The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Dynamic changes in the expression of MicroRNA-31 during inflammatory bowel disease-associated neoplastic transformation.
Alexandru V Olaru; Florin M Selaru; Yuriko Mori; Christine Vazquez; Stefan David; Bogdan Paun; Yulan Cheng; Zhe Jin; Jian Yang; Rachana Agarwal; et al. (Profiled Authors: John Kwon; Rachana Agarwal; Stephen Meltzer; Yuriko Mori; Theodore Bayless; Mary Harris; Zhe Jin; John Abraham; Alexandru Olaru; Florin Selaru)
Department of Medicine, Division of Gastroenterology and Hepatology, Johns Hopkins University, Baltimore, Maryland 21231, USA. email@example.com
Inflammatory bowel diseases 2011;17(1):221-31.
BACKGROUND: Patients with inflammatory bowel disease (IBD) are at increased risk of developing colorectal cancer. Aberrant microRNA (miR) expression has been linked to carcinogenesis; however, no reports document a relationship between IBD-related neoplasia (IBDN) and altered miR expression. In the current study we sought to identify specific miR dysregulation along the normal-inflammation-cancer axis. METHODS: miR microarrays and quantitative reverse-transcriptase polymerase chain reaction (RT-PCR) were used to detect dysregulated miRs. Receiver operating characteristic curve analysis was employed to test for potential usefulness of miR-31 as a disease marker of IBDNs. In silico prediction analysis, Western blot, and luciferase activity measurement were employed for target identification. RESULTS: Several dysregulated miRs were identified between chronically inflamed mucosae and dysplasia arising in IBD. MiR-31 expression increases in a stepwise fashion during progression from normal to IBD to IBDN and accurately discriminated IBDNs from normal or chronically inflamed tissues in IBD patients. Finally, we identified factor inhibiting hypoxia inducible factor 1 as a direct target of miR-31. CONCLUSIONS: Our study reveals specific miR dysregulation as chronic inflammation progresses to dysplasia. MiR-31 expression levels increase with disease progression and accurately discriminates between distinct pathological entities that coexist in IBD patients. The novel effect of miR-31 on regulating factor inhibiting hypoxia inducible factor 1 expression provides a new insight on the pathogenesis of IBDN.
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
Yuriko Mori; Alexandru V Olaru; Yulan Cheng; Rachana Agarwal; Jian Yang; Delgermaa Luvsanjav; Wayne Yu; Florin M Selaru; Susan Hutfless; Mark Lazarev; et al.Endocrine-related cancer 2011;18(4):465-78.
Feng Wu; Natalie Jia Guo; Hongying Tian; Michael Marohn; Susan Gearhart; Theodore M Bayless; Steven R Brant; John H KwonInflammatory bowel diseases 2011;17(1):241-50.
Feng Wu; Simin Zhang; Themistocles Dassopoulos; Mary L Harris; Theodore M Bayless; Stephen J Meltzer; Steven R Brant; John H KwonInflammatory bowel diseases 2010;16(10):1729-38.
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