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      Menstrual Factors, Reproductive Factors and Lung Cancer Risk: A Meta-analysis

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          Abstract

          Background and objective

          Epidemiological studies have suggested that menstrual and reproductive factors may influence lung cancer risk, but the results are controversial. We therefore carried out a meta-analysis aiming to examine the associations of lung cancer in women with menstrual and reproductive factors.

          Methods

          Relevant studies were searched from PubMed database, CNKI, WANFANG DATA and VIP INFORMATION up to January 2012, with no language restrictions. References listed from selected papers were also reviewed. We included studies that reported the estimates of relative risks (RRs) with 95% confidence intervals (CIs) for the association between menstrual and reproductive factors and lung cancer risk. The pooled RRs were calculated after the heterogeneity test with the software Stata 11, and publication bias and sensitivity were evaluated at the same time.

          Results

          Twenty-five articles, representing 24 independent studies, were included in this meta-analysis. Older age at menarche in North America women (RR=0.83; 95%CI: 0.73-0.94) was associated with a significant decreased risk of lung cancer. Longer length of menstrual cycle was also associated with decreased lung cancer risk (RR=0.72; 95%CI: 0.57-0.90). Other exposures were not significantly associated.

          Conclusions

          Our analysis provides evidence of the hypothesis that female sex hormones influence the risk of lung cancer in women, yet additional studies are warranted to extend this finding and to clarify the underlying mechanisms.

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          Most cited references54

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          Quantifying heterogeneity in a meta-analysis.

          Julian P T Higgins, Simon G Thompson (2002)
          The extent of heterogeneity in a meta-analysis partly determines the difficulty in drawing overall conclusions. This extent may be measured by estimating a between-study variance, but interpretation is then specific to a particular treatment effect metric. A test for the existence of heterogeneity exists, but depends on the number of studies in the meta-analysis. We develop measures of the impact of heterogeneity on a meta-analysis, from mathematical criteria, that are independent of the number of studies and the treatment effect metric. We derive and propose three suitable statistics: H is the square root of the chi2 heterogeneity statistic divided by its degrees of freedom; R is the ratio of the standard error of the underlying mean from a random effects meta-analysis to the standard error of a fixed effect meta-analytic estimate, and I2 is a transformation of (H) that describes the proportion of total variation in study estimates that is due to heterogeneity. We discuss interpretation, interval estimates and other properties of these measures and examine them in five example data sets showing different amounts of heterogeneity. We conclude that H and I2, which can usually be calculated for published meta-analyses, are particularly useful summaries of the impact of heterogeneity. One or both should be presented in published meta-analyses in preference to the test for heterogeneity. Copyright 2002 John Wiley & Sons, Ltd.
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            Cytochrome P450-mediated metabolism of estrogens and its regulation in human.

            Yuki Tsuchiya, Miki Nakajima, Tsuyoshi Yokoi (2005)
            Estrogens are eliminated from the body by metabolic conversion to estrogenically inactive metabolites that are excreted in the urine and/or feces. The first step in the metabolism of estrogens is the hydroxylation catalyzed by cytochrome P450 (CYP) enzymes. Since most CYP isoforms are abundantly expressed in liver, the metabolism of estrogens mainly occurs in the liver. A major metabolite of estradiol, 2-hydroxyestradiol, is mainly catalyzed by CYP1A2 and CYP3A4 in liver, and by CYP1A1 in extrahepatic tissues. However, CYP1B1 which is highly expressed in estrogen target tissues including mammary, ovary, and uterus, specifically catalyzes the 4-hydroxylation of estradiol. Since 4-hydroxyestradiol generates free radicals from the reductive-oxidative cycling with the corresponding semiquinone and quinone forms, which cause cellular damage, the specific and local formation of 4-hydroxyestradiol is important for breast and endometrial carcinogenesis. Changes in the expression level of estrogen-metabolizing CYP isoforms not only alter the intensity of the action of estrogen but may also alter the profile of its physiological effect in liver and target tissues. Generally, many CYP isoforms are induced by the substrates themselves, resulting in enhanced metabolism and elimination from the body. Of particular interest is a novel finding that human CYP1B1 is regulated by estradiol via the estrogen receptor. This fact suggests that the regulation of CYP enzymes involved in estrogen metabolism by estrogen itself would be physiologically significant for the homeostasis of estrogens at local organs. In this mini-review, we discuss the CYP-mediated metabolism of estrogens and the regulation of the estrogen-metabolizing CYP enzymes in relation to the risk of cancer.
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              Combined targeting of the estrogen receptor and the epidermal growth factor receptor in non-small cell lung cancer shows enhanced antiproliferative effects.

              Laura P. Stabile, Jennifer S Lyker, Christopher Gubish … (2005)
              Identifying new effective therapeutic treatments for lung cancer is critical to improving overall patient survival. We have targeted both the estrogen receptor (ER) and the epidermal growth factor receptor (EGFR) pathways using an ER antagonist, fulvestrant ("Faslodex"), and the selective EGFR tyrosine kinase inhibitor, gefitinib ("Iressa"), in non-small cell lung cancer (NSCLC) cells. Rapid activation of phospho-EGFR and phospho-p44/p42 mitogen-activated protein kinase by estrogen was observed, indicating nonnuclear ER transactivation of EGFR. Additionally, EGFR protein expression was down-regulated in response to estrogen and up-regulated in response to fulvestrant in vitro, suggesting that the EGFR pathway is activated when estrogen is depleted in NSCLC cells. Cell growth and apoptosis were examined in several NSCLC lines that express varying amounts of ERbeta, EGFR, and Neu but no full-length ERalpha. One cell line contained an EGFR mutation. Cells were exposed to 10 nmol/L estrogen and 10 ng/mL EGF and either 1 mumol/L fulvestrant or 1 mumol/L gefitinib alone or in combination. In all cell lines, the drug combination decreased cell proliferation up to 90% and increased apoptosis 2-fold. The relative responses to gefitinib and fulvestrant were similar regardless of ER and EGFR expression and mutation status. In an in vivo lung tumor xenograft model, the drug combination decreased tumor volume in severe combined immunodeficient mice by approximately 60% compared with 49% and 32% for gefitinib and fulvestrant treatment alone, respectively. Antitumor effects of the combination therapy were accompanied by biochemical and histologic evidence of increased apoptosis, decreased phospho-p44/p42 mitogen-activated protein kinase expression, and increased Ki-67 expression compared with individual treatment. These studies provide evidence of a functional interaction between the ER and the EGFR pathways in NSCLC.
              Article 0 comments Cited 65 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Baosen ZHOU
                Journal
                Journal ID (nlm-ta): Zhongguo Fei Ai Za Zhi
                Journal ID (iso-abbrev): Zhongguo Fei Ai Za Zhi
                Journal ID (publisher-id): ZGFAZZ
                Title: Chinese Journal of Lung Cancer
                Publisher: 中国肺癌杂志编辑部 (天津市和平区南京路228号300020 )
                ISSN (Print): 1009-3419
                ISSN (Electronic): 1999-6187
                Publication date (Print): 20 December 2012
                Volume: 15
                Issue: 12
                Pages: 701-719
                Affiliations
                [1 ] Department of Epidemiology, School of Public Health, China Medical University, Shenyang 110001, China
                [2 ] Key Laboratory of Cancer Etiology and Intervention, Liaoning University, Shenyang 110036, China
                [3 ] China Medical University Center For Evidence-based Medicine, Shenyang 110001, China
                Author notes
                Baosen ZHOU, E-mail: bszhou@ 123456mail.cmu.edu.cn
                Article
                Publisher ID: zgfazz-15-12-701
                DOI: 10.3779/j.issn.1009-3419.2012.12.04
                PMC ID: 6000047
                PubMed ID: 23249716
                SO-VID: 787175c7-4867-4c09-9a89-559207f0ba80
                Copyright © 版权所有©《中国肺癌杂志》编辑部2012Copyright ©2012 Chinese Journal of Lung Cancer. All rights reserved.
                License:

                This is an open access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 3.0) License. See: https://creativecommons.org/licenses/by/3.0/

                History
                Date received : 26 August 2012
                Date revision received : 15 October 2012
                Categories
                Subject: Clinical Research
                Subject: 临床研究

                Keywords: lung neoplasms,age at menarche,length of menstrual cycle,female sex hormones
                Data availability:
                Keywords: lung neoplasms, age at menarche, length of menstrual cycle, female sex hormones

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