On April 18, 2016 Oncolytics Biotech Inc. ("Oncolytics" or the "Company") (TSX: ONC) (OTCQX: ONCYF) (FRA: ONY) reported that two poster presentations covering preclinical work in multiple myeloma and colorectal cancer are being made by the Company’s research collaborators at the 2016 American Association of Cancer Research annual meeting being held from April 16th to 20th, 2016 in New Orleans, LA (Filing, 6-K, Oncolytics Biotech, APR 18, 2016, View Source [SID:1234510978]).
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"Both multiple myeloma and colorectal cancer are target indications for later-stage clinical testing of REOLYSIN," said Dr. Brad Thompson, President and CEO of Oncolytics. "These important preclinical findings continue to advance our understanding of how REOLYSIN interacts with the immune system and how immunomodulatory interventions could improve its cancer cell killing capabilities."
The first abstract/poster is titled "Successful oncolytic virotherapy in a bortezomib resistant syngeneic mouse model of multiple myeloma: implications for translation significance," and was authored by Thirukkuamaran, et al. Using the VK*MYC bortezomib resistant transplantable multiple myeloma mouse model, the authors demonstrated that mice harboring bortezomib insensitive multiple myeloma tumors significantly responded to reovirus treatment. These data are supportive of previous and ongoing preclinical and clinical work in this indication and the Company is currently enrolling patients in a Phase 1b study of REOLYSIN in combination with bortezomib in patients with relapsed or refractory multiple myeloma.
The second abstract/poster is titled "Toll like receptor 3 as an immunotherapeutic target for Kras mutated colorectal cancer," and was authored by Goel, et al. The authors hypothesized that effective expression of toll like receptors 3 ("TLR3") would dampen the infection potential of reovirus through the mounting of an innate immune response. Using a xenograft model with HCT116 colorectal cancer cells, those with TLR3 downregulated cells showed improved control of tumor growth with reovirus treatment compared to those expressing TLR3 (p=0.04). Down regulation of the host immune response improved virus mediated cell cytotoxicity and the findings could result in improved and beneficial killing of cancer cells by reovirus.