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      Parity and thyroid cancer risk: a meta‐analysis of epidemiological studies

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          Abstract

          Although observational studies have assessed the relationship between parity and thyroid cancer risk, the findings are inconsistent. To quantitatively assess the association, we conducted a systematic review and meta‐analysis. PubMed and Embase were searched up to January 2015. Prospective or case–control studies that evaluated the association between parity and thyroid cancer risk were included. We used the fixed‐effects model to pool risk estimates. After literature search, 10 prospective studies, 12 case‐control studies and 1 pooled analysis of 14 case‐control studies including 8860 patients were identified. The studies had fair methodological quality. Pooled analysis suggested that there was a significant association between parity and risk of thyroid cancer (RR for parous versus nulliparous: 1.09, 95% CI 1.03‐1.15; I2=33.4%). The positive association persisted in almost all strata of subgroup analyses based on study design, location, study quality, type of controls, and confounder adjustment, although in some strata statistical significance was not detected. By evaluating the number of parity, we identified that both parity number of 2 versus nulliparous and parity number of 3 versus nulliparous demonstrated significant positive associations (RR=1.11, 95% CI 1.01‐1.22; I2=31.1% and RR=1.16, 95% CI 1.01‐1.33; I2=19.6% respectively). The dose‐response analysis suggested neither a non‐linear nor linear relationship between the number of parity and thyroid cancer risk. In conclusion, this meta‐analysis suggests a potential association between parity and risk of thyroid cancer in females. However, the lack of detection of a dose‐response relationship suggests that further studies are needed to better understand the relationship.

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          Risk factors for thyroid cancer: an epidemiological review focused on nutritional factors.

          The present review summarizes epidemiological evidence on risk factors for thyroid cancer (TC), in particular, nutritional factors. Searches of articles on the issue were conducted using MEDLINE. Exposure to ionizing radiation, particularly during childhood, is the best-established risk factor for TC. There is also a strong association with history of benign nodules/adenoma or goiter. Iodine deficiency may induce an increasing incidence of benign thyroid conditions, but very high iodine intake also affects thyroid function and, possibly, TC risk. Among dietary factors, fish-the major natural source of iodine in human diet-is not consistently related to TC risk. High intake of cruciferous vegetables shows a weak inverse association with TC. Among other food groups, vegetables other than cruciferous are the only food group showing a favorable effect on TC, with an approximate 20% reduction in risk for subjects with the highest consumption. No effect on TC risk of alcohol, coffee, or other food-groups/nutrients emerged. Height and weight at diagnosis show a moderate positive association with TC risk. At present, the only recognized measures for reducing TC risk is to avoid ionizing radiation and iodine deficiency, particularly in childhood and young women, and to increase vegetable consumption.
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            BMI, Diet and Female Reproductive Factors as Risks for Thyroid Cancer: A Systematic Review

            Background Thyroid cancer incidence rates have been increasing worldwide but the reason behind this is unclear. Both the increasing use of diagnostic technologies allowing the detection of thyroid cancer and a true increase in thyroid cancer incidence have been proposed. This review assesses the role of body mass index (BMI), diet, and reproductive factors on the thyroid cancer trend. Methods Epidemiologic studies of the selected risk factors up to June 2010 were reviewed and critically assessed. Results Among the thirty-seven studies reviewed and despite variation in the risk estimates, most papers supported a small but positive association for BMI (risk estimate range: 1.1–2.3 in males and 1.0–7.4 in females.). Among specific dietary components, there was no consistent association of thyroid cancer risk with iodine intake through fortification (risk estimate range: 0.49–1.6) or fish consumption (risk estimate range 0.6–2.2), nor with diets high in cruciferous vegetables (risk estimate range 0.6–1.9). A small number of studies showed a consistent protective effect of diets high in non-cruciferous vegetable (risk estimate range: 0.71–0.92). Among reproductive factors (pregnancy, parity, number of live births, use of prescription hormones, menstrual cycle regularity, and menopausal status), none were consistently associated with higher thyroid cancer risk. Conclusions BMI had the strongest link to thyroid cancer risk among those examined. Detailed examinations of population-level risk factors can help identify and support prevention efforts to reduce the burden of thyroid cancer.
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              Metastatic phenotype is regulated by estrogen in thyroid cells.

              Over 200 million people worldwide are affected by thyroid proliferative diseases, including cancer, adenoma, and goiter, annually. The incidences of thyroid malignancies are three to four times higher in women, suggesting the possible involvement of estrogen. Based on this observed sex bias, we hypothesize that estrogen modulates the growth and metastatic propensity of thyroid cancer cells. In this study, two thyroid cell lines (Nthy-ori 3-1 and BCPAP) were evaluated for the presence of estrogen receptor (ER) by Western blot analysis and estrogen responsiveness by using a cell proliferation assay. In addition, the effect of estradiol (E(2)) on modulation of metastatic phenotype was determined by using in vitro adhesion, migration, and invasion assays. Thyroid cells expressed a functionally active ER-alpha and ER-beta as evidenced by 50-150% enhancement of proliferation in the presence of E(2). E(2) also enhanced adhesion, migration, and invasion of thyroid cells in an in vitro experimental model system that, based on our results, is modulated by beta-catenin. Our data provide evidence that the higher incidence of thyroid cancer in women is potentially attributed to the presence of a functional ER that participates in cellular processes contributing to enhanced mitogenic, migratory, and invasive properties of thyroid cells. These findings will enable and foster the possible development of antiestrogenic therapy targeting invasion and migration, thus affecting metastatic propensity.
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                Author and article information

                Journal
                Cancer Med
                Cancer Med
                10.1002/(ISSN)2045-7634
                CAM4
                Cancer Medicine
                John Wiley and Sons Inc. (Hoboken )
                2045-7634
                29 December 2015
                April 2016
                : 5
                : 4 ( doiID: 10.1002/cam4.2016.5.issue-4 )
                : 739-752
                Affiliations
                [ 1 ] Division of Epidemiology Department of Medicine Vanderbilt Epidemiology Center Vanderbilt‐Ingram Cancer CenterVanderbilt University School of Medicine Nashville Tennessee 37203
                [ 2 ] Program of Quantitative Methods in EducationUniversity of Minnesota Minneapolis Minnesota 55455
                [ 3 ] Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics Dongguan Scientific Research CenterGuangdong Medical University Dongguan 523808China
                [ 4 ] Oncology Institutethe Affiliated Hospital of Nanjing Medical University Changzhou No.2 People's Hospital Changzhou Jiangsu 213003China
                [ 5 ] Department of Hematologythe Affiliated Hospital of Xuzhou Medical College Xuzhou Jiangsu 221000China
                [ 6 ] Department of Neurologythe Affiliated Brain Hospital of Nanjing Medical University Nanjing Jiangsu 210000China
                [ 7 ] Department of EpidemiologyTulane University School of Public Health and Tropical Medicine New Orleans Louisiana 70112
                [ 8 ] Department of NeurologyTaihe Hospital Affiliated to Hubei University of Medicine Shiyan Hubei 442000China
                Author notes
                [*] [* ] Correspondence

                Lang Wu, Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt‐Ingram Cancer Center, Vanderbilt University School of Medicine, 2525 West End Avenue, Suite 800, Nashville, TN 37203‐1738. Tel: 1‐615‐343‐9388; Fax: 615‐343‐0719; E‐mail: lang.wu@ 123456vanderbilt.edu

                or

                Guang Jian Liu, Department of Neurology, Taihe Hospital Affiliated to Hubei University of Medicine, Shiyan City, Hubei Province 442000, China. Tel: 8613669097518; Fax: 8607198883809; E‐mail: liuguangjian@ 123456aliyun.com

                [†]

                JZ, XZ, and CT contribute equally to this study.

                Article
                CAM4604
                10.1002/cam4.604
                4831293
                26714593
                2c09b1ee-6da4-476e-b778-05e095ccbb72
                © 2015 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 29 July 2015
                : 29 October 2015
                : 11 November 2015
                Page count
                Pages: 14
                Funding
                Funded by: National Natural Science Foundation of China
                Award ID: 81541153
                Funded by: Guangdong Provincial Research Project of Science and Technology
                Award ID: 2015A050502048
                Award ID: 2014A020212295
                Award ID: 2014A020212653
                Funded by: Science and Technology Research Project in Dongguan City
                Award ID: 2013508152011
                Award ID: 2013508152002
                Funded by: Vanderbilt Molecular and GeneticEpidemiology of Cancer (MAGEC)
                Funded by: US National Cancer Institute
                Award ID: R25 CA160056
                Categories
                Original Research
                Cancer Prevention
                Original Research
                Custom metadata
                2.0
                cam4604
                April 2016
                Converter:WILEY_ML3GV2_TO_NLMPMC version:4.8.6 mode:remove_FC converted:09.04.2016

                Oncology & Radiotherapy
                epidemiology,meta‐analysis,parity,risk,thyroid cancer
                Oncology & Radiotherapy
                epidemiology, meta‐analysis, parity, risk, thyroid cancer

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