Keshteli AH, Baracos VE, Madsen KL. Hyperhomocysteinemia as a potential contributor of colorectal cancer development in inflammatory bowel diseases: A review. World J Gastroenterol 2015; 21(4): 1081-1090 [PMID: 25632180 DOI: 10.3748/wjg.v21.i4.1081]
Corresponding Author of This Article
Ammar Hassanzadeh Keshteli, MD, Department of Medicine, University of Alberta, 7-142 Katz Group Centre for Pharmacy and Health Research, Edmonton, Alberta T6G 2E1, Canada. ahassanz@ualberta.ca
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Jan 28, 2015; 21(4): 1081-1090 Published online Jan 28, 2015. doi: 10.3748/wjg.v21.i4.1081
Hyperhomocysteinemia as a potential contributor of colorectal cancer development in inflammatory bowel diseases: A review
Ammar Hassanzadeh Keshteli, Vickie E Baracos, Karen L Madsen
Ammar Hassanzadeh Keshteli, Karen L Madsen, Department of Medicine, University of Alberta, Edmonton, Alberta T6G 2E1, Canada
Vickie E Baracos, Department of Oncology, University of Alberta, Cross Cancer Institute, Edmonton, Alberta T6G 2E1, Canada
Author contributions: Keshteli AH prepared the first draft of the manuscript; Keshteli AH, Baracos VE and Madsen KL contributed equally to the selection of the topic and finalizing the manuscript for publication.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Ammar Hassanzadeh Keshteli, MD, Department of Medicine, University of Alberta, 7-142 Katz Group Centre for Pharmacy and Health Research, Edmonton, Alberta T6G 2E1, Canada. ahassanz@ualberta.ca
Telephone: +1-78-04927077 Fax: +1-78-04927593
Received: June 18, 2014 Peer-review started: June 18, 2014 First decision: July 21, 2014 Revised: August 18, 2014 Accepted: September 29, 2014 Article in press: September 30, 2014 Published online: January 28, 2015
Abstract
Homocysteine is an amino acid generated metabolically by the S-adenosylmethionine-dependent transmethylation pathway. In addition to being a well-known independent risk factor for coronary heart disease, is also a risk factor for cancer. Patients suffering from inflammatory bowel diseases (IBD) including ulcerative colitis and Crohn’s disease are at increased risk of developing colorectal cancer in comparison to healthy individuals. Furthermore, the risk of hyperhomocysteinaemia is significantly higher in IBD patients when compared with controls. In the present article, we review the mechanisms in which hyperhomocysteinemia may contribute to increased risk of colorectal cancer in IBD patients.
Core tip: There is growing evidence suggesting hyperhomocysteinemia to be associated with increased colorectal cancer risk. Taking this into account that hyperhomocysteinemia and its related contributors are prevalent among patients with inflammatory bowel disease, we suggest performing well designed epidemiological, experimental, and clinical trial studies to investigate such association in these patients.
