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Cancer Immunotherapy - At the forefront of curing cancer

Over the last twenty years, failures in harnessing the body’s own immune system and using it to eradicate cancer have overshadowed the early promises of cancer immunotherapy. Recently, this cutting edge approach made headline news when a breakthrough for melanoma treatment yielded promising outcomes and more and more similar stories are now coming to light. It is no wonder that Science magazine has hailed cancer immunotherapy as “Breakthrough of the Year in 2013” since stimulating the immune system to fight cancer marks an entirely novel approach.


Our understanding of the complex tumor immune microenvironment improved significantly over the last decade. For example, we know that tumors express a wide variety of factors capable of exploiting the immune system’s weaknesses and inhibiting the adaptive immune response thereby promoting cancer evasion and cancer progression. Recent studies have shown that tumors escape surveillance by disrupting T-cell check¬point pathways. Immune checkpoints are a multitude of hard-wired inhibitory pathways in the immune system that are crucial for maintaining self-tolerance and minimizing collateral tissue damage. Many of these checkpoints are initiated by ligand-receptor interactions, which can readily be blocked by antibodies or modulated by recombinant forms of ligands or receptors. Some of the most studied ligand-receptor interactions that regulate T-cell response to antigen include FASL and its receptor FAS, PD-L1/2 and PD-1, CD86 and CTLA-4/CD80, MHC-II and LAG-3, and Galectin-9 and Tim-3. Lately, these have all been put forward as targets for cancer immunotherapies. Ipilimumab is an example of blocking antibody against CTLA-4 and has shown great promise in the treatment of melanoma and other forms of cancers despite causing adverse side effects (Weber, 2009).

The interaction between programmed death-1 (PD-1) and its ligands (PD-L1/2) is now well characterized and has received much attention recently. PD-1 is a receptor expressed on the surface of B and T cells. PD-L1 can be found on the surface of a wide array of cancer cells. Deciphering the biology and identification of the PD-1 gene can be traced to the work of Nishimura et al. (1999) from Kyoto University School of Medicine who reported upregulation of this gene during T-cell activation and cell death. Clues to its biological function and its potential to be exploited in cancer immunotherapy were subsequently elucidated over the last decade. Efforts by Dong et al. (2001) to design antibodies to target and block these immuno-inhibitory interactions have ushered a new era of immunotherapy. Antibodies directed against PD-L1 were shown to induce tumor rejection and these findings had major implications for the design of T-cell-based cancer immunotherapy. Since then, this pathway has been shown to be often hijacked by tumors to suppress immune control (Vesely et al., 2011). Engagement of PD-1 by PD-L1 expressed on tumor cells disables the host antitumor response resulting in poor prognosis and lack of immunologic control is now recognized as one of the hallmarks of cancer (Hanahan et al., 2011). This video provides an overview of the immune checkpoint concept and how it can be deployed to target cancer pathways.



The principal method for inhibiting the PD-1 pathway has been through the development of genetically engineered monoclonal antibodies that inhibit either PD-1 or PD-L1 function. A number of these agents have been developed and have shown promising outcomes in clinical testing. From the basic understanding of how PD-1 functions in cancer to blocking this interaction with a drug was but a short intellectual leap. Many experts are of the view that among all of the therapies developed to harness the power of the immune system to fight cancer over the past several decades, PD-1/PD-L1 inhibitors have been the most promising. Cancer immunotherapy has made a remarkable journey from bench to bedside. The discovery and antibody targeting of immune regulatory mechanisms such as the PD-1/PD-L1 pathway has led to clinically meaningful anticancer results. Rapid advances have translated in obtaining regulatory approvals for this class of agents for advanced melanoma and a greater understanding of the genetic changes that occur within and surrounding cancer cell, will advance both immunotherapy and targeted drug therapy.

To that effect, Enzo Life Sciences offers comprehensive tools for advancing your research in cancer immunology including superior labeling chemistry for comparative genomic hybridization (CGH) assays, SCREEN-WELL® Compound library product family as well as CELLESTIAL® portfolio of fluorescent probes and assay kits for cellular analysis, some of which are described below:

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References:

  1. J. Weber. Ipilimumab: controversies in its development, utility and autoimmune adverse events. Cancer Immunol. Immunother. (2009) 58: 823.
  2. H. Nishimura et al. Development of lupus-like autoimmune diseases by disruption of the PD-1 gene encoding an ITIM motif-carrying immunoreceptor. Immunity. (1999) 2: 141.
  3. H. Dong et al. Tumor-associated B7-H1 promotes T-cell apoptosis: A potential mechanism of immune evasion. Nat. Med. (2001) 8: 793.
  4. M.D. Vesely et al. Natural innate and adap¬tive immunity to cancer. Annu. Rev. Immunol. (2011) 29: 235.
  5. D. Hanahan et al. Hallmarks of cancer: the next generation. Cell. (2011) 144: 646-74.

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