer in Postmenopausal Women

Journal of Obesity ◽

10.1155/2012/857510 ◽

2012 ◽

Vol 2012 ◽

pp. 1-8 ◽

Cited By ~ 4

Author(s):

Lyla Blake-Gumbs ◽

Zhengyi Chen ◽

Cheryl L. Thompson ◽

Nathan A. Berger ◽

Thomas C. Tucker ◽

...

Keyword(s):

Colon Cancer ◽

Weight Gain ◽

Cancer Risk ◽

Postmenopausal Women ◽

Early Adulthood ◽

Population Based ◽

Colon Cancer Risk ◽

Increased Risk ◽

Study Population ◽

Control Study

Purpose. We recently reported an association of adult BMI change with colon cancer risk. Here, we sought to further explore this association with respect to postmenopausal HRT use in a larger study population.Methods. We included 1,457 postmenopausal women participating in an ongoing population-based case-control study of colon cancer.Results. We confirmed a previously reported association of adulthood weight gain and increased risk of colon cancer: compared to those with <5 kg/m2change of BMI, women who reported moderate (5–10 kg/m2) and large (>10 kg/m2) BMI changes since their 20s had OR estimates of 1.54 (95% CI = 1.09–2.19) and 1.45 (95% CI = 0.90–2.33), respectively (Pfor trend = 0.05). Stratified analyses showed that this association was limited to HRT nonusers: ORs were 1.77 (95% CI = 1.02–3.05) and 2.21 (95% CI = 1.09–4.45), respectively (Pfor trend = 0.03), for BMI changes occurring between the 20s decade and time of recruitment among non-users. Similar associations were observed for BMI changes since the 30s decade. There was no association among HRT users.Conclusion. Our results suggest early adulthood weight gain increases colon cancer risk in postmenopausal women who do not use HRT.

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lncRNA-PCAT1 rs2632159 polymorphism could be a biomarker for colorectal cancer susceptibility

Bioscience Reports ◽

10.1042/bsr20190708 ◽

2019 ◽

Vol 39 (7) ◽

Cited By ~ 5

Author(s):

Ming-li Yang ◽

Zhe Huang ◽

Li-na Wu ◽

Rong Wu ◽

Han-xi Ding ◽

...

Keyword(s):

Colorectal Cancer ◽

Rectal Cancer ◽

Colon Cancer ◽

Cancer Risk ◽

Cancer Susceptibility ◽

Bioinformatic Analysis ◽

Recessive Model ◽

Eqtl Analysis ◽

Nucleotide Polymorphisms ◽

Colon Cancer Risk

AbstractBackground: Single-nucleotide polymorphisms (SNPs) in lncRNAs could be biomarkers for susceptibility to colorectal cancer (CRC), but the association of PCAT1 polymorphisms and CRC susceptibility is yet to be studied. Methods: Five tagSNPs covering the PCAT1 gene were detected through Kompetitive Allele-Specific PCR among 436 CRC patients and 510 controls. An expression quantitative trait locus (eQTL) bioinformatic analysis was then performed. Results: In the present study, PCAT1 rs2632159 polymorphism increased CRC risk by 1.37-fold and 2.19-fold in the dominant and recessive models, respectively (P=0.040 and 0.041). When the CRC cases were divided into colon cancer and rectal cancer, we found that this polymorphism affected colon cancer risk under the dominant model (P=0.022, OR = 1.51) and affected rectal cancer susceptibility under the recessive model (P=0.009, OR = 3.03). A more pronounced effect was observed in the male subgroup in that PCAT1 rs2632159 SNP increased rectal cancer risk by 3.97-fold (P=0.017). When PCAT1 rs2632159 was present, epistatic effects were observed with rs1902432 and rs785005 (P=0.011 and 0.008, respectively). eQTL analysis showed that rs2632159 could influence binding with the transcription factors EBF, LUN-1, and TCF12. Conclusion:PCAT1 rs2632159 SNP could be a biomarker for CRC risk. And the rs1902432 SNP might only have potential to be a biomarker for colon cancer risk.

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