This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bleuming, S. A. Articles by van den Brink, G. R. Search for Related Content PubMed PubMed Citation Articles by Bleuming, S. A. Articles by van den Brink, G. R.

Bone Morphogenetic Protein Signaling Suppresses Tumorigenesis at Gastric Epithelial Transition Zones in Mice

¹ Center for Experimental and Molecular Medicine and ² Department of Pathology, Academic Medical Center, Amsterdam, the Netherlands; ³ Stowers Institute for Medical Research, Kansas City, Missouri; ⁴ Department of Gastroenterology and Hepatology, Leiden University Medical Center, Leiden, the Netherlands; ⁵ Department of Cell Biology, Faculty of Medical Sciences, University of Groningen, Groningen, the Netherlands; and ⁶ Department of Pathology, University Medical Center Utrecht, Utrecht, the Netherlands

Requests for reprints: Gijs R. van den Brink, Department of Gastroenterology and Hepatology, Leiden University Medical Center, Building 1, C4-P012, P.O. Box 9600, 2300 RC Leiden, the Netherlands. Phone: 31-20-566-9111; E-mail: g.r.van_den_brink{at}lumc.nl.

Bone morphogenetic protein (BMP) signaling is known to suppress oncogenesis in the small and large intestine of mice and humans. We examined the role of Bmpr1a signaling in the stomach. On conditional inactivation of Bmpr1a, mice developed neoplastic lesions specifically in the squamocolumnar and gastrointestinal transition zones. We hypothesized that the regulation of epithelial cell fate may be less well defined in these junctional zones than in the adjacent epithelium and found that the mucosa at the squamocolumnar junction in mice shows a lack of differentiated fundic gland cell types and that foveolar cells at the gastrointestinal junctional zone lack expression of the foveolar cell marker Muc5ac. Precursor cell proliferation in both transition zones was higher than in the surrounding epithelium. Our data show that BMP signaling through Bmpr1a suppresses tumorigenesis at gastric epithelial junctional zones that are distinct from the adjacent gastric epithelium in both cellular differentiation and proliferation. [Cancer Res 2007;67(17):8149–55]

This article has been cited by other articles:

				H. Oshima, H. Itadani, H. Kotani, M. M. Taketo, and M. Oshima Induction of Prostaglandin E2 Pathway Promotes Gastric Hamartoma Development with Suppression of Bone Morphogenetic Protein Signaling Cancer Res., April 1, 2009; 69(7): 2729 - 2733. [Abstract] [Full Text] [PDF]

				S.-F. Chang, C. A. Chang, D.-Y. Lee, P.-L. Lee, Y.-M. Yeh, C.-R. Yeh, C.-K. Cheng, S. Chien, and J.-J. Chiu Tumor cell cycle arrest induced by shear stress: Roles of integrins and Smad PNAS, March 11, 2008; 105(10): 3927 - 3932. [Abstract] [Full Text] [PDF]