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      Obesity and nonalcoholic fatty liver disease associated with adenocarcinoma in patients with lung cancer

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          Abstract

          Lung cancer has become the leading cause of cancer-related deaths around the world. In addition to genetic risk factors and smoking, the metabolic risk factors remain to be elusive.

          To evaluate the associations between obesity, nonalcoholic fatty liver disease (NAFLD) and pulmonary adenocarcinoma in patients with lung cancer.

          Consecutive operation-proven lung cancer patients with assessment of metabolic disorders and liver ultrasound in 2009 and 2013 were retrospectively enrolled. T-test and multivariate logistic regression were applied to evaluate the contribution of individual factors to lung adenocarcinoma, as well as the synergistic effects between these factors.

          Among 3664 lung cancer patients with ultrasound examination, 2844 cases were enrolled for further analysis. Of them, 1053 (37.0%) were females, 1242 (43.7%) were cigarette smokers, 1658 (58.3%) were diagnosed as lung adenocarcinoma, 744 (26.2%) had obesity, and 614 (21.6%) had NAFLD. Proportion of female gender, nonsmoker, obesity, NAFLD, and serum lipid levels in patients with adenocarcinoma were significantly higher than those in other subtypes of lung cancer, and in 2013 than in 2009 (all P < .01). NAFLD and obesity were shown as independent factors and positively associated with pulmonary adenocarcinoma, along with female gender and nonsmoking, higher serum levels of cholesterol. NAFLD and other contributing factors exhibited no synergistic effects on adenocarcinoma.

          Obesity and NAFLD might increase the risk for pulmonary adenocarcinoma, especially in nonsmoking females, and underscore the need for further study into carcinogenic mechanisms and preventive interventions.

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          Most cited references24

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          Genomic alterations in lung adenocarcinoma.

          Treatment for non-small-cell lung cancer is evolving from the use of cytotoxic chemotherapy to personalised treatment based on molecular alterations. This past decade has witnessed substantial progress in the treatment of patients with EGFR mutations and ALK rearrangements, and it is now possible to study complex genomic alterations in cancer using next-generation sequencing. Sequencing data from large-scale consortia, such as The Cancer Genome Atlas, as well as several independent groups, have helped identify novel drivers and potentially targetable alterations in lung adenocarcinomas. These data clearly suggest that lung adenocarcinoma is associated with distinct genomic alterations compared with other lung cancer subtypes, and highlight the widespread molecular heterogeneity that underlies the disease. In this Review, we discuss some of the key findings from genomic studies of lung adenocarcinoma.
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            Guidelines for the diagnosis and management of nonalcoholic fatty liver disease: update 2010: (published in Chinese on Chinese Journal of Hepatology 2010; 18:163-166).

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              Relation of body mass index to cancer risk in 362,552 Swedish men.

              Obesity has been linked with increased risk for cancers of the colon, kidney, breast, endometrium and gallbladder. For other cancer sites, the relationship with obesity is less well quantified, and the effect of weight change on cancer risk is unclear. We examined the health records of 362,552 Swedish men who underwent at least one physical examination from 1971 to 1992, and were followed until death or the end of 1999. Incident cancer cases were identified by linkage to the Swedish cancer registry. Poisson regression models were used to estimate relative risks of cancer for both body-mass index (BMI) at baseline exam and, in a subgroup of 107,815 men, change in BMI after six years of follow-up, adjusting for age and smoking status. Compared to men of normal weight, obese men had a significantly increased risk of all cancers combined (RR = 1.1; 95% CI = 1.0-1.2). The risks were most pronounced for esophageal adenocarcinoma (RR = 2.7; 95% CI = 1.3-5.6), renal cell carcinoma (RR = 1.8; 95% CI = 1.4-2.4), malignant melanoma (RR = 1.4; 95% CI = 1.1-1.7), and cancers of the colon (RR = 1.7; 95% CI = 1.5-2.0), rectum (RR = 1.4; 95% CI = 1.1-1.7), and liver (RR = 3.6; 95% CI = 2.6-5.0). Risk of esophageal squamous cell carcinoma was elevated for underweight men whose BMI was less than 18.5 (RR = 3.1; 95% CI = 1.1-8.3). An excess risk for cancers of the pancreas and connective tissue was observed only among nonsmokers. Compared to men whose weight remained stable, men with more than a 15% increase in BMI after six years of follow-up had an elevated risk of pancreas and renal cell cancers. Obesity and weight gain increase the risk for several forms of cancer in men, and underscore the need for further study into carcinogenic mechanisms and preventive interventions.
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                Author and article information

                Journal
                Medicine (Baltimore)
                Medicine (Baltimore)
                MEDI
                Medicine
                Wolters Kluwer Health
                0025-7974
                1536-5964
                September 2019
                13 September 2019
                : 98
                : 37
                : e17098
                Affiliations
                [a ]Department of Gastroenterology, Gongli Hospital, The Second Military Medical University
                [b ]Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tong Ji University School of Medicine
                [c ]Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine
                [d ]Shanghai Key Lab of Pediatric Gastroenterology and Nutrition, Shanghai, China.
                Author notes
                []Correspondence: Jian-Gao Fan, Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Lab of Pediatric Gastroenterology and Nutrition, Shanghai 200092, China (e-mail: fanjiangao@ 123456xinhuamed.com.cn ).
                Article
                MD-D-19-00063 17098
                10.1097/MD.0000000000017098
                6750340
                31517837
                569c94c0-1afb-4441-9636-8f043f350811
                Copyright © 2019 the Author(s). Published by Wolters Kluwer Health, Inc.

                This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0

                History
                : 3 January 2019
                : 20 May 2019
                : 18 August 2019
                Categories
                6700
                Research Article
                Observational Study
                Custom metadata
                TRUE

                hypercholesterolemia,lung cancer,nonalcoholic fatty liver disease,obesity,pulmonary adenocarcinoma

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