Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/42583
Title: High EPHB2 mutation rate in gastric but not endometrial tumors with microsatellite instability
Authors: Davalos, V.
Dopeso, H.
Velho, S.
Ferreira, A. M.
Cirnes, L.
Díaz-Chico, N. 
Bilbao, C. 
Ramírez, R.
Rodríguez, G.
Falcón, O.
León, L.
Niessen, R. C.
Keller, G.
Dallenbach-Hellweg, G.
Espín, E.
Armengol, M.
Plaja, A.
Perucho, M.
Imai, K.
Yamamoto, H.
Gebert, J. F.
Diaz-Chico, J. C. 
Hofstra, R. M.
Woerner, S. M.
Seruca, R.
Schwartz, S.
Arango, D.
UNESCO Clasification: 320101 Oncología
Keywords: EPHB2
Cancer
Microsatellite instability
Colorectal
Stomach, et al
Issue Date: 2007
Publisher: 0950-9232
Journal: Oncogene 
Abstract: The EPH/EFN family of receptor tyrosine kinases regulates cell adhesion and migration and has an important role in controlling cell positioning in the normal intestinal epithelium. Inactivation of EPHB2 has recently been shown to accelerate tumorigenesis in the colon and rectum, and we have previously demonstrated frequent frameshift mutations (41%) in an A9 coding microsatellite repeat in exon 17 of EPHB2 in colorectal tumors with microsatellite instability (MSI). In this study, we extended these analyses to extracolonic MSI cancers, and found frameshift EPHB2 mutations in 39% (25/64) of gastric tumors and 14% (8/56) of endometrial tumors. Regression analysis of these EPHB2 mutation data on the basis of our previously proposed statistical model identified EPHB2 as a selective target of frameshift mutations in MSI gastric cancers but not in MSI endometrial carcinomas. These results suggest a functional role for EPHB2 in gastric tumor progression, and emphasize the differences between the tumorigenic processes in MSI gastrointestinal and endometrial cancer.
URI: http://hdl.handle.net/10553/42583
ISSN: 0950-9232
DOI: 10.1038/sj.onc.1209780
Source: Oncogene[ISSN 0950-9232],v. 26 (2), p. 308-311
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