alexa Associations between Markers of Colorectal Cancer Stem Cells, Mutations, Mirna, and Clinical Characteristics of Ulcerative Colitis
ISSN: 2161-1025

Translational Medicine
Open Access

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Research Article

Associations between Markers of Colorectal Cancer Stem Cells, Mutations, Mirna, and Clinical Characteristics of Ulcerative Colitis

Liu Yang1*, Edi Levi2, JianHua Du2,3, HengHua Zhou4, Rebecca Miller2,3 and Adhip PN Majumdar2,3,5

1Department of Gastroenterology, Shanghai Jiaotong University, China

2Department of Internal Medicine, Veterans Administration Medical Center, USA

3Wayne State University School of Medicine, Detroit, MI, USA

4Department of Pathology, Shanghai Ninth People’s Hospital, School of Medicine, China

5Karmanos Cancer Institute, USA

*Corresponding Author:
Liu Yang
Department of Gastroenterology
Shanghai Ninth People’s Hospital
School of Medicine, Shanghai Jiaotong University
Shanghai 200011,China
Tel: + 86 13 301782257
E-mail: [email protected]

Received Date: January 18, 2016; Accepted Date: January 29, 2016; Published Date: March 21, 2016

Citation: Yang L, Levi E, Du J, Zhou H, Miller R, et al. (2016) Associations between Markers of Colorectal Cancer Stem Cells, Mutations, Mirna, and Clinical Characteristics of Ulcerative Colitis. Transl Med (Sunnyvale) 6:168. doi:10.4172/2161-1025.1000168

Copyright: © 2016 Yang L, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Background: Several factors have been implicated in the pathogenesis of colorectal cancer (CRC) associated with ulcerative colitis (UC). We investigated markers of cancer cell pluripotency, including CD44 and CD166, microRNA-21 (miR-21) and microRNA-215 (miR-215), and APC, K-ras and DCC mutations in biopsy specimens from patients with UC to evaluate any correlations with clinical risk factors.

Methods: We observed 18 patients with UC and collected two biopsy specimens from each patient at diagnosis and at a follow-up endpoint. We examined the expression of CD44, CD166, miR-21 and miR-215 as well as APCKras and DCC mutations. We compared these markers from the two points in time and assessed their associations with clinical characteristics, including colitis duration, histological alterations, and patient age at UC onset.

Results: Most patients (16/18) had attenuated colonic lesions or remained stable during follow-up, except one patient who developed dysplasia, and one who had severe lesion aggravation during follow-up. Enhanced expression of CD44, CD166 and miR-21 with miR-215 was found in the specimens obtained at follow-up, despite attenuation of mucosal lesions. Coherence of cancer stem cell markers and microRNAs was seen in patients who had significant aggravation of mucosal alteration, dysplasia, and long duration of colitis. APC mutation occurred in only one patient, who had the longest duration of UC (23 years).

Conclusion: Enhanced markers of CRC in the follow-up colon samples support our conclusion that UC duration plays the most important role in UC-related carcinogenesis.

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