JOURNAL OF CLINICAL ONCOLOGY R E V I E W A R T I C L E Obesity and Other Cancers Lin Yang, Bettina F. Drake, and Graham A. Colditz A B S T R A C T Purpose Evidence on overweight, obesity, and an increased risk of cancer continues to accumulate and was updated in the 2016 handbook on weight control from the International Agency for Research on Cancer (IARC). The underlying primary data, together with dose-response meta-analysis and, finally, pooled analysis of individual participant data, add insight into the relation between obesity and cancer risk and prognosis. We summarize the evidence for mortality from prostate cancer, he- matologic malignancies, and kidney cancer. Methods We reviewed pooled analysis of rare end points across cohorts, regardless of primary results re- ported from the individual studies, further reducing risk of publication bias. Of these cancer sites, only kidney cancer was included in the IARC 2002 report, although mortality from prostate cancer and hematologic malignancies was noted in the American Cancer Society prospective cohort study in 2003. The 2016 update from the IARC added details for prostate and hematologic malignancies, classifying the evidence as sufficient to conclude that avoiding excess body fatness lowers the risk of multiple myeloma but found that the evidence for it lowering the risk of prostate cancer mortality or diffuse large B-cell lymphoma was limited. Results A higher body mass index is associated with an increased risk of advanced prostate cancer and prostate cancer mortality and is associated with worse survival in most subtypes of hematologic malignancies, in a dose-response fashion. Evidence for kidney cancer is built mostly on retrospective data, which supports an obesity paradox in patients with the clear cell variant; however, population- based cohort data indicate that a higher cohort-entry body mass index is associated with worse kidney cancer–specific survival. Conclusion Together, these data add support to the evidence for a growing cancer burden caused by adiposity in both early adult and later adult life, yet leave open the question of the means of weight management after diagnosis as a strategy to improve survival. J Clin Oncol 34:4231-4237. © 2016 by American Society of Clinical Oncology INTRODUCTION Here we review the current research addressing the role of adiposity/obesity in mortality and prognostic outcomes in prostate, hematologic, and renal cancers. Excess weight or adiposity is a common risk factor for cancer, progression, and nonsurvival; this provides a unique oppor- tunity to address a modifiable risk factor through primary and secondary interventions. Evidence reviewed by the International Agency for Re- search on Cancer (IARC) and the World Cancer Research Fund support the finding that being overweight or obese is an established cause of several cancers including breast, endometrium, esophagus (adenocarcinoma), renal, and colon and rectum. 1 Since the IARC report in 2002, evidence has ex- panded to suggest an association between a higher body mass index (BMI) and advanced prostate or prostate cancer mortality and several hemato- logic cancers. 2 The 2016 IARC update on body fatness and cancer concluded that the evidence was sufficient to conclude that avoiding excess body fatness lowers the risk of multiple myeloma but evidence for its lowering the risk of prostate cancer mortality and diffuse large B-cell lym- phoma is limited. Thus, for these cancer sites, the committee could not rule out bias and con- founding as contributing to the positive associ- ations observed. 2 In addition, excessive weight is a risk factor for cancer mortality overall. 3 To Lin Yang, Bettina F. Drake, and Graham A. Colditz, Washington University School of Medicine and Siteman Cancer Center, St Louis, MO; and Lin Yang, Center for Public Health, Medical University of Vienna, Vienna, Austria. Published online ahead of print at www.jco.org on November 7, 2016. Authors’ disclosures of potential conflicts of interest are found in the article online at www.jco.org. Author contributions are found at the end of this article. Corresponding author: Graham A. Colditz, MD, DrPH, Washington University School of Medicine, 660 S Euclid Ave, Campus Box 8100, St Louis, MO 63110; e-mail: colditzg@wustl.edu. © 2016 by American Society of Clinical Oncology 0732-183X/16/3435w-4231w/$20.00 DOI: 10.1200/JCO.2016.68.4837 © 2016 by American Society of Clinical Oncology 4231 VOLUME 34 • NUMBER 35 • DECEMBER 10, 2016 Downloaded from ascopubs.org by 50.19.59.234 on June 6, 2022 from 050.019.059.234 Copyright © 2022 American Society of Clinical Oncology. All rights reserved.