OBJECTIVES: Lung cancer rates increase among women in many regions of the world. To explore whether menopausal hormone therapy (MHT) plays a role. METHODS: We conducted a systematic search of the literature and performed meta-analyses of cohort studies (C), case-control studies (CC), randomized controlled trials (RCTs), and cancer registry studies (CR) to analyse the impact of estrogen therapy (ET), estrogen/progestin therapy (EPT) and any hormone therapy (HT) on lung cancer risks. We explored associations between ever-use of therapies and risks, analysed annual changes of risk, and the impact of therapies on histological subtypes. We calculated summary odds ratios, relative risks, 95% confidence intervals (CI; fixed-effects model), and assessed heterogeneity across studies. Eighteen studies were eligible (9 CC, 4 C, 3 RCT, 2 CR). RESULTS: We found a significant increase of risk - 76.2% - in non-smoking women with adenocarcinoma (CI 1.072-2.898) reporting ever-use of HT. Estrogen plus progestin therapy does not change the risk; however, the pooled analysis of 2 RCTs points at an increased risk (RR 1.359; CI 1.031-1.791). Our further results should be interpreted with caution as significances were found in analyses only when smoking and non-smoking women, various hormone regimens, or histological subtypes, respectively, were pooled. CONCLUSIONS: Dedicated studies designed to more adequately delineate the role of MHT are necessary to substantiate whether use of MHT is a risk factor for this or other types of lung cancer. Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.
OBJECTIVES:Lung cancer rates increase among women in many regions of the world. To explore whether menopausal hormone therapy (MHT) plays a role. METHODS: We conducted a systematic search of the literature and performed meta-analyses of cohort studies (C), case-control studies (CC), randomized controlled trials (RCTs), and cancer registry studies (CR) to analyse the impact of estrogen therapy (ET), estrogen/progestin therapy (EPT) and any hormone therapy (HT) on lung cancer risks. We explored associations between ever-use of therapies and risks, analysed annual changes of risk, and the impact of therapies on histological subtypes. We calculated summary odds ratios, relative risks, 95% confidence intervals (CI; fixed-effects model), and assessed heterogeneity across studies. Eighteen studies were eligible (9 CC, 4 C, 3 RCT, 2 CR). RESULTS: We found a significant increase of risk - 76.2% - in non-smoking women with adenocarcinoma (CI 1.072-2.898) reporting ever-use of HT. Estrogen plus progestin therapy does not change the risk; however, the pooled analysis of 2 RCTs points at an increased risk (RR 1.359; CI 1.031-1.791). Our further results should be interpreted with caution as significances were found in analyses only when smoking and non-smoking women, various hormone regimens, or histological subtypes, respectively, were pooled. CONCLUSIONS: Dedicated studies designed to more adequately delineate the role of MHT are necessary to substantiate whether use of MHT is a risk factor for this or other types of lung cancer. Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.
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