1
|
Bertola C, Gobbetti C, Baccarini G, Fabiani R. Wine Consumption and Lung Cancer Risk: A Systematic Review and Meta-Analysis. Nutrients 2025; 17:1322. [PMID: 40284187 PMCID: PMC12030585 DOI: 10.3390/nu17081322] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/14/2025] [Revised: 04/07/2025] [Accepted: 04/08/2025] [Indexed: 04/29/2025] Open
Abstract
Background/Objectives: Lung cancer is one of the leading causes of cancer-related mortality, with tobacco smoking being the primary risk factor. However, a significant percentage of lung cancer patients are non-smokers, suggesting the involvement of other risk factors, including alcohol consumption. The IARC classifies ethanol as a Group 1 carcinogen, but unlike other alcoholic beverages, wine contains polyphenols with potential health benefits. Some meta-analyses even suggest a protective effect, which led us to conduct our own meta-analysis to further investigate this possible correlation. Methods: We conducted a systematic review and stratified the risk across population subgroups based on smoking status and gender. We then performed a categorical "highest vs. lowest" meta-analysis, comparing heavy consumers with very occasional drinkers, using a random-effects model. Only studies examining the risk of developing lung cancer in wine drinkers were included, excluding those with different outcomes, non-primary, ineligible populations, or involving pregnant women. The literature search was conducted in three databases: PubMed, Scopus, and Web of Science. The risk of bias was assessed with the Newcastle-Ottawa quality rating scale for both case-control and cohort studies (NOS), while statistical analyses were performed using the ProMeta 3.0 software. Results: The overall analysis showed a non-statistically significant 11% reduction in lung cancer risk (OR = 0.89; 95% CI: 0.77-1.03). The analysis among smokers revealed a significant 22% reduction in lung cancer risk associated with wine consumption (OR = 0.78; 95% CI: 0.62-0.97). However, this effect was lost when the analysis was conducted separately based on the study design. Conclusions: No correlation emerged between wine consumption and lung cancer incidence, either in a protective sense or in terms of increased risk. However, further studies are needed to investigate this correlation more accurately, particularly among non-smokers.
Collapse
Affiliation(s)
- Carlotta Bertola
- Section of Hygiene and Public Health, Department of Medicine and Surgery, University of Perugia, 06132 Perugia, Italy; (C.G.); (G.B.)
| | - Camilla Gobbetti
- Section of Hygiene and Public Health, Department of Medicine and Surgery, University of Perugia, 06132 Perugia, Italy; (C.G.); (G.B.)
| | - Gaia Baccarini
- Section of Hygiene and Public Health, Department of Medicine and Surgery, University of Perugia, 06132 Perugia, Italy; (C.G.); (G.B.)
| | - Roberto Fabiani
- Department of Chemistry, Biology and Biotechnology, University of Perugia, 06123 Perugia, Italy;
| |
Collapse
|
2
|
Datta A, C GPD. Comparative investigation of lung adenocarcinoma and squamous cell carcinoma transcriptome to reveal potential candidate biomarkers: An explainable AI approach. Comput Biol Chem 2025; 115:108333. [PMID: 39787672 DOI: 10.1016/j.compbiolchem.2024.108333] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/24/2024] [Revised: 12/03/2024] [Accepted: 12/24/2024] [Indexed: 01/12/2025]
Abstract
Patients with Non-Small Cell Lung Cancer (NSCLC) present a variety of clinical symptoms, such as dyspnea and chest pain, complicating accurate diagnosis. NSCLC includes subtypes distinguished by histological characteristics, specifically lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). This study aims to compare and identify abnormal gene expression patterns in LUAD and LUSC samples relative to adjacent healthy tissues using an explainable artificial intelligence (XAI) framework. The LASSO algorithm was employed to identify the top gene features in the LUAD and LUSC datasets. An ensemble-based extreme gradient boosting (XGBoost) machine learning (ML) algorithm was trained and interpreted using SHapley Additive exPlanations (SHAP), with top features undergoing biological annotation through survival and functional enrichment analyses. The XAI-based SHAP module addresses the opaque nature of ML models. Notably, 35 and 33 genes were identified for LUAD and LUSC, respectively, using the LASSO algorithm. Performance metrics such as average accuracy and Matthew's correlation coefficient were evaluated. The XGBoost model demonstrated an average accuracy of 99.1 % for LUAD and 98.6 % for LUSC. The SFTPC gene emerged as the most significant feature across both NSCLC subtypes. For LUAD, genes such as STX11, CLEC3B, EMP2, and LYVE1 significantly influenced the XAI-SHAP framework. Conversely, GKN2, OGN, SLC39A8, and MMRN1 were identified for LUSC. Survival analysis and functional validation of these genes highlighted the physiological functions observed to be dysregulated in the NSCLC subtypes. These identified genes have the potential to enhance current medical diagnostics and therapeutics.
Collapse
Affiliation(s)
- Ankur Datta
- Laboratory of Integrative Genomics, Department of Integrative Biology, School of BioSciences and Technology, Vellore Institute of Technology, Vellore, Tamil Nadu 632014, India.
| | - George Priya Doss C
- Laboratory of Integrative Genomics, Department of Integrative Biology, School of BioSciences and Technology, Vellore Institute of Technology, Vellore, Tamil Nadu 632014, India.
| |
Collapse
|
3
|
Sodeifian F, Kian N, Atefi A, Naserghandi A, Zangiabadian M, Sadeghzade S, Namakin K, Seghatoleslami ZS, D'Ambrosio L, Nasiri MJ, Migliori GB. Pulmonary Tuberculosis and Risk of Lung Cancer: A Systematic Review and Meta-Analysis. Respiration 2024; 104:360-376. [PMID: 39733773 DOI: 10.1159/000543319] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/12/2024] [Accepted: 12/19/2024] [Indexed: 12/31/2024] Open
Abstract
INTRODUCTION Lung cancer is a leading cause of cancer-related deaths worldwide, with rising incidence in resource-limited settings. Research suggests an increased risk of lung cancer in individuals with a history of pulmonary tuberculosis (TB), but the association needs further clarification. This systematic review aims to provide a more comprehensive understanding of this relationship. METHODS We systematically searched the PubMed/Medline, EMBASE, and Scopus databases for relevant studies up to March 15, 2024. The quality of the included studies was assessed using the Joanna Briggs Institute (JBI) critical appraisal checklist. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated using either random-effects or fixed-effects models, depending on the level of heterogeneity. All statistical analyses were performed using Comprehensive Meta-Analysis Software, version 3.0. RESULTS A total of 37 studies were included (9 cohort and 28 case-control). A significant association between prior pulmonary TB and lung cancer was found in both cohort (OR: 2.3; 95% CI, 1.4-3.8) and case-control (OR: 1.9; 95% CI, 1.4-2.5) studies. Subgroup analyses revealed a stronger association in East Asia (OR: 2.4; 95% CI, 1.3-4.1). CONCLUSION Our study provides strong evidence of an increased risk of lung cancer following pulmonary TB. The findings emphasize the need for comprehensive public health strategies, including targeted screening, early detection, and smoking cessation. Future studies should investigate the mechanisms linking TB and lung cancer, as well as the effectiveness of integrated prevention programs, particularly in high-burden regions.
Collapse
Affiliation(s)
- Fatemeh Sodeifian
- Department of Microbiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| | - Naghmeh Kian
- Department of Microbiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| | - Amirhomayoun Atefi
- Student Research Committee, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran
| | - Alvand Naserghandi
- Department of Microbiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| | - Moein Zangiabadian
- Department of Microbiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| | - Sara Sadeghzade
- Department of Microbiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| | - Kosar Namakin
- Department of Microbiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| | | | | | - Mohammad Javad Nasiri
- Department of Microbiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| | - Giovanni Battista Migliori
- Servizio di Epidemiologia Clinica delle Malattie Respiratorie, Istituti Clinici Scientifici Maugeri IRCCS, Tradate, Italy
| |
Collapse
|
4
|
Flor LS, Anderson JA, Ahmad N, Aravkin A, Carr S, Dai X, Gil GF, Hay SI, Malloy MJ, McLaughlin SA, Mullany EC, Murray CJL, O'Connell EM, Okereke C, Sorensen RJD, Whisnant J, Zheng P, Gakidou E. Health effects associated with exposure to secondhand smoke: a Burden of Proof study. Nat Med 2024; 30:149-167. [PMID: 38195750 PMCID: PMC10803272 DOI: 10.1038/s41591-023-02743-4] [Citation(s) in RCA: 14] [Impact Index Per Article: 14.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/08/2023] [Accepted: 11/28/2023] [Indexed: 01/11/2024]
Abstract
Despite a gradual decline in smoking rates over time, exposure to secondhand smoke (SHS) continues to cause harm to nonsmokers, who are disproportionately children and women living in low- and middle-income countries. We comprehensively reviewed the literature published by July 2022 concerning the adverse impacts of SHS exposure on nine health outcomes. Following, we quantified each exposure-response association accounting for various sources of uncertainty and evaluated the strength of the evidence supporting our analyses using the Burden of Proof Risk Function methodology. We found all nine health outcomes to be associated with SHS exposure. We conservatively estimated that SHS increases the risk of ischemic heart disease, stroke, type 2 diabetes and lung cancer by at least around 8%, 5%, 1% and 1%, respectively, with the evidence supporting these harmful associations rated as weak (two stars). The evidence supporting the harmful associations between SHS and otitis media, asthma, lower respiratory infections, breast cancer and chronic obstructive pulmonary disease was weaker (one star). Despite the weak underlying evidence for these associations, our results reinforce the harmful effects of SHS on health and the need to prioritize advancing efforts to reduce active and passive smoking through a combination of public health policies and education initiatives.
Collapse
Affiliation(s)
- Luisa S Flor
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA.
- Department of Health Metrics Sciences, School of Medicine, University of Washington, Seattle, WA, USA.
| | - Jason A Anderson
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Noah Ahmad
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Aleksandr Aravkin
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
- Department of Health Metrics Sciences, School of Medicine, University of Washington, Seattle, WA, USA
| | - Sinclair Carr
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Xiaochen Dai
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Gabriela F Gil
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
- Department of Global Health, University of Washington, Seattle, WA, USA
| | - Simon I Hay
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
- Department of Health Metrics Sciences, School of Medicine, University of Washington, Seattle, WA, USA
| | - Matthew J Malloy
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Susan A McLaughlin
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Erin C Mullany
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Christopher J L Murray
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
- Department of Health Metrics Sciences, School of Medicine, University of Washington, Seattle, WA, USA
| | - Erin M O'Connell
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Chukwuma Okereke
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Reed J D Sorensen
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Joanna Whisnant
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Peng Zheng
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
- Department of Health Metrics Sciences, School of Medicine, University of Washington, Seattle, WA, USA
| | - Emmanuela Gakidou
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
- Department of Health Metrics Sciences, School of Medicine, University of Washington, Seattle, WA, USA
| |
Collapse
|
5
|
Dai X, Gil GF, Reitsma MB, Ahmad NS, Anderson JA, Bisignano C, Carr S, Feldman R, Hay SI, He J, Iannucci V, Lawlor HR, Malloy MJ, Marczak LB, McLaughlin SA, Morikawa L, Mullany EC, Nicholson SI, O'Connell EM, Okereke C, Sorensen RJD, Whisnant J, Aravkin AY, Zheng P, Murray CJL, Gakidou E. Health effects associated with smoking: a Burden of Proof study. Nat Med 2022; 28:2045-2055. [PMID: 36216941 PMCID: PMC9556318 DOI: 10.1038/s41591-022-01978-x] [Citation(s) in RCA: 86] [Impact Index Per Article: 28.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/11/2022] [Accepted: 07/28/2022] [Indexed: 12/17/2022]
Abstract
As a leading behavioral risk factor for numerous health outcomes, smoking is a major ongoing public health challenge. Although evidence on the health effects of smoking has been widely reported, few attempts have evaluated the dose-response relationship between smoking and a diverse range of health outcomes systematically and comprehensively. In the present study, we re-estimated the dose-response relationships between current smoking and 36 health outcomes by conducting systematic reviews up to 31 May 2022, employing a meta-analytic method that incorporates between-study heterogeneity into estimates of uncertainty. Among the 36 selected outcomes, 8 had strong-to-very-strong evidence of an association with smoking, 21 had weak-to-moderate evidence of association and 7 had no evidence of association. By overcoming many of the limitations of traditional meta-analyses, our approach provides comprehensive, up-to-date and easy-to-use estimates of the evidence on the health effects of smoking. These estimates provide important information for tobacco control advocates, policy makers, researchers, physicians, smokers and the public.
Collapse
Affiliation(s)
- Xiaochen Dai
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA.
- Department of Health Metrics Sciences, School of Medicine, University of Washington, Seattle, WA, USA.
| | - Gabriela F Gil
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Marissa B Reitsma
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Noah S Ahmad
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Jason A Anderson
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Catherine Bisignano
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Sinclair Carr
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Rachel Feldman
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Simon I Hay
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
- Department of Health Metrics Sciences, School of Medicine, University of Washington, Seattle, WA, USA
| | - Jiawei He
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
- Department of Health Metrics Sciences, School of Medicine, University of Washington, Seattle, WA, USA
| | - Vincent Iannucci
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Hilary R Lawlor
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Matthew J Malloy
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Laurie B Marczak
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Susan A McLaughlin
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Larissa Morikawa
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Erin C Mullany
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Sneha I Nicholson
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Erin M O'Connell
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Chukwuma Okereke
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Reed J D Sorensen
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Joanna Whisnant
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
| | - Aleksandr Y Aravkin
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
- Department of Applied Mathematics, University of Washington, Seattle, WA, USA
| | - Peng Zheng
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
- Department of Health Metrics Sciences, School of Medicine, University of Washington, Seattle, WA, USA
| | - Christopher J L Murray
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
- Department of Health Metrics Sciences, School of Medicine, University of Washington, Seattle, WA, USA
| | - Emmanuela Gakidou
- Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA, USA
- Department of Health Metrics Sciences, School of Medicine, University of Washington, Seattle, WA, USA
| |
Collapse
|
6
|
Cabrera-Sanchez J, Cuba V, Vega V, Van der Stuyft P, Otero L. Lung cancer occurrence after an episode of tuberculosis: a systematic review and meta-analysis. Eur Respir Rev 2022; 31:31/165/220025. [PMID: 35896272 DOI: 10.1183/16000617.0025-2022] [Citation(s) in RCA: 19] [Impact Index Per Article: 6.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/04/2022] [Accepted: 05/16/2022] [Indexed: 11/05/2022] Open
Abstract
INTRODUCTION People with tuberculosis experience long-term health effects beyond cure, including chronic respiratory diseases. We investigated whether tuberculosis is a risk factor for subsequent lung cancer. METHODS We searched PubMed, Scopus, Cochrane, Latin American and Caribbean Health Sciences Literature and the Scientific Electronic Library Online for cohort and case-control studies providing effect estimates for the association between tuberculosis and subsequent lung cancer. We pooled estimates through random-effects meta-analysis. The study was registered in PROSPERO (CDR42020178362). RESULTS Out of 6240 records, we included 29 cohort and 44 case-control studies. Pooled estimates adjusted for age and smoking (assessed quantitatively) were hazard ratio (HR) 1.51 (95% CI 1.30-1.76, I2=81%; five studies) and OR 1.74 (95% CI 1.42-2.13, I2=59%; 19 studies). The occurrence of lung cancer was increased for 2 years after tuberculosis diagnosis (HR 5.01, 95% CI 3.64-6.89; two studies), but decreased thereafter. Most studies were retrospective, had moderate to high risk of bias, and did not control for passive smoking, environmental exposure and socioeconomic status. Heterogeneity was high. CONCLUSION We document an association between tuberculosis and lung cancer occurrence, particularly in, but not limited to, the first 2 years after tuberculosis diagnosis. Some cancer cases may have been present at the time of tuberculosis diagnosis and therefore causality cannot be ascertained. Prospective studies controlling for key confounding factors are needed to identify which tuberculosis patients are at the highest risk, as well as cost-effective approaches to mitigate such risk.
Collapse
Affiliation(s)
| | - Vicente Cuba
- Facultad de Medicina, Universidad Peruana Cayetano Heredia, Lima, Peru
| | - Victor Vega
- Instituto de Medicina Tropical Alexander von Humboldt, Universidad Peruana Cayetano Heredia, Lima, Peru
| | - Patrick Van der Stuyft
- Dept of Public Health and Primary Care, Faculty of Medicine and Health Sciences, Ghent University, Ghent, Belgium
| | - Larissa Otero
- Facultad de Medicina, Universidad Peruana Cayetano Heredia, Lima, Peru.,Instituto de Medicina Tropical Alexander von Humboldt, Universidad Peruana Cayetano Heredia, Lima, Peru
| |
Collapse
|
7
|
Pulmonary Tuberculosis and Risk of Lung Cancer: A Systematic Review and Meta-Analysis. J Clin Med 2022; 11:jcm11030765. [PMID: 35160218 PMCID: PMC8836400 DOI: 10.3390/jcm11030765] [Citation(s) in RCA: 28] [Impact Index Per Article: 9.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/05/2022] [Revised: 01/27/2022] [Accepted: 01/28/2022] [Indexed: 02/06/2023] Open
Abstract
Pulmonary tuberculosis (TB) is a known risk factor for lung cancer. However, a detailed analysis of lung cancer type, age, sex, smoking, and TB burden associated with geographic and socioeconomic status has not been performed previously. We systematically appraised relevant observational studies reporting an association between pulmonary TB and lung cancer. All studies were included in the primary analysis, and studies that used robust TB diagnostic methods, such as validated medical diagnostic codes, were included in the secondary analysis. Thirty-two articles were included. The association between the history of pulmonary TB and diagnosis of lung cancer was statistically significant (OR 2.09, 95% CI: 1.62–2.69, p < 0.001). There was a high heterogeneity (I2 = 95%), without any publication bias. The analysis indicated a high association in advanced articles describing stringent pulmonary TB diagnosis (OR 2.26, 95% CI: 1.29–3.94, p = 0.004). The subgroup analyses suggested a significant association in countries with medium or high TB burdens, from East Asia and the Pacific region, and upper-middle income countries. Heterogeneity within the subgroups remained high in a majority of the subgroup analyses. A meta-regression analysis revealed that younger patients showed a significantly higher association between TB and lung cancer (regression coefficient = 0.949, p < 0.001). The history of pulmonary TB is an independent risk factor for lung cancer, especially in younger patients diagnosed with pulmonary TB. Clinicians should be aware of this association while treating young patients with a history of pulmonary TB.
Collapse
|
8
|
Abdeahad H, Salehi M, Yaghoubi A, Aalami AH, Aalami F, Soleimanpour S. Previous pulmonary tuberculosis enhances the risk of lung cancer: systematic reviews and meta-analysis. Infect Dis (Lond) 2021; 54:255-268. [PMID: 34807803 DOI: 10.1080/23744235.2021.2006772] [Citation(s) in RCA: 11] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/23/2022] Open
Abstract
PURPOSE The possible association between history of pulmonary tuberculosis (TB) and lung cancer (LC) has attracted researchers' attention for several decades. This systematic review and meta-analysis aim to assess the association between previous pulmonary TB infection and LC risk. METHODS A Systematic and comprehensive search was performed in the following databases: PubMed, Embase, clinical key, Web of Science and Google Scholar, in articles and abstracts published from 1987 to 2021. Thirty-two articles (involving 50,290 cases and 846,666 controls) met the inconclusive criteria. The Comprehensive Meta-Analysis version 2.2 software was used for this meta-analysis. RESULTS The result of this meta-analysis demonstrates that pre-existing active pulmonary TB increases the risk of LC (RR = 2.170, 95% confidence interval [CI] 1.833-2.569, p < .001, I2 = 91.234%). The results showed that the risk of the history of active pulmonary TB infection in adenocarcinoma was 2.605 (95% CI 1.706-3.979, p < .001, I2 = 55.583%), in small-cell carcinoma was 2.118 (95% CI 1.544-2.905, p < .001, I2 = 0.0%), in squamous-cell carcinoma, was 3.570 (95% CI 2.661 - 4.791, p < .001, I2 = 42.695%) and 2.746 (95% CI 2.300-3.279, p < .001, I2 = 41.686%) for other histological types of LCs. According to these results, a history of active pulmonary TB increases the risk of LC. CONCLUSIONS This study emphasizes the importance of LC screening in pulmonary TB patients even after the infection is treated. With the increased chances of LC in a patient who had a history of active pulmonary TB, there could be a need for a further follow-up period after pulmonary TB recovery.
Collapse
Affiliation(s)
- Hossein Abdeahad
- Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT, USA.,Department of Medical Biochemistry, Faculty of Medicine, Mashhad University of Medical, Sciences, Mashhad, Iran
| | - Maryam Salehi
- Department of Community Medicine, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
| | - Atieh Yaghoubi
- Antimicrobial Resistance Research Center, Bu-Ali Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran.,Department of Microbiology and Virology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
| | - Amir Hossein Aalami
- Department of Biology, Mashhad Branch, Islamic Azad University, Mashhad, Iran
| | - Farnoosh Aalami
- Student Research Committee, Mashhad University of Medical Sciences, Mashhad, Iran
| | - Saman Soleimanpour
- Antimicrobial Resistance Research Center, Bu-Ali Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran.,Department of Microbiology and Virology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.,Tuberculosis Reference Laboratory-Northeast of Iran, Mashhad University of Medical Sciences, Mashhad, Iran
| |
Collapse
|
9
|
Chung HF, Gete DG, Mishra GD. Age at menopause and risk of lung cancer: A systematic review and meta-analysis. Maturitas 2021; 153:1-10. [PMID: 34654521 DOI: 10.1016/j.maturitas.2021.07.010] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/11/2021] [Revised: 07/06/2021] [Accepted: 07/16/2021] [Indexed: 12/31/2022]
Abstract
Previous reviews have found that menstrual and reproductive factors are associated with lung cancer risk, but evidence on a possible association with age at menopause is inconsistent. This review aimed to determine the association of early and late menopause with lung cancer risk. Publications were reviewed and obtained through PubMed, EMBASE and Scopus database search up to March 2021. The pooled relative risks (RRs) or odds ratios (ORs) and corresponding 95% CIs were estimated using a random-effects meta-analysis. Twenty-eight studies were included in at least one meta-analysis, of age at menopause (lowest vs highest; n=26), early menopause (≤45 vs ≥50/51 years or middle; n=11), late menopause (≥55 vs <50 years or middle; n=6), or continuous (per additional year; n=6). We found that early menopause was associated with lung cancer in both cohort studies (RR 1.26, 1.10-1.41; n=6) and case-control studies (OR 1.38, 1.11-1.66; n=5). Three large cohort studies showed that the increased risk was primarily evident among smokers (RR 1.38, 1.10-1.66) but not among non-smokers (RR 1.02, 0.63-1.40). Four case-control studies found that late menopause was also associated with lung cancer (OR 1.29, 1.08-1.51); conversely, the association was mainly observed among non-smokers (OR 1.35, 1.11-1.59) but not among smokers (OR 1.05, 0.75-1.36). In conclusion, evidence from this review indicates an increased risk of lung cancer in women who experience early menopause (≤45 years), although this risk is primarily among smokers. Large prospective cohort studies are needed to confirm the association between late menopause (≥55 years) and lung cancer risk among non-smokers. PROSPERO registration: CRD42020205429.
Collapse
Affiliation(s)
- Hsin-Fang Chung
- School of Public Health, The University of Queensland, Queensland, Brisbane, Australia.
| | - Dereje G Gete
- School of Public Health, The University of Queensland, Queensland, Brisbane, Australia.
| | - Gita D Mishra
- School of Public Health, The University of Queensland, Queensland, Brisbane, Australia.
| |
Collapse
|
10
|
Pulmonary Tuberculosis and the Incidence of Lung Cancer among Patients with Chronic Obstructive Pulmonary Disease. Ann Am Thorac Soc 2021; 19:640-648. [PMID: 34478360 DOI: 10.1513/annalsats.202010-1240oc] [Citation(s) in RCA: 24] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/27/2022] Open
Abstract
RATIONALE While the history of pulmonary tuberculosis (PTB) is a risk factor for developing both chronic obstructive pulmonary disease (COPD) and lung cancer, it remains unclear whether the history of PTB affects lung cancer development in COPD patients. OBJECTIVES To investigate whether a history of PTB is associated with an increased risk of lung cancer development in a population with COPD. METHODS This cohort study included a nationwide representative sample of 13,165 Korean men and women with COPD, aged between 50-84 years. In addition, to assess whether the relationship between PTB and lung cancer risk differs between participants with and without COPD, a matched cohort without COPD was included. Participants were matched 1:3 for age, sex, smoking history, and PTB status based on the index health screening exam of corresponding participants with COPD. The two cohorts were followed up for 13 years (January 1st, 2003, to December 31st, 2015). PTB was diagnosed based on the results of chest radiography, and incident lung cancer was identified from hospitalization and outpatient visit claims (International Classification of Diseases, Tenth Revision diagnosis code C33 or C34). RESULTS During 370,617 person-years (PY) of follow-up (median follow-up, 7.7 years), in the COPD group, we observed 430 incident cases of lung cancer in participants without a history of PTB (incidence rate 524 per 100,000 PY) and 148 cases in those with a history of PTB (incidence rate 931 per 100,000 PY). Compared to participants without a PTB history, the fully adjusted subdistribution hazard ratio (95% confidence interval) for lung cancer in those with a history of PTB was 1.24 (1.03, 1.50). The association of PTB history and lung cancer development was more evident in never-smokers with COPD. In contrast, among participants without COPD, the corresponding hazard ratio (95% confidence interval) was 0.98 (0.78, 1.22). There was no interaction between PTB, smoking status, and COPD. CONCLUSIONS The history of PTB was associated with an increased risk of developing lung cancer among COPD patients in our country with an intermediate TB burden. COPD patients with a history of PTB, particularly the never-smokers, might benefit from periodical screening or assessment for lung cancer development.
Collapse
|
11
|
Wang J, Gao J, Xu HL, Qian Y, Xie L, Yu H, Qian BY. Citrus fruit intake and lung cancer risk: A meta-analysis of observational studies. Pharmacol Res 2021; 166:105430. [PMID: 33529754 DOI: 10.1016/j.phrs.2021.105430] [Citation(s) in RCA: 12] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/15/2020] [Revised: 12/19/2020] [Accepted: 01/06/2021] [Indexed: 11/29/2022]
Abstract
OBJECTIVE To explore the hypothesis that Citrus intake may reduce the risk of lung cancer. DESIGN Meta-analyses of Dichotomy and dose-response relationship. DATA SOURCES We searched online literature databases including PubMed, Embase, and Cochrane Library to screen relevant articles available up to 27 July 2020. Search terms included (i) Citrus, Fruit, Diet, Dietary; (ii) cancer, neoplasm, tumor (iii)lung; (iv)case-control, cohort, prospective. STUDY SELECTION The selection of studies and the meta-analysis were carried out by following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. The following inclusion criteria were chosen: (i) epidemiological studies with case-control or cohort design; (ii) human participants; (iii) studies investigated the relationship between Citrus fruit intake and lung cancer risk; (iv) if data were duplicated in more than two studies, we brought the most recent or all-sided study into this analysis. We collected all full-text articles that met the inclusion criteria. We applied the following exclusion criteria to the full-text articles, including possible articles listed by manual search: (i) there was no represented odds ratio (OR) or relative risk (RR) estimate and its corresponding 95 % confidence interval (95 % CI) (or data to calculate them) for the highest versus lowest levels of Citrus fruit consumption (ii) reviews, systematic reviews and meta-analyses; (iii) there was no data of Citrus fruit intake at the individual level. DATA EXTRACTION Two reviewers independently performed the extraction of data from eligible studies. STATISTICAL METHODS Adjusted odds ratios (ORs) and 95 % CIs were combined and weighted by the method of "Dersimonian and Laird" to produce pooled ORs using a random-effects model. Moreover, we utilized the method reported by "Longnecker and Greenland" to evaluate linear trends and 95 % CIs by the ORs' natural logs and corresponding CIs from categories of Citrus intake. Finally, we evaluated the risk of publication bias and selection bias by inspecting for asymmetry in the pre-specified funnel plots of the study OR against the standard error of the OR's logarithm and by "Egger's test". RESULTS We included twenty-one studies in the final review. Pooled analyses suggested that those with the highest Citrus fruit intake compared to the lowest intake had a 9% reduction in lung cancer risk [OR 0.91 (95 % CI 0.84-0.98)]. We found a nonlinear association between Citrus intake and lung cancer risk in the dose-response analysis (p = 0.0054) and that the risk reached the minimum (OR = 0.91) around 60 g/d. However, no obvious dose-response association was observed with intakes above 80 g/d. CONCLUSION We found that Citrus fruit intake was negatively associated with the risk of lung cancer. Besides, there was a nonlinear dose-response relationship between Citrus intake and lung cancer risk within a certain range.
Collapse
Affiliation(s)
- Jie Wang
- Hongqiao International Institute of Medicine, Shanghai Tongren Hospital / School of Public Health, Shanghai Jiao Tong University School of Medicine, No. 227, South Chongqing Road, Shanghai, 200025, China
| | - Jing Gao
- Hongqiao International Institute of Medicine, Shanghai Tongren Hospital / Clinical Research Institute, Shanghai Jiao Tong University School of Medicine, No. 227, South Chongqing Road, Shanghai, 200025, China.
| | - Hong-Li Xu
- Hongqiao International Institute of Medicine, Shanghai Tongren Hospital / Clinical Research Institute, Shanghai Jiao Tong University School of Medicine, No. 227, South Chongqing Road, Shanghai, 200025, China
| | - Ying Qian
- Hongqiao International Institute of Medicine, Shanghai Tongren Hospital / School of Public Health, Shanghai Jiao Tong University School of Medicine, No. 227, South Chongqing Road, Shanghai, 200025, China
| | - Li Xie
- Hongqiao International Institute of Medicine, Shanghai Tongren Hospital / Clinical Research Institute, Shanghai Jiao Tong University School of Medicine, No. 227, South Chongqing Road, Shanghai, 200025, China
| | - Herbert Yu
- Cancer Epidemiology Program, University of Hawaii Cancer Center, 701 Ilalo Street, Honolulu, HI, 96813, USA
| | - Bi-Yun Qian
- Hongqiao International Institute of Medicine, Shanghai Tongren Hospital / Clinical Research Institute, Shanghai Jiao Tong University School of Medicine, No. 227, South Chongqing Road, Shanghai, 200025, China; Shanghai Clinical Research Promotion and Development Center, Shanghai Shenkang Hospital Development Center, No. 2 Kangding Road, Shanghai, 200041, China.
| |
Collapse
|
12
|
Yin X, Zhu Z, Hosgood HD, Lan Q, Seow WJ. Reproductive factors and lung cancer risk: a comprehensive systematic review and meta-analysis. BMC Public Health 2020; 20:1458. [PMID: 32977782 PMCID: PMC7519481 DOI: 10.1186/s12889-020-09530-7] [Citation(s) in RCA: 14] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/24/2020] [Accepted: 09/10/2020] [Indexed: 12/24/2022] Open
Abstract
BACKGROUND A number of studies have investigated the association between reproductive factors and lung cancer risk, however findings are inconsistent. This meta-analysis aimed to evaluate the association between female reproductive factors and lung cancer risk. METHODS We conducted a comprehensive systematic search to identify relevant and eligible studies published before 18th December 2019. Inter-study heterogeneity was assessed using the Q test and I2 statistic. Based on the heterogeneity of each reproductive factor, fixed or random effects models were used to calculate the summary odds ratios (ORs) and 95% confidence intervals (CIs). Subgroup analyses by study design, lung cancer subtypes, smoking status, and ethnicity were also performed. RESULTS A total of 66 studies with 20 distinct reproductive factors were included in this meta-analysis. Comparing the highest and lowest categories (reference) of each reproductive factor, parity (OR = 0.83, 95% CI = 0.72-0.96), menstrual cycle length (OR = 0.79, 95% CI = 0.65-0.96), and age at first birth (OR = 0.85, 95% CI = 0.74-0.98), were significantly associated with a lower risk of overall lung cancer. On the contrary, non-natural menopause was significantly associated with higher lung cancer risk (OR = 1.52, 95% CI = 1.25-1.86). Among never-smokers, a significant negative association was found between parity and lung cancer risk. Both parity and non-natural menopause were statistically significant in case-control studies. CONCLUSION These results suggest that certain reproductive factors may be associated with lung cancer risk. Future studies should further validate the associations, and investigate the underlying mechanisms.
Collapse
Affiliation(s)
- Xin Yin
- Saw Swee Hock School of Public Health, National University of Singapore and National University Health System, Singapore, 117549, Singapore
| | - Zhiying Zhu
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, 20850, USA
- Dermatology Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, 10065, USA
| | - H Dean Hosgood
- Department of Epidemiology and Population Health, Albert Einstein College of Medicine, The Bronx, NY, 10461, USA
| | - Qing Lan
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, 20850, USA
| | - Wei Jie Seow
- Saw Swee Hock School of Public Health, National University of Singapore and National University Health System, Singapore, 117549, Singapore.
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, 20850, USA.
- Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore and National University Health System, Singapore, 119228, Singapore.
| |
Collapse
|
13
|
Female reproductive factors and the risk of lung cancer in postmenopausal women: a nationwide cohort study. Br J Cancer 2020; 122:1417-1424. [PMID: 32203211 PMCID: PMC7188895 DOI: 10.1038/s41416-020-0789-7] [Citation(s) in RCA: 25] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/10/2019] [Revised: 02/18/2020] [Accepted: 02/27/2020] [Indexed: 02/08/2023] Open
Abstract
Background Reproductive factors and hormone use in postmenopausal women have been hypothesised to affect the risk of developing lung cancer, but the epidemiological evidence is inconsistent. Methods Using the Korean National Health Insurance System database, we identified 4,775,398 postmenopausal women older than 40 years who had undergone both cardiovascular health- and cancer screening between 1 January 2009 and 31 December 2014. Information about reproductive factors was obtained from a self-administered questionnaire. The risk of lung cancer was estimated using Cox proportional hazard regression models. Results During a median follow-up of 4.4 years, 16,556 women (15,223 non-smokers) were diagnosed with lung cancer. The risk of lung cancer was not significantly influenced by early menarche age (adjusted hazard ratio [aHR] 1.03 for menarche ≥18 vs. ≤14; 95% confidence interval [CI], 0.98–1.09) or late age at menopause (aHR 1.02 for menopause ≥55 vs. <40; 95% CI, 0.91–1.14). Furthermore, the number of children, duration of breastfeeding and use of hormone replacement therapy were not associated with the risk of lung cancer. Conclusions No statistically significant association was found between reproductive factors and the risk of lung cancer in postmenopausal Korean women.
Collapse
|
14
|
Ni X, Xu N, Wang Q. Meta-Analysis and Systematic Review in Environmental Tobacco Smoke Risk of Female Lung Cancer by Research Type. INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH 2018; 15:E1348. [PMID: 29954105 PMCID: PMC6068922 DOI: 10.3390/ijerph15071348] [Citation(s) in RCA: 19] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 06/06/2018] [Revised: 06/23/2018] [Accepted: 06/25/2018] [Indexed: 12/14/2022]
Abstract
More than 50% of women worldwide are exposed to Environmental Tobacco Smoke (ETS). The impact of ETS on lung cancer remains unclear. Cohort studies since the late 1990s have provided new evidence of female lung cancer risk due to ETS. The objective of this meta-analysis and systematic review was to analyze the association of ETS with female lung cancer risk from 1997 to 2017, organised based on research design. According to our applied inclusion and exclusion criteria, 41 published studies were included. The relative risk (RR) from the cohort studies or odds ratio (OR) from case-control studies were extracted to calculate the pooled risks based on the type of study. The summary risks of ETS were further explored with the modulators of ETS exposure sources and doses. The pooled risks of lung cancer in non-smoking women exposed to ETS were 1.35 (95% CI: 1.17⁻1.56), 1.17 (95% CI: 0.94⁻1.44), and 1.33 (95% CI: 1.17⁻1.51) for case-control studies, cohort studies, and both types of studies, respectively. The summary RR estimate of the cohort studies was not statistically significant, but the RR increased with increasing doses of ETS exposure (p trend < 0.05). Based on the results of this study, ETS might be an important risk factor of female lung cancer in non-smokers.
Collapse
Affiliation(s)
- Xue Ni
- National Institute of Environmental Health, Chinese Center for Disease Control and Prevention, No. 29 Nanwei Road, Beijing 100050, China.
| | - Ning Xu
- National Institute of Environmental Health, Chinese Center for Disease Control and Prevention, No. 29 Nanwei Road, Beijing 100050, China.
| | - Qiang Wang
- National Institute of Environmental Health, Chinese Center for Disease Control and Prevention, No. 29 Nanwei Road, Beijing 100050, China.
| |
Collapse
|
15
|
Min L, Wang F, Liang S, Yang J, Xu X. Menopausal status and the risk of lung cancer in women: A PRISMA-compliant meta-analysis. Medicine (Baltimore) 2017; 96:e7065. [PMID: 28658099 PMCID: PMC5500021 DOI: 10.1097/md.0000000000007065] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/13/2023] Open
Abstract
BACKGROUND Quantification of the association between menopausal status and risk of lung cancer is inconsistent. We carried out a meta-analysis of available studies to examine this issue. METHODS Relevant articles were identified by searching PudMed and Embase databases. Reference lists from selected papers were also reviewed. A random-effect model was used to calculate summary odds ratios (OR) and relative risk (RR) with 95% confidence interval (CI). Publication bias was estimated using Egger regression asymmetry test. RESULTS Eight eligible studies, including 5 case-control studies and 3 cohort studies, provided data for meta-analysis. Postmenopausal women had a statistically significant increased risk of lung cancer in all included studies (RR = 1.44, 95% CI: 1.12-1.85) and cohort studies (RR = 1.39, 95% CI: 1.05-1.86), but not in case-control studies (OR = 1.46, 95% CI: 0.95-2.24). CONCLUSIONS Overall, there was evidence that postmenopause is related to increased lung cancer risk. However, studies have produced slightly heterogeneous results (I = 38.40%). To obtain a better indication of relationship, well-designed large prospective studies are required.
Collapse
Affiliation(s)
- Lingfeng Min
- Department of Respiration, Clinical Medical School of Yangzhou University, Subei People's Hospital of Jiangsu Province, Yangzhou
| | - Fang Wang
- Department of Respiration, Clinical Medical School of Yangzhou University, Subei People's Hospital of Jiangsu Province, Yangzhou
| | - Sudong Liang
- Department of Urology, Taizhou People's Hospital, Taizhou, Jiangsu, China
| | - Junjun Yang
- Department of Respiration, Clinical Medical School of Yangzhou University, Subei People's Hospital of Jiangsu Province, Yangzhou
| | - Xingxiang Xu
- Department of Respiration, Clinical Medical School of Yangzhou University, Subei People's Hospital of Jiangsu Province, Yangzhou
| |
Collapse
|
16
|
Lee PN, Fry JS, Forey BA, Hamling JS, Thornton AJ. Environmental tobacco smoke exposure and lung cancer: A systematic review. World J Meta-Anal 2016; 4:10. [DOI: 10.13105/wjma.v4.i2.10] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/24/2015] [Revised: 01/19/2016] [Accepted: 03/14/2016] [Indexed: 02/05/2023] Open
|
17
|
Tan HS, Tan MH, Chow KY, Chay WY, Lim WY. Reproductive factors and lung cancer risk among women in the Singapore Breast Cancer Screening Project. Lung Cancer 2015; 90:499-508. [PMID: 26476714 DOI: 10.1016/j.lungcan.2015.10.003] [Citation(s) in RCA: 16] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/06/2015] [Revised: 09/26/2015] [Accepted: 10/04/2015] [Indexed: 11/17/2022]
Abstract
OBJECTIVES A growing body of literature suggests that female hormones play a role in lung cancer risk. Our study aims to examine the relationship between reproductive factors and lung cancer incidence in a large prospectively enrolled cohort in Singapore. MATERIALS AND METHODS Multivariate Cox proportional hazard regression models were used to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs) of lung cancer for each exposure, adjusting for smoking, age at entry, ethnicity and body mass index. RESULTS Among 28,222 women aged 50-64 years enrolled in the Singapore Breast Cancer Screening Project from October 1994 to February 1997, we identified 311 incident lung cancer cases (253 in non-smokers) over an average of 15.8 years of follow-up to 31 December 2011. Higher parity was associated with decreased lung cancer risk. Compared with nulliparous women, those with 1-2, 3-4, and ≥5 deliveries had a hazard ratio (HR) of 0.56, 0.55 and 0.45, respectively (P(trend)<0.01). This association was observed in both smokers and non-smokers, and in both adenocarcinomas and non-adenocarcinomas. Reproductive period, breastfeeding, oral contraceptive and hormone replacement therapy use did not seem to influence the risk of getting lung cancer. CONCLUSION Our findings add to the existing evidence that parous women have a lower lung cancer risk than nulliparous women.
Collapse
Affiliation(s)
- Hui Shan Tan
- Saw Swee Hock School of Public Health, National University of Singapore, Singapore; Division of Medical Oncology, National Cancer Centre Singapore, Singapore
| | - Min-Han Tan
- Saw Swee Hock School of Public Health, National University of Singapore, Singapore; Division of Medical Oncology, National Cancer Centre Singapore, Singapore; Institute of Bioengineering and Nanotechnology, Singapore
| | | | - Wen Yee Chay
- Division of Medical Oncology, National Cancer Centre Singapore, Singapore
| | - Wei-Yen Lim
- Saw Swee Hock School of Public Health, National University of Singapore, Singapore.
| |
Collapse
|
18
|
Fan WC, Ting WY, Lee MC, Huang SF, Chiu CH, Lai SL, Chen YM, Shih JF, Lin CH, Kao SJ, Wu MF, Tsao TCY, Wu CH, Yang KY, Lee YC, Feng JY, Su WJ. Latent TB infection in newly diagnosed lung cancer patients - A multicenter prospective observational study. Lung Cancer 2014; 85:472-8. [PMID: 25063540 DOI: 10.1016/j.lungcan.2014.07.001] [Citation(s) in RCA: 23] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/11/2014] [Revised: 06/20/2014] [Accepted: 07/01/2014] [Indexed: 01/06/2023]
Abstract
OBJECTIVES Lung cancer and tuberculosis (TB) share common risk factors and are associated with high morbidity and mortality. Coexistence of lung cancer and TB were reported in previous studies, with uncertain pathogenesis. The association between lung cancer and latent TB infection (LTBI) remains to be explored. METHODS Newly diagnosed, treatment-naïve lung cancer patients were prospectively enrolled from four referral medical centers in Taiwan. The presence of LTBI was determined by QuantiFERON-TB Gold In-Tube (QFT-GIT). Demographic characteristics and cancer-related factors associated with LTBI were investigated. The survival status was also analyzed according to the status of LTBI. RESULTS A total of 340 lung cancer patients were enrolled, including 96 (28.2%) LTBI, 214 (62.9%) non-LTBI, and 30 (8.8%) QFT-GIT results-indeterminate cases. Non-adenocarcinoma cases had higher proportion of LTBI than those of adenocarcinoma, especially in patients with younger age. In multivariate analysis, COPD (OR 2.41, 95% CI 1.25-4.64), fibrocalcified lesions on chest radiogram (OR 2.73, 95% CI 1.45-5.11), and main tumor located in typical TB areas (OR 2.02, 95% CI 1.15-3.55) were independent clinical predictors for LTBI. Kaplan-Meier survival analysis demonstrated patients with indeterminate QFT-GIT results had significantly higher 1-year all-cause mortality than those with LTBI (p<0.001) and non-LTBI (p=0.003). In multivariate analysis, independent predictors for 1-year all-cause mortality included BMI<18.5 (HR 2.09, 95% CI 1.06-4.14, p=0.033), advanced stage of lung cancer (RR 7.76, 95% CI 1.90-31.78, p=0.004), and indeterminate QFT-GIT results (RR 2.40, 95% CI 1.27-4.54, p=0.007). CONCLUSIONS More than one-quarter of newly diagnosed lung cancer patients in Taiwan have LTBI. The independent predictors for LTBI include COPD, fibrocalcified lesions on chest radiogram, and main tumor located in typical TB areas. The survival rate is comparable between LTBI and non-LTBI cases. However, indeterminate QFT-GIT result was an independent predictor for all-cause mortality in lung cancer patients.
Collapse
Affiliation(s)
- Wen-Chien Fan
- Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan, ROC
| | - Wen-Ying Ting
- Department of Chest Medicine, Taipei Veterans General Hospital, Taipei, Taiwan, ROC
| | - Ming-Che Lee
- Department of Chest Medicine, Taipei Veterans General Hospital, Taipei, Taiwan, ROC
| | - Shiang-Fen Huang
- School of Medicine, National Yang-Ming University, Taipei, Taiwan, ROC; Division of Infectious Disease, Department of Internal Medicine, Taipei Veterans General Hospital, Taiwan, ROC
| | - Chao-Hua Chiu
- Department of Chest Medicine, Taipei Veterans General Hospital, Taipei, Taiwan, ROC; School of Medicine, National Yang-Ming University, Taipei, Taiwan, ROC
| | - Shinn-Liang Lai
- Department of Chest Medicine, Taipei Veterans General Hospital, Taipei, Taiwan, ROC; School of Medicine, National Yang-Ming University, Taipei, Taiwan, ROC
| | - Yuh-Min Chen
- Department of Chest Medicine, Taipei Veterans General Hospital, Taipei, Taiwan, ROC; School of Medicine, National Yang-Ming University, Taipei, Taiwan, ROC; College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan, ROC
| | - Jen-Fu Shih
- Department of Chest Medicine, Taipei Veterans General Hospital, Taipei, Taiwan, ROC; School of Medicine, National Yang-Ming University, Taipei, Taiwan, ROC
| | - Ching-Hsiung Lin
- Division of Chest Medicine, Department of Internal Medicine, Changhua Christian Hospital, Changhua, Taiwan, ROC; Department of Respiratory Care, College of Health Sciences, Chang Jung Christian University, Tainan, Taiwan, ROC; School of Medicine, Chung Shan Medical University, Taichung, Taiwan, ROC
| | - Shang-Jyh Kao
- Pulmonary Division, Department of Internal Medicine, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan, ROC; Taipei Medical University, Taipei, Taiwan, ROC
| | - Ming-Fang Wu
- School of Medicine, Chung Shan Medical University, Taichung, Taiwan, ROC; Divisions of Chest Medicine and Medical Oncology, Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan, ROC
| | - Thomas Chang Yao Tsao
- Department of Chest Medicine, Chung Shan Medical University and Chung Shan Medical University Hospital, Taichung, Taiwan, ROC
| | - Chieh-Hung Wu
- Department of Chest Medicine, Taipei Veterans General Hospital, Taipei, Taiwan, ROC; Institute of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan, ROC
| | - Kuang-Yao Yang
- Department of Chest Medicine, Taipei Veterans General Hospital, Taipei, Taiwan, ROC; Infection and Immunity Research Center, School of Medicine, National Yang-Ming University, Taipei, Taiwan, ROC
| | - Yu-Chin Lee
- Department of Chest Medicine, Taipei Veterans General Hospital, Taipei, Taiwan, ROC; School of Medicine, National Yang-Ming University, Taipei, Taiwan, ROC
| | - Jia-Yih Feng
- Department of Chest Medicine, Taipei Veterans General Hospital, Taipei, Taiwan, ROC; Institute of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan, ROC.
| | - Wei-Juin Su
- Department of Chest Medicine, Taipei Veterans General Hospital, Taipei, Taiwan, ROC; School of Medicine, National Yang-Ming University, Taipei, Taiwan, ROC.
| |
Collapse
|
19
|
Zhang Y, Yin Z, Shen L, Wan Y, Zhou B. Menstrual factors, reproductive factors and lung cancer risk: a meta-analysis. ZHONGGUO FEI AI ZA ZHI = CHINESE JOURNAL OF LUNG CANCER 2013; 15:701-19. [PMID: 23249716 PMCID: PMC6000047 DOI: 10.3779/j.issn.1009-3419.2012.12.04] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Indexed: 11/05/2022]
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.
Collapse
Affiliation(s)
- Yue Zhang
- Department of Epidemiology, School of Public Health, China Medical University, Shenyang 110001, China
| | | | | | | | | |
Collapse
|
20
|
Increased lung cancer risk among patients with pneumococcal pneumonia: a nationwide population-based cohort study. Lung 2013; 192:159-65. [PMID: 24150601 DOI: 10.1007/s00408-013-9523-z] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/06/2013] [Accepted: 10/04/2013] [Indexed: 12/23/2022]
Abstract
BACKGROUND The possible effects of pneumonia on subsequent lung cancer have been reported, but no relevant publications have focused on the association between pneumococcal pneumonia and lung cancer. The purpose of this study was to perform a nationwide population-based cohort study to investigate the risk of lung cancer after pneumococcus infection. METHODS This nationwide population-based cohort study was based on data obtained from the Taiwan National Health Insurance Database. In total, 22,034 pneumococcal pneumonia patients and 88,136 controls, matched for age and sex, were recruited for the study from 1997 to 2010. RESULTS The incidence rate of lung cancer (28.2 per 1,000 person-years) was significantly higher in pneumococcal pneumonia patients than in controls (8.7 per 1,000 person-years; incidence rate ratio, 3.25; 95 % confidence interval, 3.09-3.42; p < 0.001). Cox proportional hazards regression analysis showed a hazard ratio of 4.24 (95 % confidence interval, 3.96-4.55) for the pneumococcal pneumonia cohort after adjustment for age, gender, and comorbidities. CONCLUSIONS Pneumococcal pneumonia is associated with an increased risk of lung cancer. Thus, physicians should remain aware of this association when assessing patients with pneumococcal pneumonia.
Collapse
|
21
|
Pesatori AC, Carugno M, Consonni D, Caporaso NE, Wacholder S, Tucker M, Landi MT. Reproductive and hormonal factors and the risk of lung cancer: the EAGLE study. Int J Cancer 2013; 132:2630-9. [PMID: 23129166 PMCID: PMC3609937 DOI: 10.1002/ijc.27926] [Citation(s) in RCA: 33] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/17/2012] [Accepted: 10/18/2012] [Indexed: 12/15/2022]
Abstract
Evidence about the role for reproductive and hormonal factors in the etiology of lung cancer in women is conflicting. To clarify this question, we examined 407 female cases and 499 female controls from the Environment And Genetics in Lung cancer Etiology population-based case-control study. Subjects were interviewed in person using a computer-assisted personal interview to assess demographics, education, smoking history, medical history, occupational history, reproductive and hormonal factors. Associations of interest were investigated using logistic regression models, adjusted for catchment area and age (matching variables), cigarette smoking (status, pack-years and time since quitting). Additional confounding variables were investigated but did not substantially affect the results. We observed a reduced risk of lung cancer among women with later age at first live birth [≥31 years: odds ratio (OR) = 0.57, 95% confidence interval (CI) = 0.31-1.06, p-trend = 0.05], later age at menopause (≥51 years: OR = 0.49, 95%CI = 0.31-0.79, p-trend = 0.003) and longer reproductive periods (≥41 years: OR = 0.44, 95%CI = 0.25-0.79, p-trend = 0.01). A reduced risk was also observed for hormone replacement therapy (OR = 0.63, 95%CI = 0.42-0.95, p = 0.03) and oral contraceptive use (OR = 0.67, 95%CI = 0.45-1.00, p = 0.05) but no trend with duration of use was detected. Menopausal status (both natural and induced) was associated with an augmented risk. No additional associations were identified for other reproductive variables. This study suggests that women who continue to produce estrogens have a lower lung cancer risk. Large studies with great number of never smoking women, biomarkers of estrogen and molecular classification of lung cancer are needed for a more comprehensive view of the association between reproductive factors and lung cancer risk.
Collapse
Affiliation(s)
- Angela Cecilia Pesatori
- Department of Clinical Sciences and Community Health, EPOCA, Epidemiology Research Center, Università degli Studi di Milano, Milan, Italy.
| | | | | | | | | | | | | |
Collapse
|
22
|
The Role of Bacteria in Cancer Development. Infect Agent Cancer 2013. [DOI: 10.1007/978-94-007-5955-8_3] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/25/2022] Open
|
23
|
Barrera-Rodriguez R, Morales-Fuentes J. Lung cancer in women. LUNG CANCER-TARGETS AND THERAPY 2012; 3:79-89. [PMID: 28210127 DOI: 10.2147/lctt.s37319] [Citation(s) in RCA: 31] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Key Words] [Subscribe] [Scholar Register] [Indexed: 01/01/2023]
Abstract
Recent biological advances in tumor research provide clear evidence that lung cancer in females is different from that in males. These differences appear to have a direct impact on the clinical presentation, histology, and outcomes of lung cancer. Women are more likely to present with lung adenocarcinoma, tend to receive a diagnosis at an earlier age, and are more likely to be diagnosed with localized disease. Women may also be more predisposed to molecular aberrations resulting from the carcinogenic effects of tobacco, but do not appear to be more susceptible than men to developing lung cancer. The gender differences found in female lung cancer make it mandatory that gender stratification is used in clinical trials in order to improve the survival rates of patients with lung cancer.
Collapse
Affiliation(s)
- Raúl Barrera-Rodriguez
- Biochemistry and Environmental Medicine Laboratory, National Institute of Respiratory Disease
| | - Jorge Morales-Fuentes
- Lung Cancer Medical Service, National Institute of Respiratory Disease, Tlalpan, Mexico City, Distrito Federal, Mexico
| |
Collapse
|
24
|
Yang WS, Wong MY, Vogtmann E, Tang RQ, Xie L, Yang YS, Wu QJ, Zhang W, Xiang YB. Meat consumption and risk of lung cancer: evidence from observational studies. Ann Oncol 2012; 23:3163-3170. [PMID: 22855553 PMCID: PMC3501234 DOI: 10.1093/annonc/mds207] [Citation(s) in RCA: 68] [Impact Index Per Article: 5.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/08/2012] [Revised: 05/23/2012] [Accepted: 05/23/2012] [Indexed: 02/04/2023] Open
Abstract
BACKGROUND A number of epidemiological studies have reported inconsistent findings on the association between meat consumption and lung cancer. DESIGN We therefore conducted a systematic review and meta-analysis to investigate the relationship between meat consumption and lung cancer risk in epidemiological studies. RESULTS Twenty-three case-control and 11 cohort studies were included. All studies adjusted for smoking or conducted in never smokers. The summary relative risks (RRs) of lung cancer for the highest versus lowest intake categories were 1.35 (95% confidence interval (CI) 1.08-1.69) for total meat, 1.34 (95% CI 1.18-1.52) for red meat, and 1.06 (95% CI 0.90-1.25) for processed meat. An inverse association was found between poultry intake and lung cancer (RR = 0.91, 95% CI 0.85-0.97), but not for total white meat (RR = 1.06, 95% CI 0.82-1.37) or fish (RR = 1.01, 95% CI 0.96-1.07). CONCLUSIONS The relationship between meat intake and lung cancer risk appears to depend on the types of meat consumed. A high intake of red meat may increase the risk of lung cancer by about 35%, while a high intake of poultry decreases the risk by about 10%. More well-designed cohort studies on meat mutagens or heme iron, meat cooking preferences, and doneness level are needed to fully characterize this meat-lung cancer association.
Collapse
Affiliation(s)
- W S Yang
- State Key Laboratory of Oncogene and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai; Department of Epidemiology, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China
| | - M Y Wong
- Department of Mathematics, The Hong Kong University of Science & Technology, Hong Kong, China
| | - E Vogtmann
- State Key Laboratory of Oncogene and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai; Department of Epidemiology, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China; Department of Epidemiology, University of Alabama at Birmingham, Birmingham, USA
| | - R Q Tang
- State Key Laboratory of Oncogene and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai; Department of Epidemiology, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China
| | - L Xie
- State Key Laboratory of Oncogene and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai; Department of Epidemiology, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China
| | - Y S Yang
- Department of Mathematics, The Hong Kong University of Science & Technology, Hong Kong, China
| | - Q J Wu
- State Key Laboratory of Oncogene and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai; Department of Epidemiology, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China
| | - W Zhang
- State Key Laboratory of Oncogene and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai; Department of Epidemiology, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China
| | - Y B Xiang
- State Key Laboratory of Oncogene and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai; Department of Epidemiology, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
| |
Collapse
|
25
|
Cheng MH, Tsai SS, Chen CC, Ho SC, Chiu HF, Wu TN, Yang CY. Parity and risk of death from lung cancer among a cohort of premenopausal parous women in Taiwan. J Epidemiol 2012; 22:364-9. [PMID: 22522149 PMCID: PMC3798656 DOI: 10.2188/jea.je20110123] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/18/2022] Open
Abstract
Background We examined the association between parity and risk of lung cancer. Methods The study cohort consisted of all women with a record of a first singleton birth in the Taiwanese Birth Register between 1978 and 1987. We tracked each woman from the time of their first childbirth to 31 December 2009. Follow-up was terminated when the mother died, when she reached age 50 years, or on 31 December 2009, whichever occurred first. The vital status of mothers was ascertained by linking records with the computerized mortality database. Cox proportional hazard regression models were used to estimate hazard ratios (HRs) for death from lung cancer associated with parity. Results There were 1375 lung cancer deaths during 32 243 637.08 person-years of follow-up. The mortality rate of lung cancer was 4.26 cases per 100 000 person-years. As compared with women who had given birth to only 1 child, the adjusted HR was 1.13 (95% CI, 0.94–1.35) for women who had 2 children, 1.10 (0.91–1.33) for those who had 3 children, and 1.22 (0.96–1.54) for those who had 4 or more children. Conclusions The findings suggest that premenopausal women of higher parity tended to have an increased risk of lung cancer, although the trend was not statistically significant.
Collapse
Affiliation(s)
- Meng-Hsuan Cheng
- Division of Pulmonary and Critical Medicine, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
| | | | | | | | | | | | | |
Collapse
|
26
|
Brinton LA, Schwartz L, Spitz MR, Park Y, Hollenbeck AR, Gierach GL. Unopposed estrogen and estrogen plus progestin menopausal hormone therapy and lung cancer risk in the NIH-AARP Diet and Health Study Cohort. Cancer Causes Control 2012; 23:487-96. [PMID: 22367699 PMCID: PMC3328187 DOI: 10.1007/s10552-012-9904-2] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/21/2011] [Accepted: 01/23/2012] [Indexed: 10/28/2022]
Abstract
PURPOSE Previous studies have reported that lung cancer risk may be decreased, increased, or unaffected by prior use of menopausal hormone therapy (MHT). METHODS To assess this issue further, we examined relationships among 118,008 women, ages 50-71 years who were recruited during 1995-1996 for the NIH-AARP Diet and Health Study and in whom 2,097 incident lung carcinomas were identified during follow-up through 2006. Multivariable Cox proportional hazards models estimated relative risks (RR) and 95% confidence intervals (CIs) associated with various measures of self-reported MHT use. RESULTS We found no evidence that either estrogen therapy (ET)-only or estrogen plus progestin therapy (EPT) use was substantially related to subsequent lung cancer risk (respective RRs and 95% CIs for ever use = 0.97, 0.86-1.09 and 1.03, 0.90-1.17). There were no significant variations according to currency or duration of use of either formulation, nor was there evidence that risks varied within subgroups defined by cigarette smoking or body size. The absence of effect was seen for nearly all lung cancer subtypes, with the exception of an increased risk of undifferentiated/large cell cancers associated with long-term ET-only use (p (trend) = 0.02), a relationship not observed among EPT users. CONCLUSIONS Our results failed to support any substantial alterations in lung cancer risk associated with use of either unopposed estrogen or estrogen plus progestin MHT, even when detailed exposure measures and other risk predictors were considered.
Collapse
Affiliation(s)
- Louise A Brinton
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD 20852, USA.
| | | | | | | | | | | |
Collapse
|
27
|
Brinton LA, Gierach GL, Andaya A, Park Y, Schatzkin A, Hollenbeck AR, Spitz MR. Reproductive and hormonal factors and lung cancer risk in the NIH-AARP Diet and Health Study cohort. Cancer Epidemiol Biomarkers Prev 2011; 20:900-11. [PMID: 21467241 PMCID: PMC3507989 DOI: 10.1158/1055-9965.epi-10-1325] [Citation(s) in RCA: 58] [Impact Index Per Article: 4.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/29/2022] Open
Abstract
BACKGROUND Lung cancer exhibits unique patterns among women including high adenocarcinoma rates among nonsmokers. Inconsistent findings about hormonal factors on risk may reflect incomplete control for confounding, misclassification of exposures, or insufficient attention to variation by histology. METHODS Among 185,017 women, ages 50 to 71 years, recruited during 1995 and 1996 for the NIH-AARP (American Association of Retired Persons) Diet and Health Study, we identified 3,512 incident lung cancers (including 276 in never smokers) in follow-up through December 2006. Multivariable Cox proportional hazards models estimated relative risks (RR) and 95% CIs for self-reported hormonally related risk factors. RESULTS After adjustment for smoking and other confounders, subjects with late menarche were at reduced risk, with the association specific for adenocarcinomas (RR = 0.72 for menarche 15+ vs. <11, P(trend) < 0.01). Subjects with early ages at ovarian cessation (either from natural menopause or bilateral oophorectomy) were at an increased risk for adenocarcinomas and squamous cell tumors, but the associations were strongest for smokers, suggesting either residual confounding or an enhanced effect of menopausally related factors among subjects with decreased endogenous estrogens. In contrast, we saw no relationships of risk with either parity, age at first birth, or exogenous hormone use. CONCLUSIONS Elevated levels of hormones may adversely affect lung function early in life while assisting with cellular and immunologic responses later in life. Additional attention toward the role of hormonal factors may further our understanding of lung carcinogenesis. IMPACT Our findings provide some support for a role of hormonal factors in the etiology of lung cancer, although the mechanisms appear complicated.
Collapse
Affiliation(s)
- Louise A Brinton
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Rockville, MD 20852, USA.
| | | | | | | | | | | | | |
Collapse
|
28
|
Increased lung cancer risk among patients with pulmonary tuberculosis: a population cohort study. J Thorac Oncol 2011; 6:32-7. [PMID: 21150470 DOI: 10.1097/jto.0b013e3181fb4fcc] [Citation(s) in RCA: 148] [Impact Index Per Article: 10.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
INTRODUCTION Given one third of the human population have been infected with tuberculosis, it is important to delineate the relationship between tuberculosis and lung cancer. This study explored whether contracting pulmonary tuberculosis is associated with an increased risk of developing lung cancers. METHODS In a cohort of 716,872 insured subjects, free from cancers, aged 20 years and older, 4480 patients with newly diagnosed tuberculosis were identified from the universal insurance claims in 1998-2000 and tracked until 2007 with the remaining insured without tuberculosis. We compared the incidence of lung cancers between the two cohorts and measured the associated hazard of developing lung cancer. RESULTS The incidence of lung cancers was approximately 11-fold higher in the cohort of patients with tuberculosis than nontuberculosis subjects (26.3 versus 2.41 per 10,000 person-years). Cox proportional hazard regression analysis showed a hazard ratio of 4.37 (95% confidence interval [CI]: 3.56-5.36) for the tuberculosis cohort after adjustment for the sociodemographic variables or 3.32 (95% CI: 2.70-4.09) after further adjustment for chronic obstructive pulmonary disease (COPD), smoking-related cancers (other than lung cancer), etc. The hazard ratio increased to 6.22 (95% CI: 4.87-7.94) with the combined effect with COPD or to 15.5 (95% CI: 2.17-110) with the combined effect with other smoking-related cancers. CONCLUSIONS This study provides a compelling evidence of increased lung cancer risk among individuals with tuberculosis. The risk may increase further with coexisting COPD or other smoking-related cancers.
Collapse
|
29
|
Abstract
Lung cancer in never smokers (LCINS) has lately been recognized as a unique disease based on rapidly gained knowledge from genomic changes to treatment responses. The focus of this article is on current knowledge and challenges with regard to LCINS expanded from recent reviews highlighting five areas: (1) distribution of LCINS by temporal trends, geographic regions, and populations; (2) three well-recognized environmental risk factors; (3) other plausible environmental risk factors; (4) prior chronic lung diseases and infectious diseases as risk factors; and (5) lifestyles as risk or protective factors. This article will also bring attention to recently published literature in two pioneering areas: (1) histological characteristics, clinical features with emerging new effective therapies, and social and psychological stigma; and (2) searching for susceptibility genes using integrated genomic approaches.
Collapse
Affiliation(s)
- Ping Yang
- Department of Health Sciences Research, College of Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA.
| |
Collapse
|
30
|
Brenner DR, McLaughlin JR, Hung RJ. Previous lung diseases and lung cancer risk: a systematic review and meta-analysis. PLoS One 2011; 6:e17479. [PMID: 21483846 PMCID: PMC3069026 DOI: 10.1371/journal.pone.0017479] [Citation(s) in RCA: 242] [Impact Index Per Article: 17.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/09/2010] [Accepted: 02/05/2011] [Indexed: 01/09/2023] Open
Abstract
BACKGROUND In order to review the epidemiologic evidence concerning previous lung diseases as risk factors for lung cancer, a meta-analysis and systematic review was conducted. METHODS Relevant studies were identified through MEDLINE searches. Using random effects models, summary effects of specific previous conditions were evaluated separately and combined. Stratified analyses were conducted based on smoking status, gender, control sources and continent. RESULTS A previous history of COPD, chronic bronchitis or emphysema conferred relative risks (RR) of 2.22 (95% confidence interval (CI): 1.66, 2.97) (from 16 studies), 1.52 (95% CI: 1.25, 1.84) (from 23 studies) and 2.04 (95% CI: 1.72, 2.41) (from 20 studies), respectively, and for all these diseases combined 1.80 (95% CI: 1.60, 2.11) (from 39 studies). The RR of lung cancer for subjects with a previous history of pneumonia was 1.43 (95% CI: 1.22-1.68) (from 22 studies) and for subjects with a previous history of tuberculosis was 1.76 (95% CI=1.49, 2.08), (from 30 studies). Effects were attenuated when restricting analysis to never smokers only for COPD/emphysema/chronic bronchitis (RR=1.22, 0.97-1.53), however remained significant for pneumonia 1.36 (95% CI: 1.10, 1.69) (from 8 studies) and tuberculosis 1.90 (95% CI: 1.45, 2.50) (from 11 studies). CONCLUSIONS Previous lung diseases are associated with an increased risk of lung cancer with the evidence among never smokers supporting a direct relationship between previous lung diseases and lung cancer.
Collapse
Affiliation(s)
- Darren R. Brenner
- Samuel Lunenfeld Research Institute
of Mount Sinai Hospital, Toronto, Canada
- The Dalla Lana School of Public
Health, University of Toronto, Toronto, Canada
| | - John R. McLaughlin
- Samuel Lunenfeld Research Institute
of Mount Sinai Hospital, Toronto, Canada
- The Dalla Lana School of Public
Health, University of Toronto, Toronto, Canada
- Cancer Care Ontario, Toronto, Canada
| | - Rayjean J. Hung
- Samuel Lunenfeld Research Institute
of Mount Sinai Hospital, Toronto, Canada
- The Dalla Lana School of Public
Health, University of Toronto, Toronto, Canada
- * E-mail:
| |
Collapse
|
31
|
Meinhold CL, Berrington de González A, Bowman ED, Brenner AV, Jones RT, Lacey JV, Loffredo CA, Perlmutter D, Schonfeld SJ, Trivers GE, Harris CC. Reproductive and hormonal factors and the risk of nonsmall cell lung cancer. Int J Cancer 2011; 128:1404-13. [PMID: 20473922 PMCID: PMC3010247 DOI: 10.1002/ijc.25434] [Citation(s) in RCA: 35] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/04/2023]
Abstract
Although exposure to estrogen may directly influence or modify the association between cigarette smoking and lung cancer risk, results from epidemiologic studies examining the association between reproductive and hormonal factors and risk of lung cancer among women have been inconsistent. Between 1998 and 2008, 430 women diagnosed with nonsmall cell lung cancer, 316 hospital controls and 295 population controls were recruited into the multi-center Maryland Lung Cancer Study. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) according to reproductive and hormonal exposures adjusting for age, smoking, passive smoking, education and household income. Results were similar for hospital and population based controls, so the control groups were combined. Reduced risks of lung cancer were observed among women with greater parity (≥ 5 vs. 1-2 births: OR = 0.50, 95% CI = 0.32, 0.78, p-trend = 0.002) and later ages at last birth (≥ 30 vs. <25 years old: OR = 0.68, 95% CI = 0.48, 0.98, p-trend = 0.04). After mutual adjustment parity, but not age at last birth, remained significantly inversely associated with risk (p-trend = 0.01). No associations were found for nonsmall cell lung cancer risk with age at menarche, age at first birth, menopausal status, oral contraceptive use or menopausal hormone use, including use of oral estrogens. Compatible with findings from recent epidemiologic studies, we observed a reduction in the risk of nonsmall cell lung cancer with increasing number of births. Other reproductive and hormonal exposures, including menopausal hormone therapy use, were not associated with risk.
Collapse
Affiliation(s)
- Cari L Meinhold
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Rockville, MD 20852, USA.
| | | | | | | | | | | | | | | | | | | | | |
Collapse
|
32
|
Baik CS, Strauss GM, Speizer FE, Feskanich D. Reproductive factors, hormone use, and risk for lung cancer in postmenopausal women, the Nurses' Health Study. Cancer Epidemiol Biomarkers Prev 2010; 19:2525-33. [PMID: 20739629 PMCID: PMC2952036 DOI: 10.1158/1055-9965.epi-10-0450] [Citation(s) in RCA: 71] [Impact Index Per Article: 4.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022] Open
Abstract
BACKGROUND There is increasing evidence suggesting that female hormones may play a significant role in lung cancer development. We evaluated the associations between reproductive factors, exogenous hormone use, and lung cancer incidence in the Nurses' Health Study. METHODS We assessed age at menopause, age at menarche, type of menopause, parity, age at first birth, postmenopausal hormone (PMH) use, and past oral contraceptive use in 107,171 postmenopausal women. Cox models were used to estimate the hazard ratios for each exposure, adjusting for smoking and other covariates. RESULTS We identified 1,729 lung cancer cases during follow-up from 1984 to 2006. Menopause onset before 44 years of age (hazard ratio, 1.39; 95% confidence interval, 1.14-1.70) and past oral contraceptive use for >5 years (hazard ratio, 1.22; 95% confidence interval, 1.05-1.42) were associated with increased lung cancer risk. These associations were strongest in current smokers and small cell histology. In never smokers, increased parity was associated with decreased risk among parous women (P trend = 0.03), whereas in current smokers, older age at first birth was associated with increased risk (P trend = 0.02). PMH use was not associated with overall lung cancer incidence. However, nonsignificant results of increased risk in adenocarcinoma were seen with current PMH use. CONCLUSIONS Our findings suggest female hormones may influence lung carcinogenesis, although the effect is likely modest, varied by histologic subtype, and altered by smoking. IMPACT Further investigation of the pathophysiology of female hormones in lung cancer subtypes and their interaction with smoking will lead to better understanding of lung carcinogenesis.
Collapse
Affiliation(s)
- Christina S Baik
- Division of Hematology-Oncology, Tufts Medical Center, Boston, Massachusetts, USA.
| | | | | | | |
Collapse
|
33
|
Clément-Duchêne C, Vignaud JM, Stoufflet A, Bertrand O, Gislard A, Thiberville L, Grosdidier G, Martinet Y, Benichou J, Hainaut P, Paris C. Characteristics of never smoker lung cancer including environmental and occupational risk factors. Lung Cancer 2010; 67:144-50. [DOI: 10.1016/j.lungcan.2009.04.005] [Citation(s) in RCA: 31] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/14/2008] [Revised: 01/25/2009] [Accepted: 04/15/2009] [Indexed: 10/20/2022]
|
34
|
Liang HY, Li XL, Yu XS, Guan P, Yin ZH, He QC, Zhou BS. Facts and fiction of the relationship between preexisting tuberculosis and lung cancer risk: a systematic review. Int J Cancer 2009; 125:2936-44. [PMID: 19521963 DOI: 10.1002/ijc.24636] [Citation(s) in RCA: 180] [Impact Index Per Article: 11.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/22/2022]
Abstract
There has been conflicting evidence concerning the possible association between tuberculosis (TB) and subsequent risk of lung cancer. To investigate whether currently published epidemiological studies can clarify this association, we performed a systematic review of 37 case-control and 4 cohort studies (published between January 1966 and January 2009) and a meta-analysis of risk estimates, with particular attention to the role of smoking, passive smoking and the timing of diagnosis of TB on this relationship. Data for the review show a significantly increased lung cancer risk associated with preexisting TB. Importantly, the association was not due to confounding by the effects of tobacco use (RR=1.8, 95% confidence interval (CI)=1.4-2.2, among never smoking individuals), lifetime environmental tobacco smoke exposure (RR=2.9, 95%CI=1.6-5.3, after controlling) or the timing of diagnosis of TB (the increased lung cancer risk remained 2-fold elevated for more than 20 years after TB diagnosis). Interestingly, the association was significant with adenocarcinoma (RR=1.6, 95%CI=1.2-2.1), but no significant associations with squamous and small cell type of lung cancer were observed. Although no causal mechanism has been demonstrated for such an association, present study supports a direct relation between TB and lung cancer, especially adenocarcinomas.
Collapse
Affiliation(s)
- Hui-Ying Liang
- Department of Epidemiology, School of Public Health, China Medical University, Shenyang, China
| | | | | | | | | | | | | |
Collapse
|
35
|
Relationships between lung adenocarcinoma and gender, age, smoking and occupational risk factors: A case-case study. Lung Cancer 2009; 68:146-53. [PMID: 19586681 DOI: 10.1016/j.lungcan.2009.06.007] [Citation(s) in RCA: 19] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/29/2009] [Revised: 06/08/2009] [Accepted: 06/11/2009] [Indexed: 11/24/2022]
Abstract
BACKGROUND The hypothesis that some risk factors for lung cancer may have more specific associations with particular histologic types remains controversial. The aim of this study was to investigate possible associations between adenocarcinoma and gender, age, smoking characteristics and selected occupational carcinogens in relation to other histologic types. METHODS This study included all histologically confirmed lung cancer cases diagnosed consecutively in two French University hospitals from 1997 to 2006. All medical data were obtained by face-to-face patient interviews. Occupational carcinogen exposures of each patient were assessed by an industrial hygienist. Relationships between risk factors and adenocarcinoma were analyzed by case-case comparisons using unconditional logistic regressions (ULRs). RESULTS A total of 1493 subjects were enrolled in this study, comprising 1303 men (87.3%), 67 nonsmokers (4.5%) and 489 adenocarcinomas (32.7%). Using ULR, no associations were observed between adenocarcinoma and age, gender or smoking characteristics except for a negative relationship with smoking duration (p<0.0001). Significant associations were observed between ADC and exposure to welding fumes and silica in the whole population and with polycyclic aromatic hydrocarbons in ever smokers. CONCLUSION This study demonstrated that some risk factors, such as duration of smoking and certain occupational exposures but not gender or age, have a more important influence on the incidence of lung ADC than on other histologic types. As the distribution of histologic types may reflect underlying biological mechanisms, these findings also suggest that lung carcinogenesis pathways should be studied in relation to smoking duration and other lung cancer risk factors.
Collapse
|
36
|
Berardi R, Verdecchia L, Paolo MDP, Giampieri R, Scartozzi M, Pierantoni C, Bianconi M, Mazzanti P, Cascinu S. Women and lung cancer: clinical and molecular profiling as a determinate for treatment decisions: a literature review. Crit Rev Oncol Hematol 2009; 69:223-236. [PMID: 18722785 DOI: 10.1016/j.critrevonc.2008.06.008] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/06/2008] [Revised: 06/23/2008] [Accepted: 06/24/2008] [Indexed: 11/26/2022] Open
Abstract
In the past decade the incidence of lung cancer among women has risen, whereas among men it has slightly declined. Important differences in lung cancer have been demonstrated between men and women, although many areas still remain controversial. Some biologic differences may justify the increase in response of women to therapy for lung cancer and can partially explain the improved survival of women compared with men. We extensively reviewed the published scientific literature on this topic in order to investigate the clinical and genetic profiling underlying lung cancer in women and to use this information as a tool for medical therapy.
Collapse
Affiliation(s)
- Rossana Berardi
- Clinica di Oncologia Medica, Azienda Ospedaliero-Universitaria Ospedali Riuniti Umberto I - GM Lancisi - G Salesi di Ancona, Italy
| | | | | | | | | | | | | | | | | |
Collapse
|
37
|
Stojsic J, Milovanovic I, Radojicic J, Milenkovic B. Lung cancer in women: histological type and patient age from 1985 to 2005. Med Oncol 2008; 26:265-8. [PMID: 18982463 DOI: 10.1007/s12032-008-9112-9] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/14/2008] [Accepted: 10/14/2008] [Indexed: 12/21/2022]
Abstract
The aim of the study was to analyse changes in histological type and age of presentation in female lung cancer patients during a period of 20 years. The obtained results are compared with those available from the literature published in various parts of the world.
Collapse
Affiliation(s)
- Jelena Stojsic
- Institute for Lung Diseases and Tuberculosis, Clinical Centre of Serbia, Belgrade, Serbia.
| | | | | | | |
Collapse
|
38
|
Chao C. Associations between beer, wine, and liquor consumption and lung cancer risk: a meta-analysis. Cancer Epidemiol Biomarkers Prev 2008; 16:2436-47. [PMID: 18006934 DOI: 10.1158/1055-9965.epi-07-0386] [Citation(s) in RCA: 44] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022] Open
Abstract
OBJECTIVE Epidemiologic studies suggest that the effect on lung cancer risk may be different for beer, wine, and liquor. We conducted dose-specific meta-analyses and dose-response meta-regression to summarize findings from the current literature on the association between consumption of beer, wine, or liquor and lung cancer risk. RESULTS Average beer consumption of one drink or greater per day was associated with an increased risk of lung cancer [relative risk (RR), 1.23; 95% confidence interval (95% CI), 1.06-1.41]. This association was observed in both men and women, although it was only significant in men. A J-shaped dose-response curve was suggested for beer intake. An inverse association was observed for both average wine consumption of less than one drink per day (RR, 0.77; 95% CI, 0.59-1.00) and one drink or greater per day (RR, 0.78; 95% CI, 0.60-1.02) in the drinking range incurred in the source studies. Average liquor consumption of one drink or greater per day was found to be associated with increased risk in men (RR, 1.33; 95% CI, 1.10-1.62). No association was observed for liquor drinking in women. The presence of heterogeneity between studies was detected. Study design, country, gender, adjustment factors, and lung cancer histologic type were not significant predictors of the heterogeneity. CONCLUSIONS The results from this meta-analysis suggest that high consumption of beer and liquors may be associated with increased lung cancer risk, whereas modest wine consumption may be inversely associated with risk. More research with improved control of confounding is needed to confirm these findings and to establish the dose-response relationship, particularly risk at high consumption levels.
Collapse
Affiliation(s)
- Chun Chao
- Department of Research and Evaluation, Kaiser Permanente Southern California, Pasadena, California 91101-2453, USA.
| |
Collapse
|
39
|
Sone S, Nakayama T, Honda T, Tsushima K, Li F, Haniuda M, Takahashi Y, Suzuki T, Yamanda T, Kondo R, Hanaoka T, Takayama F, Kubo K, Fushimi H. Long-term follow-up study of a population-based 1996–1998 mass screening programme for lung cancer using mobile low-dose spiral computed tomography. Lung Cancer 2007; 58:329-41. [PMID: 17675180 DOI: 10.1016/j.lungcan.2007.06.022] [Citation(s) in RCA: 92] [Impact Index Per Article: 5.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/17/2007] [Revised: 06/22/2007] [Accepted: 06/28/2007] [Indexed: 10/23/2022]
Abstract
Early diagnosis and treatment are important for improvement of the low survival rate of patients with lung cancer. The objective of this study was to evaluate the long-term survival rate of patients identified to have lung cancer by our population-based baseline and annual repeat low-radiation dose computed tomography (low-dose CT) screenings, conducted in 1996-1998. A total of 13,037 CT scans were obtained from 5480 subjects (2969 men, 2511 women) aged 40-74 years at the initial CT screening. Lung cancer was detected in 63 subjects (57 were detected by CT scans and underwent surgery; 1 was detected by sputum cytology and underwent surgery; 3 rejected treatment; and 2 were interval cases that developed symptoms prior to the next annual repeat CT screening). Follow-up study included review of medical records. Death certificates were examined to check for any deceased interval case among participants. Postoperative follow-up of the 50 survived patients ranged from 70 to 117 (median, 101) months. Eight patients died during follow-up (6 due to lung cancer from 20 to 67 months after surgery and 2 deaths unrelated to lung cancer, each 7 and 60 months following surgery). Three patients who rejected treatment died 14 months to 6 years after positive screening CT scans, and the 2 interval cases died at each 17 and 30 months, respectively, following negative screening CT scans. Survival was analysed in 59 patients with lung cancer detected by low-dose CT screening (excluding two patients; one was detected by sputum cytology and the other had mass lesion already noted on the chest radiograph of the previous year). The 10-year survival calculated by the Kaplan-Meier method was 83.1% (95% CI: 0.735-0.927) for death from all causes and 86.2% (95% CI: 0.773-0.951) for death from lung cancer. The survival rate was excellent for never-smokers, patients with BAC and adenocarcinoma/mixed types with non-solid CT density pattern, associated with Noguchi's type A or B and pathologic stage IA. A poorer prognosis was noted in smokers with adenocarcinomas/mixed types, associated with part-solid or solid CT density pattern and Noguchi's type C or D. All patients with non-solid tumours measuring 6-13.5mm at presentation are alive, patients with part-solid tumours, measuring 17mm or more, or solid tumours, measuring 13mm or more at presentation were associated with increased risk of lung cancer-related morbidity or mortality. The estimated rate of possible over-diagnosis was 13% in total and we failed to cure 17% of patients encountered in the programme. Low-dose CT screening substantially improves the 10-year survival for lung cancer with minimal use of invasive treatment procedures.
Collapse
Affiliation(s)
- Shusuke Sone
- Department of Radiology, JA Nagano Azumi General Hospital, Ikeda, Nagano 399-8695, Japan
| | | | | | | | | | | | | | | | | | | | | | | | | | | |
Collapse
|
40
|
Mazières J, Rouquette I, Brouchet L. Cancer bronchique de la femme et de la femme enceinte : vers une origine hormonale ? Rev Mal Respir 2007; 24:983-97. [DOI: 10.1016/s0761-8425(07)92763-1] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/25/2022]
|
41
|
Taylor R, Najafi F, Dobson A. Meta-analysis of studies of passive smoking and lung cancer: effects of study type and continent. Int J Epidemiol 2007; 36:1048-59. [PMID: 17690135 DOI: 10.1093/ije/dym158] [Citation(s) in RCA: 117] [Impact Index Per Article: 6.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/26/2022] Open
Abstract
BACKGROUND To calculate a pooled estimate of relative risk (RR) of lung cancer associated with exposure to passive smoking in never smoking women exposed to smoking spouses. This study is an updated meta-analysis that also assesses the differences between estimated risks according to continent and study type using meta-regression. METHODS From a total of 101 primary studies, 55 studies are included in this meta-analysis, of which, 7 are cohort studies, 25 population-based case-control and 23 non-population-based case-control studies. Twenty previously published meta-analyses are also reviewed. Fixed and random effect models and meta-regression are used to obtain pooled estimates of RR and P-value functions are used to demonstrate consistency of results. RESULTS The pooled RR for never-smoking women exposed to passive smoking from spouses is 1.27 (95% CI 1.17-1.37). The RR for North America is 1.15 (95% CI 1.03-1.28), Asia, 1.31 (95% CI 1.16-1.48) and Europe, 1.31 (1.24-1.52). Sequential cumulative meta-analysis shows no trend. There is no strong evidence of publication bias. CONCLUSIONS The abundance of evidence, consistency of finding across continent and study type, dose-response relationship and biological plausibility, overwhelmingly support the existence of a causal relationship between passive smoking and lung cancer.
Collapse
Affiliation(s)
- Richard Taylor
- School of Population Health, University of Queensland, Australia.
| | | | | |
Collapse
|
42
|
Kirk GD, Merlo C, O' Driscoll P, Mehta SH, Galai N, Vlahov D, Samet J, Engels EA. HIV infection is associated with an increased risk for lung cancer, independent of smoking. Clin Infect Dis 2007; 45:103-10. [PMID: 17554710 PMCID: PMC4078722 DOI: 10.1086/518606] [Citation(s) in RCA: 282] [Impact Index Per Article: 15.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/06/2006] [Accepted: 02/28/2007] [Indexed: 11/03/2022] Open
Abstract
BACKGROUND Human immunodeficiency virus (HIV)-infected persons have an elevated risk for lung cancer, but whether the increase reflects solely their heavy tobacco use remains an open question. METHODS The Acquired Immunodeficiency Syndrome (AIDS) Link to the Intravenous Experience Study has prospectively observed a cohort of injection drug users in Baltimore, Maryland, since 1988, using biannual collection of clinical, laboratory, and behavioral data. Lung cancer deaths were identified through linkage with the National Death Index. Cox proportional hazards regression was used to examine the effect of HIV infection on lung cancer risk, controlling for smoking status, drug use, and clinical variables. RESULTS Among 2086 AIDS Link to the Intravenous Experience Study participants observed for 19,835 person-years, 27 lung cancer deaths were identified; 14 of the deaths were among HIV-infected persons. All but 1 (96%) of the patients with lung cancer were smokers, smoking a mean of 1.2 packs per day. Lung cancer mortality increased during the highly active antiretroviral therapy era, compared with the pre-highly active antiretroviral therapy period (mortality rate ratio, 4.7; 95% confidence interval, 1.7-16). After adjusting for age, sex, smoking status, and calendar period, HIV infection was associated with increased lung cancer risk (hazard ratio, 3.6; 95% confidence interval, 1.6-7.9). Preexisting lung disease, particularly noninfectious diseases and asthma, displayed trends for increased lung cancer risk. Illicit drug use was not associated with increased lung cancer risk. Among HIV-infected persons, smoking remained the major risk factor; CD4 cell count and HIV load were not strongly associated with increased lung cancer risk, and trends for increased risk with use of highly active antiretroviral therapy were not significant. CONCLUSIONS HIV infection is associated with significantly increased risk for developing lung cancer, independent of smoking status.
Collapse
Affiliation(s)
- Gregory D Kirk
- Department of Epidemiology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA.
| | | | | | | | | | | | | | | |
Collapse
|
43
|
Pauk N, Kubík A, Zatloukal P, Krepela E. Lung cancer in women. Lung Cancer 2005; 48:1-9. [PMID: 15777966 DOI: 10.1016/j.lungcan.2004.10.009] [Citation(s) in RCA: 49] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/22/2004] [Revised: 10/18/2004] [Accepted: 10/19/2004] [Indexed: 01/10/2023]
Abstract
Lung cancer is one of the most important avoidable causes of death around the world, it is the most widespread carcinoma with a very poor prognosis, and is the leading cause of cancer death in both developed and developing countries. At present more men than women die each year from lung cancer, but in recent years a rapid increase in lung cancer mortality has been observed among women in developed countries, contrasting with a levelling off or decrease among men. The rising trend in female lung cancer mortality has been observed to parallel with the past and current prevalence of cigarette smoking among women in the United States and elsewhere. An important role of other factors acting either as independent risk factors or interacting with the effect of smoking has been suggested by some studies among women, among them genetic, biologic and hormonal factors, and probably some factors related to the environment and lifestyle. There is a controversy concerning the claim that women have a different susceptibility to tobacco carcinogens, which might or might not be greater than men do. Since tobacco is far and away the strongest epidemiological risk factor for the development of lung cancer, comprehensive smoking control efforts are the priority in the prevention of lung cancer among women.
Collapse
Affiliation(s)
- Norbert Pauk
- Department of Pneumology and Thoracic Surgery, Charles University, 3rd Faculty of Medicine, University Hospital Na Bulovce, and Postgraduate Medical Institute, Budínova 2, 18081 Prague, Czech Republic.
| | | | | | | |
Collapse
|