Immunology and Biotherapies

Learn how decades of #immunotherapy research is resulting in new cancer therapies: http://t.co/xMDUCNNN37 http://t.co/bAkC5xMmtH

Via Krishan Maggon

The promise of cancer immunotherapy was validated officially in March 2011 when the FDA approved Yervoy (ipilimumab; Bristol-Myers Squibb) for the treatment of unresectable or metastatic melanoma. The approval was based on results of a randomized, double-blind clinical trial establishing that ipilimumab (a humanized anti-CTLA-4 monoclonal antibody) treatment extended the overall survival of patients with advanced melanoma. CTLA-4 is a member of the so-called family of checkpoint regulators, which are expressed on immune cells that activate or inhibit an immune response. An increasing number of immune checkpoint regulators are now being identified and targeted for immunotherapy. At the 2014 meeting of the American Society of Clinical Oncology (ASCO), it was reported that checkpoint blockade as a monotherapy or combination therapy was used successfully to treat advanced melanoma and non–small cell lung cancer. Checkpoint blockade immunotherapy was also used successfully for the treatment of other cancers, most notably genitourinary cancers such as urothelial bladder cancer and metastatic renal cell carcinoma. This report is a compiled summary of cancer immunotherapy highlights presented at the 2014 ASCO meeting by various investigators. Cancer Immunol Res; 2(8); 714–9. ©2014 AACR.

Via Krishan Maggon

TG4010, a novel MUC1 targeting immunotherapy, is in development for the treatment of metastatic non-small cell lung cancer (NSCLC) in combination with first-line chemotherapy.

 

TG4010 is a recombinant vaccinia virus of the Ankara strain (MVA) expressing the coding sequences of the MUC1 antigen and of the cytokine, Interleukin-2 (IL2). In healthy cells, the MUC1 protein is normally found on the surface of epithelial cells in many types of tissue and works to protect these cells. In tumor cells, several modifications of MUC1 can occur: over expression, hypo-glycosylation and changes in cellular localization. These changes transform the MUC1 protein into a highly immunogenic tumor associated antigen (TAA) and make it an attractive target for cancer immunotherapy. Thus, the strategy is to induce MUC1 antigen expression in a non-tumor environment, i.e., where the immune system is fully functional, in order to induce both innate and MUC1 specific adaptive immunity. In addition to lung cancer, the MUC1 TAA is expressed in many other solid tumor types, such as breast, colorectal, kidney and prostate cancers.

Via Krishan Maggon