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A new oncolytic virus therapy is turning heads in cutaneous cancer treatment. VET3-TGI, given alone or with atezolizumab, achieved a 71% response rate in patients with advanced skin cancers that had stopped responding to checkpoint inhibitors. Remarkably, responses appeared in both injected and non-injected tumors — and no dose-limiting toxicities were reported.
A new oncolytic virus is showing real promise for patients with advanced skin cancers who've run out of options. In the phase 1/1b STEALTH-001 trial, VET3-TGI — a modified vaccinia virus engineered to carry a TGF-β inhibitor and interleukin-12 — was administered directly into tumors, alone or alongside the immunotherapy atezolizumab. Among 12 efficacy-evaluable patients, the overall response rate was 42%, but in the cutaneous malignancy subgroup (n=7), that number jumped to 71%. Crucially, no dose-limiting toxicities were observed, and all responders were still on treatment at data cutoff.
What makes this therapy particularly exciting is its effect on non-injected lesions: responses were seen not just in injected tumors, but also in tumors that were never directly treated. Translational analyses showed dramatic increases in immune cell activity, suggesting the virus is converting immunologically "cold" tumors into "hot" ones capable of sustaining a durable immune response.
By the Numbers
Why it matters: Patients with checkpoint inhibitor–refractory cutaneous cancers have very few treatment options. VET3-TGI's ability to generate responses — including in non-injected lesions — without severe toxicity could represent a meaningful new path forward for this underserved population.
