alexa Resistance to Anti-EGFR Therapy and Strategies to Overcome it: Possible Role of BDNF/TrkB
ISSN: 1948-5956

Journal of Cancer Science & Therapy
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Short Communication

Resistance to Anti-EGFR Therapy and Strategies to Overcome it: Possible Role of BDNF/TrkB

de Farias CB1,2*, Schwartsmann G1,3 and Roesler R1,4

1Cancer and Neurobiology Laboratory, Clinical Hospital, Federal University of Rio Grande do Sul, RS, Brazil

2Children’s Cancer Institute, Porto Alegre, RS, Brazil

3Department of Internal Medicine, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil

4Department of Pharmacology, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil

*Corresponding Author:
de Farias CB
Cancer and Neurobiology Laboratory
Experimental Research Center, Clinical Hospital
Federal University of Rio Grande do Sul. Rua Ramiro Barcelos
2350, CPE, 2° Andar, 90035-003 Porto Alegre, RS, Brazil
Tel: +555151 33597616
Fax: +5551 33598012
E-mail: [email protected]

Received Date: December 30, 2015 Accepted Date: February 24, 2016 Accepted Date: February 26, 2016

Citation: de Farias CB, Schwartsmann G, Roesler R (2016) Resistance to Anti- EGFR Therapy and Strategies to Overcome it: Possible Role of BDNF/TrkB. J Cancer Sci Ther 8:046-047. doi: 10.4172/1948-5956.1000387

Copyright: © 2016 de Farias CB, 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

Acquired resistance to anti-epidermal growth factor receptor (EGFR) monoclonal antibodies such as cetuximab and panitumumab represents an important limitation to the treatment of colorectal cancer (CRC), and research efforts have increasingly been directed towards understanding molecular mechanisms of resistance. We propose that neurotrophin signaling mediated by brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosinrelated kinase B (TrkB), might be a compensatory mechanism contributing to decreased response to anti-EGFR therapy in CRC. The combined targeting of EGFR and TrkB is a novel strategy worth of further investigation.

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