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44 - Esophageal cancer

from Part 3.1 - Molecular pathology: carcinomas

Published online by Cambridge University Press:  05 February 2015

By
DuyKhanh P. Ceppa  and
Thomas A. D’Amico
Edited by
Edward P. Gelmann ,
Charles L. Sawyers  and
Frank J. Rauscher, III
DuyKhanh P. Ceppa
Affiliation:
Division ofhoracic Surgery, Indiana University School of Medicine, Indianapolis, IN, USA
Thomas A. D’Amico
Affiliation:
Division of horacic Surgery, Duke University Health System, Durham, NC, USA
Edward P. Gelmann
Affiliation:
Columbia University, New York
Charles L. Sawyers
Affiliation:
Memorial Sloan-Kettering Cancer Center, New York
Frank J. Rauscher, III
Affiliation:
The Wistar Institute Cancer Centre, Philadelphia
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Summary

Introduction

The incidence of esophageal carcinoma is increasing, with the incidence of esophageal adenocarcinoma increasing faster than any other malignancy in the United States (1). Estimates for 2013 predict 17990 new cases of esophageal carcinoma, accounting for 15210 deaths (2). While the incidence of squamous cell carcinoma of the esophagus is decreasing by 3.6% per year, the incidence of adenocarcinoma of the esophagus is increasing by 2.1% per year (3).

Adenocarcinoma of the esophagus

The most important risk factor for the development of adenocarcinoma of the esophagus is the presence of columnar-lined esophagus (CLE), or Barrett's esophagus (4). CLE is present in approximately 10% of patients with gastroesophageal reflux (5) and it is estimated that up to 90% of all esophageal adenocarcinomas arise from CLE. The presence of CLE is associated with an increased risk of adenocarcinoma by a factor of between 30 and 125 (4,6).

LOH data

Loss-of-heterozygosity (LOH) studies of specific oncogenes involved in the neoplastic progression of the esophagus have identiied important loss of function atmultiple sites (7–11). In a study performed on 23 cases of adenocarcinoma of the esophagus the chromosomal abnormalitieswith the highest incidence of LOH were 3p (64%), 5q (45%), 9p (52%), 11p (61%), 13q (50%), 17p (96%), 17q (55%), and 18q (70%; 71).

Type
Chapter
Information
Molecular Oncology
Causes of Cancer and Targets for Treatment
 , pp. 526 - 531
Publisher: Cambridge University Press
Print publication year: 2013

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References

Blot, WJ, Devesa, SS, Kneller, RW, et al. Rising incidence of adenocarcinoma of the esophagus and gastric cardia. Journal of the American Medical Association 1991;265:1287–9.CrossRefGoogle ScholarPubMed
Siegel, R, Naishadham, D, Jemal, A. Cancer Statistics 2013. CA, A Cancer Journal for Clinicians 2013;63:(1):11–30.
Trivers, KF, Sabatino, SA, Stewart, SL.Trends in esophageal cancer incidence by histology, United States, 1998–2003. International Journal of Cancer 2008;123:1422–8.CrossRefGoogle ScholarPubMed
Spechler, SJ, Robbins, AH, Rubins, HB, et al. Adenocarcinoma and Barrett's esophagus. Gastroenterology 1984;87:927–33.
Altorki, NK, Oliveria, S, Schrump, DS. Epidemiology and molecular biology of Barrett's adenocarcinoma. Seminars on Surgical Oncology 1997;13:270–80.3.0.CO;2-2>CrossRef
Clark, GW, Smyrk, TC, Mirvish, SS, et al. Effect of gastroduodenal juice and dietary fat on the development of Barrett's esophagus and esophageal neoplasia: an experimental rat model. Annals of Surgical Oncology 1994;1:252–61.CrossRef
Blount, PL, Ramel, S, Raskind, WH, et al. 17p allelic deletions and p53 overexpression in Barrett's adenocarcinoma. Cancer Research 1991;51:5482–6.
Huang, Y, Boynton, RF, Blount, PL, et al. Loss of heterozygosity involves multiple tumour suppressor genes in human esophageal cancers. Cancer Research 1992;52:6525–30.
Moskaluk, CA, Rumpel, CA. Allelic deletion in 11p15 is a common occurrence in esophageal and gastric adenocarcinoma. Cancer 1998;83:232–9.3.0.CO;2-S>CrossRef
Neshat, K, Sanchez, CA, Galipeau, PC, et al. Barrett's esophagus: a model of human neoplastic progression. Cold Spring Harbor Symposia on Quantitative Biology 1994;59:577–83.CrossRef
Wu, T, Watanabe, T, Heitmiller, R, et al. Genetic alterations in Barrett esophagus and adenocarcinomas of the esophagus and esophagogastric junction region. American Journal of Pathology 1998;153:287–94.CrossRefGoogle ScholarPubMed
Montesano, R, Hollstein, M, Hainaut, P.Genetic alterations in esophageal cancer and their relevance to etiology and pathogenesis: a review. International Journal of Cancer 1996;69:225–35.3.0.CO;2-6>CrossRefGoogle ScholarPubMed
Casson, AG, Tammenagi, M, Eskandarian, S, et al. p53 alterations in oesophageal cancer: association with clinicopathological features, risk factors, and survival. Journal of Clinical Pathology and Molecular Pathology 1998;51:71–9.CrossRefGoogle Scholar
Schneider, PM, Casson, AG, Levin, B, et al. Mutations of p53 in Barrett's esophagus and Barrett's cancer: a prospective study of ninety-eight cases. Journal of Thoracic and Cardiovascular Surgery 1996;111:323–33.CrossRefGoogle ScholarPubMed
Ramel, S, Reid, BJ, Sanchez, CA, et al. Evaluation of p53 protein expression in Barrett's esophagus by two-parameter flow cytometry. Gastroenterology 1992;102:1220–8.CrossRef
Younes, M, Ertan, A, Lechago, LV, et al. p53 protein accumulation is a specific marker of malignant potential in Barrett's metaplasia. Digestive Diseases and Sciences 1997;42:697–701.CrossRef
Symonds, H, Krall, L, Remington, L, et al. p53 dependent apoptosis suppressed tumor growth and progression in vivo. Cell 1994;78:703–11.CrossRef
Suzuki, H, Zhou, X, Yin, J, et al. Intragenic metations of CDKN2B and CDKN2A in primary human esophageal cancer. Human Molecular Genetics 1995;4:1883–7.CrossRef
Zhou, X, Suzuki, H, Shimada, Y, et al. Genomic DNA and messenger RNA expression alterations of the CDKN2B and CDKN2 genes in esophageal squamous carcinoma cell lines. Genes, Chromosomes and Cancer 1995;13:285–90.CrossRef
Yacoub, L, Goldman, H, Odze, RD. Transforming growth factor-a, epidermal growth factor receptor, and MiB-1 expression in Barrett's associated neoplasia: correlation with prognosis. Modern Pathology 1997;10:105–12.
Jankowski, J, Murphy, S, Coghill, G, et al. Epidermal growth factor receptors in the esophagus. Gut 1992;33:439–43.CrossRef
Jankowski, J, Coghill, G, Tregaskis, B, et al. Epidermal growth factor in the esophagus. Gut 1992;33:1448–53.CrossRef
Jankowski, J, Sharma, O. Review article: approaches to Barrett's esophagus treatment-the role of proton pump inhibitors and other interventions. Alimentary Pharmacology and Therapeutics 2004;19:54–9.CrossRef
Jankowski, JA, Wright, NA, Meltzer, SJ, et al. Molecular evolution of the metaplasia-dysplasia-adenocarcinoma sequence in the esophagus. American Journal of Pathology 1999;154:965–73.CrossRefGoogle ScholarPubMed
Al Kasspooles, M, Moore, JH, Orringer, M, et al. Amplification and over-expression of EGFr and erb-B2 genes in human esophageal adenocarcinoma. International Journal of Cancer 1993;54:213–19.CrossRefGoogle Scholar
Shimada, Y, Imamura, M, Shibagaki, I, et al. Genetic alterations in patients with esophageal cancer with short- and long-term survival rates after curative esophagectomy. Annals of Surgery 1997;226:162–8.CrossRef
Jiang, W, Zhang, YJ, Kahn, SM, et al. Altered expression of the cyclin D1 and retinoblastoma genes in human esophageal cancer. Proceedings of the National Academy of Sciences USA 1993;90:9026–30.CrossRef
Brown, LM, Silverman, DT, Pottern, LM, et al. Adenocarcinoma of the esophagus in white men in the United States: alcohol, tobacco, and socioeconomic factors. Cancer Causes and Control 1994;5:333–40.CrossRef
Gammon, MD, Schoenberg, JB, Ahsan, H, et al. Tobacco, alcohol, and socioeconomic status and adenocarcinomas of the esophagus and gastric cardia. Journal of the National Cancer Institute 1997;89:1277–84.CrossRefGoogle ScholarPubMed
Kabat, GC, Ng, SKC, Wynder, EL. Tobacco, alcohol intake, and diet in relation to adenocarcinoma of the esophagus and gastric cardia. Cancer Causes and Control 1993;41:123–32.CrossRef
Zhang, ZF, Kurtz, RC, Sun, M, et al. Adenocarcinomas of the esophagus and gastric cardia: medical conditions, tobacco, alcohol, and socioeconomic factors. Cancer Epidemiology, Biomarkers and Prevention 1996;5:761–8.
Ribeiro, U, Posner, MC, Safatle-Ribiero, AV, et al. Risk factors for squamous cell carcinoma of the esophagus. British Journal of Surgery 1996;83:1174–85.CrossRefGoogle Scholar
Lehrbach, DM, Nita, ME, Cecconello, I, Clinical Genomics of Esophageal Cancer Group. Molecular aspects of esophageal squamous cell carcinoma carcinogensis. Arqivos de Gastroenterologia 2003;4:256–61.CrossRef
Hiyama, T, Yoshihara, M, Tanaka, S, Chayama, K.Genetic polymorphisms and esophageal cancer risk. International Journal of Cancer 2007;121:1643–58.CrossRefGoogle ScholarPubMed
Hori, H, Kawano, T, Endo, M, et al. Genetic polymorphisms of tobacco- and alcohol-related metabolizing enzymes and human esophageal squamous cell carcinoma susceptibility. Journal of Clinical Gastroenterology 1997;25:568–75.CrossRefGoogle ScholarPubMed
Lewis, SJ, Smith, GD. Alcohol, ALDH2, and esophageal cancer: a meta-analysis which illustrates the potentials and limitations of a Mendelian randomization approach. Cancer Epidemiology, Biomarkers and Prevention 2005;14:1967–71.CrossRef
Wu, CF, Wu, DC, Hsu, HK, et al. Relationship between genetic polymorphisms of alcohol and aldehyde dehydrogenases and esophageal squamous cell carcinoma risk in males. World Journal of Gastroenterology 2005;11:5103–8.CrossRefGoogle ScholarPubMed
Yokoyama, A, Kato, H, Yokoyama, T, et al. Genetic polymorphisms of alcohol and aldehyde dehydrogenase and glutathione S-transferase M1 and drinking, smoking, and diet in Japanese men with esophageal squamous cell carcinoma. Carcinogenesis 2002;23:1851–9.CrossRef
Hong, Y, Miao, X, Zhang, X, et al. The role of p53 and mdm2 polymorphisms in the risk of esophageal squamous cell carcinoma. Cancer Research 2005;65:9582–7.CrossRef
Lee, JM, Lee, YC, Yang, SY, et al. Genetic polymorphisms of p53 and GSTP1, but not NAT2, are associated with susceptibility to squamous cell carcinoma of the esophagus. International Journal of Cancer 2000;89:458–64.3.0.CO;2-R>CrossRefGoogle Scholar
Hiyama, T, Yokozaki, H, Kitadai, Y, et al. Overexpression of human telomerase RNA is an early event in esophageal carcinogenesis. Virchows Archiv 1999;434:483–7.CrossRef
Aklilu, M, Ilson, DH. Targeted agents and esophageal cancer: the next step? Seminars in Radiation Oncology 2006;17:62–9.
Lin, CC, Papadopoulos, KP. Novel targeted therapies for advanced esophageal cancer. Diseases of the Esophagus 2007;20:365–71.CrossRef
Peters, CJ, Fitzgerald, RC. Systematic review: the application of molecular pathogenesis to prevention and treatment of esophageal adenocarcinoma. Alimentary Pharmacology and Therapeutics 2007;25:1253–69.CrossRef
Syrigos, KN, Zalonis, A, Kotteas, E, Saif, MW. Targeted therapy for esophageal cancer: an overview. Cancer Metastasis Review 2008;27:273–88.CrossRef
Tew, WP, Kelsen, DP, Ilson, DH. Targeted therapies for esophageal cancer. The Oncologist 2005;15:590–601.
Bax, DA, Siersema, PD, Van Vliet, AH, et al. Molecular alterations during the development of esophageal adenocarcinoma. Journal of Surgical Oncology 2005;92:89–98.CrossRefGoogle ScholarPubMed
Geddert, H, Zeriouh, M, Wolter, M, et al. Gene amplification and protein overexpression of c-erb-b2 in Barrett carcinoma and its precursor lesions. American Journal of Clinical Pathology 2002;118:60–6.CrossRefGoogle ScholarPubMed
Brieu, TP.Odze, RD, Sheehan, CE, et al. Her2/neu gene amplification by FISH predicts poor survival in Barrett's esophagus-associated adenocarcinoma. Human Pathology 2000;31:35–9.CrossRef
Wainberg, Z, Hecht, JR. Panitumumab in colon cancer: a review and summary of ongoing trials. Expert Opinion on Biological Therapy 2006;6:1229–35.CrossRef
Saba, NF, Khuri, FR, Shin, DM. Targeting epidermal growth factor receptor. Trials in head and neck and lung cancer. Onology 2006;20:153–61.
Fukuoka, M, Yano, S, Giaccone, G, et al. Multi-institutional randomized Phase II trial of gefitinib for previously treated patients with advanced non-small cell lung cancer (The IDEAL 1 Trial). Journal of Clinical Oncology 2003;21:2237–46.CrossRefGoogle Scholar
Lynch, T, Bell, DW, Sordella, R, et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small cell lung cancer to gefitinib. New England Journal of Medicine 2004;350:2129–39.CrossRefGoogle ScholarPubMed
Kleespies, A, Guba, M, Jauch, K, et al. Vascular endothelial growth factor in esophageal. Journal of Surgical Oncology 2004;87:95–104.CrossRefGoogle ScholarPubMed
Shimizu, D, Vallbohmer, D, Kuramochi, H, et al. Increasing cyclooxygenase-2 (cox-2) gene expression in the progression of Barrett's esophagus to adenocarcinoma correlates with that of Bcl-2. International Journal of Cancer 2006;119:765–70.CrossRefGoogle ScholarPubMed
Zimmerman, KC, Sarbia, M, Weber, AA, et al. Cyclooxygenase-2 expression in human esophageal cancer. Cancer Research 1999;59:198–204.
Tangers, JA, Albert, PS, Lanza, E, et al. Non-steroidal anti-inflammatory drug use is associated with reduction in recurrence of advanced and non-advanced and nonadvanced colorectal adenomas. Cancer Causes and Control 2003;14:403–11.CrossRef
Kaur, BS, Khamnehei, N, Iravani, M, et al. Rofecoxib inhibits cyclooxygenase 2 expression and activity and reduces cell proliferation in Barrett's esophagus. Gastroenterology 2002;123:60–7.CrossRef
Murray, GI, Duncan, ME, O’Neill, P, et al. Matrix metalloproteinase-1 is associated with poor prognosis in esophageal cancer. Journal of Pathology 1998;185:256–61.3.0.CO;2-A>CrossRefGoogle Scholar
Nelson, AR, Fingleton, B, Rothenberg, ML, Matrisian, LM.Matrix metalloproteinase's: biologic activity and clinical implications. Journal of Clinical Oncology 2000;18:1135–49.CrossRefGoogle Scholar
Davies, B, Brown, PD, East, N, et al. A synthetic matrix metalloproteinase inhibitor decreases tumor burden and prolongs survival of mice bearing human ovarian carcinoma xenografts. Cancer Research 1993;53:2087–91.
Wang, X, Fu, X, Brown, PD, et al. Matrix metalloproteinase inhibitor BB-94 (batimastat) inhibits human colon tumor growth and spread in a patient-like orthotopic model in nude mice. Cancer Research 1994;54:4726–8.
Nemunaitis, J, Poole, C, Primrose, J, et al. Combined analysis of studies of the effects of the matrix metalloproteinase inhibitor marimastat on serum tumor markers in advanced cancer: selection of a biologically active and tolerable dose for longer-term studies. Clinical Cancer Research 1998;4:1101–9.
Bramhall, SR, Hallissey, MT, Whiting, J, et al. Marimastat as maintenance therapy for patients with advanced gastric cancer: a randomized trial. British Journal of Cancer 2002;86:1864–70.CrossRefGoogle Scholar
Swanton, C. Cell-cycle targeted therapies. Lancet Oncology 2004;5:27–36.CrossRef
Sato, S, Kajiyama, Y, Saguno, M, et al. Flavopiridol as a radiosensitizer for esophageal cancer cell lines. Diseases of the Esophagus 2004;17:338–44.CrossRef
Senderowicz, AM. Small molecular cyclin-dependent kinase modulators. Oncogene 2003;22:6609–20.CrossRef
Schwartz, GK, O’Reilly, E, Ilson, D, et al. Phase I study of the cyclin-dependent kinase inhbitor flavopiridol in combination with paclitaxel in patients with advanced solid tumors. Journal of Clinical Oncology 2002;20:2157–70.CrossRefGoogle Scholar
Shah, MA, Kortmansky, J, Gonen, M, et al. Phase I study of weekly irinotecan, cisplatin and flavopiridol. Proceedings of the American Society of Clinical Oncology 2004;23:319.Google Scholar
Shah, MA, Holen, K, Singh, D, et al. A multicenter, two-stage, Phase II study of PS-341 in patients with unresectable or metastatic gastric or gastroesophageal junction adenocarcinoma. Program and Abstracts of the American Society of Clinical Oncology Meeting 2005;103, abstr 41.
Dolan, K, Garde, J, Gosney, J, et al. Allelotype analysis of oesophageal adenocarcinoma: Loss of heterozygosity occurs at multiple sites. British Journal of Cancer 1998;78:950–7.CrossRefGoogle ScholarPubMed

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