Oncolytics Biotech Inc. has announced that translational data from its GOBLET and AWARE-1 trials will be presented at the 2026 American Society of Clinical Oncology (ASCO) Annual Meeting, scheduled for May 29 to June 2 in Chicago. The findings highlight pelareorep, an investigational systemic immunotherapy, which has been shown to activate both innate and adaptive immune responses. According to the company’s press release, pelareorep works by expanding pre-existing tumor-reactive immune cells and has demonstrated the ability to induce an antiviral response within tumors via double-stranded RNA signaling.
The data from the Phase 1/2 GOBLET study in advanced pancreatic cancer indicate that treatment with pelareorep led to the expansion of virus-specific T cells and the subsequent activation of tumor-specific T cells. Notably, the expansion of pre-existing tumor-infiltrating lymphocyte (TIL) clones correlated with reductions in tumor volume in pancreatic cancer patients. Additionally, T-cell receptor sequencing confirmed the expansion of mutant KRAS-specific T-cell clones, suggesting that pelareorep may effectively drive immune responses against KRAS-driven tumors. In the AWARE-1 window-of-opportunity study in early-stage breast cancer, gene expression profiling of serial tumor biopsies showed significant increases in antiviral and immune gene expression, consistent with the activation of toll-like receptor 3 (TLR3). This was linked to the induction of CXCL13, a chemokine involved in the formation of tertiary lymphoid structures.
The company will present a dedicated abstract, “Influence of pelareorep on mutant KRAS-specific blood TIL clonal expansion” (Abstract Number: 2664), on May 30, 2026. Oncolytics’ CEO Jared Kelly noted that these translational data help bridge the gap between clinical observations and mechanistic understanding, providing confidence in the company's development plans for difficult-to-treat cancers. A copy of the ASCO presentation will be made available on the company’s website after the meeting.