alexa Cancer Treatment in the Checkpoint Inhibitor Era
ISSN: 1745-7580

Immunome Research
Open Access

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Cancer Treatment in the Checkpoint Inhibitor Era

Ghazaleh Shoja E Razavi*

Department of Clinical Development- Oncology and Respiratory, Global Allied Pharmaceutical, 160 Vista Oak Dr.Longwood, FL 32779, USA

*Corresponding Author:
Ghazaleh Shoja E Razavi
Department of Clinical Development-Oncology and Respiratory
Global Allied Pharmaceutical
160 Vista Oak Dr.Longwood, FL 32779, USA
Tel: 1+ 416-520-8835
E-mail: [email protected]

Received date: April 22, 2016; Accepted date: April 23, 2016; Published date: April 25, 2016

Citation: Razavi GSE (2016) Cancer Treatment in the Checkpoint Inhibitor Era. Immunome Res 12:e105. doi:10.4172/1745-7580.10000e105

Copyright: © 2016 Razavi GSE. 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.



Cross talk between antigen presenting cells, effector T cells and immune regulatory cells through co-stimulatory and inhibitory signals orchestrates the anti-tumor immune response that eventuates in either the effective tumor directed immune activity leading to the tumor removal or an immune suppressed tumor microenvironment leading to the tumor progression and metastasis. The co-stimulatory signals have been shown to be mediated by CD28 and members of the tumor necrosis factor receptor (TNFR) family, such as CD40, OX-40, 4-1BB, CD30, and CD27, while the regulatory signals are generally mediated through cytotoxic T lymphocyte activator-4 (CTLA-4) and programmed death -1 (PD-1) receptors that share structural homology with the CD28 co-stimulatory class and also bind to the B7 family members. Despite the observed similarities in their structure and receptors, CTLA-4 and PD-1 show the main regulatory role and considered as checkpoints. Targeting these co-stimulatory or inhibitory receptors with either stimulating or blocking antibodies may lead to the enhanced immune response within tumor microenvironment and clinical benefits.


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