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Journal of Clinical Microbiology, April 2009, p. 959-968, Vol. 47, No. 4
0095-1137/09/$08.00+0     doi:10.1128/JCM.02330-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Polymorphism in the CagA EPIYA Motif Impacts Development of Gastric Cancer{triangledown} ,§

Kathleen R. Jones,1,{dagger} Young Min Joo,2,{dagger} Sungil Jang,2 Yun-Jung Yoo,2 Hak Sung Lee,3 In-Sik Chung,3 Cara H. Olsen,4 Jeannette M. Whitmire,1 D. Scott Merrell,1* and Jeong-Heon Cha2*

Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 20814,1 Department of Oral Biology, Oral Science Research Center, BK21 Project, Yonsei University College of Dentistry, Seoul, South Korea,2 Division of Gastroenterology, Department of Internal Medicine, College of Medicine, the Catholic University of Korea, Seoul, South Korea,3 Department of Preventive Medicine and Biometrics, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 208144

Received 3 December 2008/ Returned for modification 27 December 2008/ Accepted 10 January 2009

Helicobacter pylori causes diseases ranging from gastritis to peptic ulcer disease to gastric cancer. Geographically, areas with high incidences of H. pylori infection often overlap with areas with high incidences of gastric cancer, which remains one of the leading causes of cancer-related deaths worldwide. Strains of H. pylori that carry the virulence factor cytotoxin-associated gene A (cagA) are much more likely to be associated with the development of gastric cancer. Moreover, particular C-terminal polymorphisms in CagA vary by geography and have been suggested to influence disease development. We conducted a large-scale molecular epidemiologic analysis of South Korean strains and herein report a statistical link between the East Asian CagA EPIYA-ABD genotype and the development of gastric cancer. Characterization of a subset of the Korean isolates showed that all strains from cancer patients expressed and delivered phosphorylatable CagA to host cells, whereas the presence of the cagA gene did not strictly correlate to expression and delivery of CagA in all noncancer strains.

* Corresponding author. Mailing address for D. Scott Merrell: Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Rd., Bethesda, MD 20814. Phone: (301) 295-1584. Fax: (301) 295-3773. E-mail: dmerrell{at}usuhs.mil. Mailing address for Jeong-Heon Cha: Department of Oral Biology, Yonsei University College of Dentistry, 134 Sinchon-dong, Seodaemoon-gu, Seoul 120-752, South Korea. Phone: 82-2-2228-3061. Fax: 82-2-2227-7903. E-mail: Jcha{at}yuhs.ac

{triangledown} Published ahead of print on 21 January 2009.

§ Supplemental material for this article may be found at http://jcm.asm.org/.

{dagger} These authors contributed equally to this work.

Journal of Clinical Microbiology, April 2009, p. 959-968, Vol. 47, No. 4
0095-1137/09/$08.00+0     doi:10.1128/JCM.02330-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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