Acta Scientific Cancer Biology

Literature ReviewVolume 2 Issue 3

GLP-1 Receptor Agonists and Cancers

Aqsa Iqbal1* and Anum Iqbal2

1Physiology and Biophysics Department, University of Illinois at Chicago, USA
1Liaquat University of Medical and Health Sciences, Pakistan

*Corresponding Author: Aqsa Iqbal, Physiology and Biophysics Department, University of Illinois at Chicago, USA. E-mail:

Received: March 21, 2018; Published: April 06, 2018

Citation: Aqsa Iqbal and Anum Iqbal. “GLP-1 Receptor Agonists and Cancers”. Acta Scientific Cancer Biology 2.3 (2018).


  Diabetes mellitus is associated with various types of cancers and presence of diabetes as a co-morbidity worsens the prognosis of cancer [1]. Glucagon-like peptide-1 receptor agonist (GLP-1RA) is a class of drug, which is used as a treatment of type 2 diabetes. Studies linking GLP-1RAs with cancers have found that GLP-1 RAs are associated with increased risks of pancreatic and thyroid can- cers and decreased risks of breast, prostate, endometrial, colon, ovarian cancers and various other cancers. This review discusses the impact of GLP-1RAs on different cancers and pathways involved in carcinogenic and anti-carcinogenic effects of GLP-1RAs. GLP-1RAs exerts their carcinogenic and anti-carcinogenic effects by attenuating various pathways including mTOR, ERK ½, and MAPK. Studying and understanding core pathways of GLP-1RAs directs more research on GLP-1RAs and guides the future management of diabetes mellitus.

Keywords: Diabetes Mellitus; Pancreatitis; Glucagon-like receptor agonists (GLP-RAs); Pancreatitis; Insulin; Pancreatic Cancer; Breast Cancer; Prostate Cancer; Endometrial Cancer; Ovarian Cancer; Thyroid Cancer; Exenatide; Liraglutide; Exendin -4; MAPK; mTOR; Akt; Apoptosis; Carcinogenic; Anti-carcinogenic

Copyright: © 2018 Aqsa Iqbal and Anum Iqbal. 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.

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