Energy Balance and Cancer

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2 Energy Balance and Cancer Series Editor: Nathan A. Berger, Case Western Reserve University, Cleveland, OH, USA For further volumes:

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4 Sanford D. Markowitz Editors Nathan A. Berger Energy Balance and Gastrointestinal Cancer

5 Editors Sanford D. Markowitz Case Western Reserve University Cleveland, OH, USA Nathan A. Berger Case Western Reserve University Cleveland, OH, USA ISBN e-isbn DOI / Springer New York Dordrecht Heidelberg London Library of Congress Control Number: Springer Science+Business Media, LLC 2012 All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science+Business Media, LLC, 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. Printed on acid-free paper Springer is part of Springer Science+Business Media ( )

6 Preface As the worldwide pandemic of overweight and obesity continues to expand, with over 1 billion overweight and 315 million obese adults estimated worldwide [1 3], obesity is increasingly recognized as a significant risk factor for cancer. In the USA, approximately 20% of all cancer deaths in women and 14% in men have been attributed to overweight and obesity [4]. Epidemiological studies indicate an association between obesity and specific malignancies in multiple organ systems including colon, postmenopausal breast, endometrial, esophageal adenocarcinoma and renal cell cancer [5 7]. In addition to colon and esophageal adenocarcinoma, more recent evidence supports an association of obesity with other gastrointestinal malignancies including pancreatic, gallbladder, and hepatocellular cancer [4, 7, 8]. In 2009, the American Cancer Society estimated that the combined deaths in the USA from gastrointestinal cancers, including pancreas, colon, and rectum, esophageal, liver, and bile ducts exceeded 135,000 [9]. During the same year, there were 100,000 new cases and 50,000 deaths from colon cancer [9]. The relative risk of mortality from colon cancer according to body mass index in a prospective population study of more than 900,000 US adults [4] was found to be 1.20 for overweight and for obese men, and 1.1 for overweight and for obese women. In contrast, a recent study showed that in men with nonmetastatic colorectal cancer at diagnosis, increased physical activity was associated with improved colorectal cancer mortality and overall mortality [10]. Thus, gastrointestinal cancer in general and colorectal cancer more specifically causes an enormous burden of morbidity and mortality in the USA with significant impact from obesity and benefit associated with physical activity. Persistence of this vexing problem both at the personal and public health levels can be attributed, in part, to the multicomponent and complex nature of the relation between energy balance and cancer in which many of the cytokines, hormones, and other obesity-associated factors may act in combination with environmental and lifestyle factors as both mutagens and cancer promoters. Persistence of the problem is associated also with the difficulty in implementing effective and sustainable biobehavioral interventions to control obesity and associated mediators and comorbidities. v

7 vi Preface This volume assembles a panel of leading investigators to present a transdisciplinary view of the state of the science regarding the linkages between gastrointestinal malignancy and energy balance. In addition to analyzing the extensive epidemiologic data associating energy balance with gastrointestinal malignancies, this volume details the significant progress being made to increase mechanistic understandings and to identify possible mediators of these relationships and the potential interventions that are just beginning to be identified and tested. Chapter 1 presents a comprehensive evaluation by Dr. Nora Nock of the epidemiologic association of obesity with major gastrointestinal malignancies. In Chap. 2, Dr. Graham Casey reviews both the common and the rare genetic changes associated with colon cancer susceptibility. In Chap. 3, Dr. Leonard Augenlicht and associates provide an overview of their ongoing research on the effects of dietary modulation, especially of vitamin D, calcium, and fat, on the incidence of colon cancer in the mouse and new insights on potential mechanisms influenced by diet focused on cellular interactions between macrophages and intestinal epithelial cells. In Chap. 4, Dr. Nathan Berger provides an overview of mouse model studies investigating the effect of exercise on gastrointestinal malignancies. In Chaps. 5 and 6, Drs. Rom Leidner, Amitabh Chak, and Donghui Li review recent studies investigating the relation between obesity, Barrett s esophagus, esophageal cancer, and pancreatic cancer. In Chaps. 7 and 8, Dr. Li Li explains the important contribution of insulin resistance pathways to the relation of obesity and colon cancer and Drs. Fred Bunz and Nickolas Papadopoulos explain the relation of Ras/Raf mutation to the process. Dr. Jeffrey Meyerhardt, in Chap. 9, evaluates studies on the effect of energy balance on colorectal cancer recurrence and survival in clinical situations and Dr. Monica Bertagnolli describes the role of chronic inflammation in colorectal malignancies. Overall, this volume should provide an important basis for studies to advance the state of the science linking energy balance to gastrointestinal malignancy and serve, also, as a background to develop new therapeutic interventions for prevention and control. Cleveland, OH, USA Sanford D. Markowitz Nathan A. Berger References 1. Caterson ID, Gill TP (2002) Obesity: epidemiology and possible prevention. Best Pract Res Clin Endocrinol Metab 16: Ogden CL, Carroll MD, Curtin LR et al (2008) Prevalence of overweight and obesity in the United States, JAMA 295: World Health Organization (2003) World cancer report. IARC Nonserial Publication, Geneva 4. Calle EE, Rodriguez C, Walker-Thurmond K et al (2003) Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med 348(17):

8 Preface vii 5. World Health Organization (2000) Obesity: preventing and managing the global epidemic. Report of a WHO consultation. Rep. 894, World Health Organization 6. World Cancer Research Fund and American Institute for Cancer Research (2007) Food, nutrition, physical activity, and the prevention of cancer: a global perspective. AICR, Washington, DC 7. Renehan AG, Tyson M, Egger M et al (2008) Body-mass index and incidence of cancer: a systematic review and meta-analysis of prospective observational studies. Lancet 371: Li D, Morris JS, Liu J et al (2009) Body mass index and risk, age of onset, and survival in patients with pancreatic cancer. JAMA 301: American Cancer Society (2009) Cancer facts & figures American Cancer Society, Atlanta Meyerhardt JA, Giovannucci EL, Ogino S, Kirkner GS, Chan AT, Willett W, Fuch CS (2009) Physical activity and male colorectal cancer survival. Arch Intern Med 169:

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10 Contents 1 Obesity and Gastrointestinal Cancers: Epidemiology... 1 Nora L. Nock 2 Genetics of Colon Cancer Susceptibility Graham Casey 3 Dietary Modulation of Colon Cancer: Effects on Intermediary Metabolism, Mucosal Cell Differentiation, and Inflammation Lidija Klampfer, Barbara G. Heerdt, Anna Velcich, Erin Gaffney-Stomberg, Donghai Wang, Elaine Lin, and Leonard H. Augenlicht 4 The Apc Min/+ Mouse Model to Study the Effects of Exercise on Gastrointestinal Malignancy Nathan A. Berger 5 Obesity and the Pathogenesis of Barrett s Esophagus Rom Leidner and Amitabh Chak 6 Obesity and Pancreatic Cancer Donghui Li 7 Obesity, Insulin Resistance Pathway Factors, and Colon Cancer Li Li 8 Ras/Raf and Their Influence in Glycolysis in Colon Cancer Fred Bunz and Nickolas Papadopoulos ix

11 x Contents 9 Energy Balance and Other Modifiable Host Factors on Colorectal Cancer Prognosis Jeffrey Meyerhardt 10 Cyclooxygenase-2 and Chronic Inflammation: Drivers of Colorectal Tumorigenesis Monica M. Bertagnolli Index

12 Contributors Leonard H. Augenlicht Montefiore Medical Center and Albert Einstein Cancer Center, Albert Einstein College of Medicine, Bronx, NY, USA Nathan A. Berger Center for Science, Health and Society, Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, OH, USA Monica M. Bertagnolli Division of Surgical Oncology, Dana Farber Cancer Institute, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA Fred Bunz Department of Radiation Oncology and Molecular Radiation Sciences, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA Graham Casey Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA Amitabh Chak Department of Medicine, Case Western Reserve University, Cleveland, OH, USA Erin Gaffney-Stomberg Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY, USA Barbara G. Heerdt Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY, USA Lidija Klampfer Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY, USA Rom Leidner Department of Medicine, Case Western Reserve University, Cleveland, OH, USA Donghui Li Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA xi

13 xii Contributors Li Li Department of Family Medicine Research Division, Case Western Reserve University, Cleveland, OH, USA Elaine Lin Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY, USA Jeffrey Meyerhardt Division of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA Nora L. Nock Department of Epidemiology and Biostatistics, Case Western Reserve University, Cleveland, OH, USA Nickolas Papadopoulos The Ludwig Center for Cancer Genetics and Therapeutics, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA Anna Velcich Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY, USA Donghai Wang Department of Hematology, Peking University First Hospital, Beijing, China

14 Chapter 1 Obesity and Gastrointestinal Cancers: Epidemiology Nora L. Nock Abstract There is strong and consistent evidence for associations between obesity and multiple gastrointestinal (GI) cancers. The most consistent and compelling evidence exists for the association between obesity and colon cancer; however, there is emerging evidence for associations between obesity and esophageal adenocarcinoma and, pancreatic and liver cancers. The number of studies evaluating obesity and gastric and gallbladder cancers is limited and results, thus far, have been inconsistent. In this chapter, the epidemiological evidence linking obesity to the development and survival of GI cancers is reviewed. Because obesity plays an integral role in manifestation of the Metabolic Syndrome (MetSyn), epidemiological evidence for associations between MetSyn and GI cancers is also summarized. Other environmental and genetic risk factors for GI cancers and the putative mechanisms linking obesity, MetSyn, and GI cancers are discussed in subsequent chapters of this book. 1 Obesity: Definitions Obesity is often defined using surrogates of body size, most commonly, body mass index (BMI), which is expressed as weight adjusted for height in units of kilograms (kg) per meter squared (m 2 ). The most widely adopted definitions of adult overweight and obesity are those established by the World Health Organization (WHO) [ 1 ] as follows: N.L. Nock, Ph.D. (*) Department of Epidemiology and Biostatistics, Case Western Reserve University, 2103 Cornell Road, Cleveland, OH , USA nln@case.edu S.D. Markowitz and N.A. Berger (eds.), Energy Balance and Gastrointestinal Cancer, Energy Balance and Cancer 4, DOI / _1, Springer Science+Business Media, LLC

15 2 N.L. Nock 1. Overweight: BMI ³ 25.0 to <30.0 kg/m 2 2. Class I obesity: BMI ³ 30.0 to <35.0 kg/m 2 3. Class II obesity: BMI ³ 35.0 to <40.0 kg/m 2 4. Class III obesity: BMI ³ 40.0 kg/m 2 Non-standardized definitions of overweight or obesity, such as BMI percentiles (e.g., quartiles) or unit changes in BMI (e.g., 5 kg/m 2 ), have also been extensively utilized which makes drawing conclusions across studies more challenging. Nevertheless, as discussed in the subsequent sections, associations between obesity (predominantly measured using BMI) and certain GI cancers are quite strong regardless of the definition or threshold applied. Central obesity has been assessed using waist circumference and waist-to-hip ratio (WHR) measures. Waist circumference and WHR essentially serve as a proxy for visceral fat, which is more biologically active than subcutaneous fat [ 2 4 ]; and, individuals with more visceral vs. subcutaneous fat are at markedly higher risk of developing insulin resistance, metabolic syndrome (MetSyn) and cancer [ 5 8 ]. The threshold values or cut-points for waist circumference, however, are quite inconsistent across studies, in part, because of substantial sex- and ethnic-specific differences in body size and composition. In the most recent joint interim statement for harmonizing the definition of MetSyn, it was proposed that central obesity be defined using sex-, ethnic-, and population-specific cut-points of waist circumference [ 9 ]. For example, for Caucasian women in the USA, a waist circumference of ³ 88 cm would confer central obesity and an increased risk of type II diabetes mellitus (T2DM) and cardiovascular disease (CVD), while a circumference of ³ 80 cm would increase the risk of insulin resistance. For Caucasian men in the USA, a waist circumference of ³ 102 cm and ³ 94 cm would confer central obesity and an increased risk of T2DM/CVD and insulin resistance, respectively. In contrast, Asian men and women with a waist circumference ³ 90 cm and ³ 80 cm, respectively, would be classified as having central obesity and an increased risk of metabolic diseases [ 9, 10 ]. Obesity can be more accurately defined in terms of body fat. Dual energy X-ray absorptiometry (DXA) scans can differentiate between total and regional fat, lean and bone mass, and; computed tomography (CT) and magnetic resonance imaging (MRI) scans can provide direct estimates of visceral adiposity [ 11, 12 ]. However, because these technologies are more costly and less convenient than simple anthropometric measures, very few studies have utilized these types of scans in large(r) epidemiological studies to evaluate obesity and GI carcinogenesis. 2 Obesity Rates The rates of overweight (BMI ³ 25.0 to <30.0 kg/m 2 ) and obesity (BMI ³ 30.0 kg/ m 2 ) are increasing in epidemic proportions in both developed and developing nations with an estimated one billion overweight and 315 million obese adults worldwide [ ].