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      Body weight trajectories and risk of oesophageal and gastric cardia adenocarcinomas: a pooled analysis of NIH-AARP and PLCO Studies

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          Abstract

          Background:

          Elevated body mass index (BMI, kg m −2) has been consistently associated with oesophageal adenocarcinoma (EA) and gastric cardia adenocarcinoma (GCA) incidence. However, effects of adiposity over the life course in relation to EA/GCA have not been thoroughly explored.

          Methods:

          We pooled two prospective cohort studies: NIH-AARP Diet and Health Study and Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial, with data on 409 796 individuals (633 EA, 415 GCA). At baseline, participants reported their height and weight at ages 20 and 50 years, and current. Body mass index trajectories were determined using latent class analysis. Hazard ratios (HRs) and 95% confidence intervals (CI) were estimated using proportional hazards regression.

          Results:

          Compared with individuals with a BMI<25 kg m −2 at all time points, exceeding a BMI of 25 kg m −2 at age 20 was associated with increased risks of EA (HR=1.76, 95% CI: 1.35–2.29) and GCA (HR=1.62, 95% CI: 1.16–2.25). Similarly, a BMI trajectory of overweight (⩾25–<30 kg m −2) at age 20 progressing to obesity (⩾30 kg m −2) by age 50 was associated with increased risks of EA (HR=2.90, 95% CI: 1.67–5.04) and GCA (HR=4.07, 95% CI: 2.32–7.15), compared with individuals with a normal weight (⩾18.5–<25 kg m −2) trajectory. Weight gain of ⩾20 kg between age 20 and baseline was also associated with a two times increased risk of EA (HR=1.97, 95% CI: 1.43–2.73) and more modestly with GCA (HR=1.40, 95% CI: 0.96–2.05).

          Conclusions:

          Being overweight in early adulthood and weight gain later in life were each associated with increased risks of EA and GCA. This underscores the potential of weight control programs for reducing EA and GCA risk.

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          Most cited references46

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          Tracking of childhood overweight into adulthood: a systematic review of the literature

          Obesity Reviews, 9(5), 474-488
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            Changing patterns in the incidence of esophageal and gastric carcinoma in the United States.

            Incidence rates for esophageal adenocarcinoma previously were reported to be increasing rapidly, especially among white males. Rates for gastric cardia adenocarcinoma also were observed to be rising, although less rapidly. In this article, the authors update the incidence trends through 1994 and further consider the trends by age group. Surveillance, Epidemiology, and End Results (SEER) program data were used to calculate age-adjusted incidence rates for esophageal carcinoma by histologic type and gastric adenocarcinoma by anatomic subsite. Among white males, the incidence of adenocarcinoma of the esophagus rose > 350% since the mid-1970s, surpassing squamous cell carcinoma around 1990. Rates also rose among black males, but remained at much lower levels. To a lesser extent, there were continuing increases in gastric cardia adenocarcinoma among white and black males, which nearly equaled the rates for noncardia tumors of the stomach in white men. The upward trend for both tumors was much greater among older than younger men. Although the incidence also rose among females, rates remained much lower than among males. Previously reported increases of esophageal adenocarcinoma are continuing, most notably among white males. Cigarette smoking may contribute to the trend through an early stage carcinogenic effect, along with obesity, which may increase intraabdominal pressure and predispose to gastroesophageal reflux disease. Further research into esophageal and gastric cardia adenocarcinoma is needed to clarify the risk factors and mechanisms responsible for the upward trends as well as the racial and gender disparities in incidence.
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              Cancers with increasing incidence trends in the United States: 1999 through 2008.

              Despite declines in incidence rates for the most common cancers, the incidence of several cancers has increased in the past decade, including cancers of the pancreas, liver, thyroid, and kidney and melanoma of the skin, as well as esophageal adenocarcinoma and certain subsites of oropharyngeal cancer associated with human papillomavirus (HPV) infection. Population-based incidence data compiled by the North American Association of Central Cancer Registries were used to examine trends in incidence rates from 1999 through 2008 for the 7 cancers listed by sex, age group, race/ethnicity, and stage at diagnosis. Joinpoint regression was used to calculate average annual percent changes in incidence rates (1999-2008). Rates for HPV-related oropharyngeal cancer, esophageal adenocarcinoma, cancer of the pancreas, and melanoma of the skin increased only in whites, except for esophageal adenocarcinoma, which also increased in Hispanic men. Liver cancer rates increased in white, black, and Hispanic men and in black women only. In contrast, incidence rates for thyroid and kidney cancers increased in all racial/ethnic groups, except American Indian/Alaska Native men. Increases in incidence rates by age were steepest for liver and HPV-related oropharyngeal cancers among those aged 55 [corrected] to 64 years and for melanoma of the skin in those aged 65 years and older. Notably, for HPV-related oropharyngeal cancer in men and thyroid cancer in women, incidence rates were higher in those aged 55 to 64 years than in those aged 65 years and older. Rates increased for both local and advanced stage diseases for most cancer sites. The reasons for these increasing trends are not entirely known. Part of the increase (for esophageal adenocarcinoma and cancers of the pancreas, liver, and kidney) may be linked to the increasing prevalence of obesity as well as increases in early detection practices for some cancers. These rising trends will exacerbate the growing cancer burden associated with population expansion and aging. Additional research is needed to determine the underlying reasons for these increasing trends. CA Cancer J Clin 2012. © 2012 American Cancer Society. Copyright © 2012 American Cancer Society, Inc.
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                Author and article information

                Journal
                Br J Cancer
                Br. J. Cancer
                British Journal of Cancer
                Nature Publishing Group
                0007-0920
                1532-1827
                28 March 2017
                14 February 2017
                : 116
                : 7
                : 951-959
                Affiliations
                [1 ]Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS , Bethesda, MD, USA
                Author notes
                Article
                bjc201729
                10.1038/bjc.2017.29
                5379141
                28196067
                8fd4e511-1f54-4ac4-8285-0352555aac41
                Copyright © 2017 Cancer Research UK

                From twelve months after its original publication, this work is licensed under the Creative Commons Attribution-NonCommercial-Share Alike 4.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/

                History
                : 07 October 2016
                : 10 January 2017
                : 15 January 2017
                Categories
                Epidemiology

                Oncology & Radiotherapy
                adenocarcinoma,body mass index,latent class analysis
                Oncology & Radiotherapy
                adenocarcinoma, body mass index, latent class analysis

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