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Differentiation of Tumor CellsWenjuan Li, Zheng Ge, Cheng Liu, et al. Clin Cancer Res 2008;14:3722-3728. Published online June 16, 2008.
Downloaded from clincancerres.aacrjournals.org on January 7, 2011 Copyright © 2008 American Association for Cancer Research
Human Cancer Biology
Gastric cancer is one of the most common malignancies worldwide and ranks second in terms of global cancer-related mortality (1, 2). Helicobacter pylori infection has been shown to initiate the pathogenesis of gastric cancer by causing a chronic gastritis, the precursor to all the pathophysiologic abnormal- ities characteristic of gastric carcinogenesis (1, 3, 4). However, these precursor lesions only develop in a proportion of infected
Authors’Affiliations: 1Department of Microbiology/Key Laboratory for Experimental Teratology of Chinese Ministry of Education; 2 Department of Biochemistry, School of Medicine, Shandong University, Jinan, People’s Republic of China and 3 Department of Medicine, Division of Hematology, Karolinska University Hospital Solna and Karolinska Institutet, Stockholm, Sweden Received 9/8/07; revised 3/20/08; accepted 3/23/08. Grant support: Swedish Cancer Society, Swedish Research Council, Cancer Society in Stockholm, Swedish Society of Medicine, Karolinska Institutet Foundation, National Natural Science Foundation of China grants 30770118 and 30772545, National Basic Research Program of China 973 Program 2007CB512001, and Science Foundation of Shandong Province grants 2005GG3202087 andY2004C03. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with18 U.S.C. Section1734 solely to indicate this fact. Requests for reprints: JihuiJia, Department of Microbiology, School of Medicine, Shandong University, Jinan, 250012, PR China. Phone: 86 -531-88382672; Fax: 86-531-88382502; E-mail: jiajihui@sdu.edu.cn. F 2008 American Association for Cancer Research. doi:10.1158/1078 -0432.CCR-07-4137 subjects and do not necessarily progress into invasive cancers. The host genetic, bacterial virulence, environmental, and many other factors have been implicated in affecting the gastric oncogenic process, but the underlying molecular mechanism is poorly understood (1, 3). Moreover, because of lack of reliable early diagnostic markers, the prognosis of gastric cancer remains poor. Therefore, better defining the pathogenesis of gastric cancer, looking for useful biomarkers, and exploring novel therapeutic targets for treatment are urgently demanding tasks (1 – 3). A hallmark of cancer is unlimited cellular proliferation due to the aberrant expression of key factors regulating cell cycle progression, apoptosis, senescence, and differentiation (5). One of these molecules, named cancerous inhibitor of protein phosphatase 2A (PP2A; CIP2A), has recently been identified to stabilize c-MYC protein by inhibiting its degradation mediated by PP2A in cancer cells and to be required for the malignant cell growth (6). When overexpressed, CIP2A transforms immortal- ized human cells. Furthermore, CIP2A was observed to be highly expressed in human neck and head carcinomas and colon cancers (6). Taken together, CIP2A functions as an oncoprotein contributing to malignant transformation of human cells. In the present study, we compared CIP2A expression between normal and malignant gastric tissues to determine whether CIP2A could serve as a diagnostic marker for gastric cancer; moreover, we sought to investigate the
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