Skip to main content Accessibility help
×
Hostname: page-component-76fb5796d-wq484 Total loading time: 0 Render date: 2024-04-25T21:12:20.939Z Has data issue: false hasContentIssue false

45 - Gastric cancer

from Part 3.1 - Molecular pathology: carcinomas

Published online by Cambridge University Press:  05 February 2015

Yoshiaki Ito
Affiliation:
Cancer Science Institute, National University of Singapore, Center for Translational Medicine, Singapore
Khay Guan Yeoh
Affiliation:
Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore and National University Health System, Singapore
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
Get access

Summary

Etiology

Although the worldwide incidence of gastric cancer has declined in recent years, it is still the second most frequent cause of cancer-related death in the world.

Environmental factors play critical roles in the pathogenesis of gastric cancer, with the major risk factors being Helicobacter pylori (H. pylori) infection, diet, and smoking (1). H. pylori infection is the most important single risk factor for gastric cancer development and has been defined as a Class 1 carcinogen by the World Health Organization (WHO). Populations with high incidences of gastric cancer can be found in geographic areas with high prevalence of H. pylori infection. High salt intake, often due to traditional diet in the form of salted fish, is the best-documented dietary risk factor for atrophic gastritis (2).

Epstein–Barr virus (EBV) infection is correlated with Burkitt’s lymphoma in Africa and nasopharyngeal carcinoma in South-East Asia. In addition, this virus has been recognized as an etiological agent in 5–10% of gastric cancers (3). Infectious agents, therefore, play important causative roles in gastric carcinogenesis.

Type
Chapter
Information
Molecular Oncology
Causes of Cancer and Targets for Treatment
, pp. 532 - 541
Publisher: Cambridge University Press
Print publication year: 2013

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Lochhead, P, El-Omar, EM. Gastric cancer. British Medical Bulletin 2008;85:87–100.CrossRef
Tsugane, S, Sasazuki, S. Diet and the risk of gastric cancer: review of epidemiological evidence. Gastric Cancer 2007;10:75–83.CrossRef
Iwakiri, D, Takada, K. Epstein–Barr virus and gastric cancers. In: Robertson ES, editor. Epstein–Barr Virus. Norwich, UK:Caister Academic Press; 2005:157–69.
Correa, P. Human gastric carcinogenesis: a multistep and multifactorial process–First American Cancer Society Award Lecture on Cancer Epidemiology and Prevention. Cancer Research 1992;52:6735–40.
Goldenring, JR, Nam, KT. Oxyntic atrophy, metaplasia and gastric cancer. Progress in Molecular Biology and Translational Science 2010;96:117–31CrossRef
Karin, M. Inflammation and cancer: the long reach of Ras. Nature Medicine 2005;11:20–1.CrossRef
Brandt, S, Kwok, T, Hartig, R, Konig, W, Backert, S. NF-kappaB activation and potentiation of proinflammatory responses by the Helicobacter pylori CagA protein. Proceedings of the National Academy of Sciences USA 2005;102:9300–5.CrossRef
Houghton, J, Stoicov, C, Nomura, S, et al. Gastric cancer originating from bone marrow-derived cells. Science 2004;306:1568–71.CrossRef
El-Omar, EM, Rabkin, CS, Gammon, MD, et al. Increased risk of noncardia gastric cancer associated with proinflammatory cytokine gene polymorphisms. Gastroenterology 2003;124:1193–201.CrossRef
Figueiredo, C, Machado, JC, Pharoah, P, et al. Helicobacter pylori and interleukin 1 genotyping: an opportunity to identify high-risk individuals for gastric carcinoma. Journal of the National Cancer Institute 2002;94:1680–7.CrossRef
Tu, S, Bhagat, G, Cui, G, et al. Overexpression of interleukin-1beta induces gastric inflammation and cancer and mobilizes myeloid-derived suppressor cells in mice. Cancer Cell 2008;14:408–19.CrossRef
Smith, MG, Hold, GL, Tahara, E, El-Omar, EM. Cellular and molecular aspects of gastric cancer. World Journal of Gastroenterology 2006;12:2979–90.CrossRefGoogle ScholarPubMed
Rohde, M, Püls, J, Buhrdorf, R, Fischer, w, Haas, R. A novel sheathed surface organelle of the Helicobacter pylori cag-type IV secretion system. Molecular Microbiology 2003;49:219–34.CrossRef
Odenbreit, S, Puls, J, Sedlmaier, B, et al. Translocation of Helicobacter pylori CagA into gastric epithelial cells by type IV secretion. Science 2000;287:1497–500.CrossRef
Higashi, H, Tsutsumi, R, Muto, S, et al. SHP-2 tyrosine phosphatase as an intracellular target of Helicobacter pylori CagA protein. Science 2002;295:683–6.CrossRef
Amieva, MR, Vogelmann, R, Covacci, A, et al. Disruption of the epithelial apical-junctional complex by Helicobacter pylori CagA. Science 2003;300:1430–4.CrossRef
Bagnoli, F, Buti, L, Tompkins, L, Covacci, A, Amieva, MR. Helicobacter pylori CagA induces a transition from polarized to invasive phenotypes in MDCK cells. Proceedings of the National Academy of Sciences USA 2005;102:16 339–44.
Saadat, I, Higashi, H, Obuse, C, et al. Helicobacter pylori CagA targets PAR1/MARK kinase to disrupt epithelial cell polarity. Nature 2007;447:330–3.CrossRef
Poppe, M, Feller, SM, Romer, G, Wessler, S. Phosphorylation of Helicobacter pylori CagA by c-Abl leads to cell motility. Oncogene 2007;26:3462–72.CrossRef
Suzuki, M, Mimuro, H, Kiga, K, et al. Helicobacter pylori CagA phosphorylation-independent function in epithelial proliferation and inflammation. Cell Host and Microbe 2009;5:23–34.CrossRef
Murata-Kamiya, N, Kurashima, Y, Teishikata, Y, et al. Helicobacter pylori CagA interacts with E-cadherin and deregulates the beta-catenin signal that promotes intestinal transdifferentiation in gastric epithelial cells. Oncogene 2007;26:4617–26.CrossRef
Ito, K, Lim, AC, Salto-Tellez, M, et al. RUNX3 attenuates β-catenin/T cell factors in intestinal tumorigenesis. Cancer Cell 2008;14:226–37.CrossRef
Barker, N, Huch, M, Kujala, P, et al. Lgr5+ve stem cells drive self-renewal in the stomach and build long- lived gastric units in vitro. Cell Stem Cell 2010;6:25–36.CrossRef
de Lau, W, Barker, N, Low, TY, et al. Lgr5 homologues associate with Wnt receptors and mediate R- spondin signaling. Nature 2011;476:293–7.CrossRef
Schepers, AG, Snippert, HJ, Stange, DE, et al. Lineage tracing reveals Lgr5+ stem cell activity in mouse intestinal adenomas. Science 2012;337:730–5.CrossRef
Wang, K, Kan, J, Yuen, ST, et al. Exome sequencing identifies frequent mutation of ARID1A in molecular subtypes of gastric cancer. Nature Genetics 2011;43:1219–23CrossRef
Zang, ZJ, Cutcutache, I, Poon, SL, et al. Exome sequencing of gastric adenocarcinoma identifies recurrent somatic mutations in cell adhesion and chromatin remodeling genes. Nature Genetics 2012;44:570–4.CrossRef
Ushijima, K, Hattori, N. Molecular pathways: involvement of Helicobacter pylori-triggered inflammation in the formation of an epigenetic field defect, and its usefulness as cancer risk and exposure markers. Clinical Cancer Research 2011;18:923–9.CrossRef
Ramalho-Santos, M, Melton, DA, McMahon, AP. Hedgehog signals regulate multiple aspects of gastrointestinal development. Development 2000;127:2763–72.
Horii, A, Nakatsuru, S, Miyoshi, Y, et al. The APC gene, responsible for familial adenomatous polyposis, is mutated in human gastric cancer. Cancer Research 1992;52:3231–3.
Clements, WM, Wang, J, Sarnaik, A, et al. beta-Catenin mutation is a frequent cause of Wnt pathway activation in gastric cancer. Cancer Research 2002;62:3503–6.
Tomita, H, Yamada, Y, Oyama, T, et al. Development of gastric tumors in Apc(Min/+) mice by the activation of the beta-catenin/Tcf signaling pathway. Cancer Research 2007;67:4079–87.CrossRef
Silberg, DG, Sullivan, J, Kang, E, et al. Cdx2 ectopic expression induces gastric intestinal metaplasia in transgenic mice. Gastroenterology 2002;122:689–96.CrossRef
Li, QL, Ito, K, Sakakura, C, et al. Causal relationship between the loss of RUNX3 expression and gastric cancer. Cell 2002;109:113–24.CrossRef
Powell, SM, Harper, JC, Hamilton, SR, Robinson, CR, Cummings, OW. Inactivation of Smad4 in gastric carcinomas. Cancer Research 1997;57:4221–4.
Yoshida, K, Yokozaki, H, Niimoto, M, et al. Expression of TGF-beta and procollagen type I and type III in human gastric carcinomas. International Journal of Cancer 1989;44:394–8.CrossRefGoogle Scholar
Derynck, R, Akhurst, RJ, Balmain, A. TGF-beta signaling in tumor suppression and cancer progression. Nature Genetics 2001;29:117–29.CrossRef
Tamura, G, Kihana, T, Nomura, K, et al. Detection of frequent p53 gene mutations in primary gastric cancer by cell sorting and polymerase chain reaction single-strand conformation polymorphism analysis. Cancer Research 1991;51:3056–8.
Yokota, J, Yamamoto, T, Toyoshima, K, et al. Amplification of c-erbB-2 oncogene in human adenocarcinomas in vivo. Lancet 1986;1:765–7.CrossRef
Yokozaki, H, Yasui, W, Tahara, E. Genetic and epigenetic changes in stomach cancer. International Review of Cytology 2001;204:49–95.CrossRef
Yasui, W, Oue, N, Aung, PP, et al. Molecular-pathological prognostic factors of gastric cancer: a review. Gastric Cancer 2005;8:86–94.CrossRef
Jenkins, BJ, Grail, D, Nheu, T, et al. Hyperactivation of Stat3 in gp130 mutant mice promotes gastric hyperproliferation and desensitizes TGF-beta signaling. Nature Medicine 2005;11:845–52.CrossRef
Oshima, H, Matsunaga, A, Fujimura, T, et al. Carcinogenesis in mouse stomach by simultaneous activation of the Wnt signaling and prostaglandin E2 pathway. Gastroenterology 2006;131:1086–95.CrossRef
Matsumoto, Y, Marusawa, H, Kinoshita, K, et al. Helicobacter pylori infection triggers aberrant expression of activation-induced cytidine deaminase in gastric epithelium. Nature Medicine 2007;13:470–6.CrossRef
Akama, Y, Yasui, W, Yokozaki, H, et al. Frequent amplification of the cyclin E gene in human gastric carcinomas. Japanese Journal of Cancer Research 1995;86:617–21.CrossRefGoogle ScholarPubMed
Yasui, W, Naka, K, Suzuki, T, et al. Expression of p27Kip1, cyclin E and E2F-1 in primary and metastatic tumors of gastric carcinoma. Oncology Reports 1999;6:983–7.CrossRef
El-Rifai, W, Powell, SM. Molecular biology of gastric cancer. Seminars on Radiation Oncology 2002;12:128–40.CrossRef
Leung, SY, Yuen, ST, Chung, LP, et al. hMLH1 promoter methylation and lack of hMLH1 expression in sporadic gastric carcinomas with high-frequency microsatellite instability. Cancer Research 1999;59:159–64.
Ooi, CH, Ivanova, T, Wu, J, et al. Oncogenic pathway combinations predict clinical prognosis in gastric cancer. PLoS Genetics 2009;5:e1000676.
Guilford, P, Hopkins, J, Harraway, J, et al. E-cadherin germline mutations in familial gastric cancer. Nature 1998;392:402–5.CrossRef
Huntsman, DG, Carneiro, F, Lewis, FR, et al. Early gastric cancer in young, asymptomatic carriers of germ-line E-cadherin mutations. New England Journal of Medicine 2001;344:1904–9.CrossRefGoogle ScholarPubMed
Brooks-Wilson, AR, Kaurah, P, Suriano, G, et al. Germline E-cadherin mutations in hereditary diffuse gastric cancer: assessment of 42 new families and review of genetic screening criteria. Journal of Medical Genetics 2004;41:508–17.CrossRefGoogle ScholarPubMed
Keller, G, Vogelsang, H, Becker, I, et al. Diffuse type gastric and lobular breast carcinoma in a familial gastric cancer patient with an E-cadherin germline mutation. American Journal of Pathology 1999;155:337–42.CrossRefGoogle Scholar
Machado, J, Carneiro, F, Sobrinho-Simoes, M. E-cadherin mutations in gastric carcinoma. Journal of Pathology 2000;191:466–8.3.0.CO;2-Q>CrossRefGoogle ScholarPubMed
Mani, SA, Guo, W, Liao, MJ, et al. The epithelial-mesenchymal transition generates cells with properties of stem cells. Cell 2008;133:704–15.CrossRef
Hayashi, T, Senda, M, Morohashi, H, et al. Ternary structure-function analysis reveals the pathogenic signaling potentiation mechanism of Helicobacter pylori oncogenic effector, CagA. Cell Host and Microbe 2012;12:20–33.CrossRef
Hatakeyama, M. SagA of CagA in Helicobacter pylori pathogenesis. Current Opinion in Microbiology 2008;11:30–7.CrossRef

Save book to Kindle

To save this book to your Kindle, first ensure coreplatform@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

  • Gastric cancer
    • By Yoshiaki Ito, Cancer Science Institute, National University of Singapore, Center for Translational Medicine, Singapore, Khay Guan Yeoh, Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore and National University Health System, Singapore
  • Edited by Edward P. Gelmann, Columbia University, New York, Charles L. Sawyers, Memorial Sloan-Kettering Cancer Center, New York, Frank J. Rauscher, III
  • Book: Molecular Oncology
  • Online publication: 05 February 2015
  • Chapter DOI: https://doi.org/10.1017/CBO9781139046947.046
Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

  • Gastric cancer
    • By Yoshiaki Ito, Cancer Science Institute, National University of Singapore, Center for Translational Medicine, Singapore, Khay Guan Yeoh, Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore and National University Health System, Singapore
  • Edited by Edward P. Gelmann, Columbia University, New York, Charles L. Sawyers, Memorial Sloan-Kettering Cancer Center, New York, Frank J. Rauscher, III
  • Book: Molecular Oncology
  • Online publication: 05 February 2015
  • Chapter DOI: https://doi.org/10.1017/CBO9781139046947.046
Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

  • Gastric cancer
    • By Yoshiaki Ito, Cancer Science Institute, National University of Singapore, Center for Translational Medicine, Singapore, Khay Guan Yeoh, Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore and National University Health System, Singapore
  • Edited by Edward P. Gelmann, Columbia University, New York, Charles L. Sawyers, Memorial Sloan-Kettering Cancer Center, New York, Frank J. Rauscher, III
  • Book: Molecular Oncology
  • Online publication: 05 February 2015
  • Chapter DOI: https://doi.org/10.1017/CBO9781139046947.046
Available formats
×