Resensitization of Ovarian Cancer to Carboplatin Using Oncolytic Vaccine
Posted: Friday, November 13, 2020
A team of researchers found that patients with platinum-resistant or -refractory ovarian cancer may become responsive to carboplatin doublet therapies after oncolytic virotherapy, leading to potential increases in objective response rates and progression-free survival. This group was led by Robert W. Holloway, MD, of the AdventHealth Cancer Institute in Orlando, Florida, who presented the findings at the European Society for Medical Oncology (ESMO) Virtual Congress 2020 (Abstract 837P).
“Virus-induced changes in the tumor microenvironment may explain the apparent reversal of platinum resistance,” suggested the authors.
The trial enrolled 27 patients who had progressive ovarian cancer after treatment with a median of 4 prior lines of therapy. Patients had a median progression-free survival of 4.6 months from their last line of therapy before enrolling in this trial. Patients received an intraperitoneal infusion of the oncolytic virus for 2 consecutive days, followed by a median of six cycles of carboplatin doublet therapy with or without bevacizumab. Maintenance therapy was continued afterward using single-agent carboplatin with or without bevacizumab. Biopsies and blood samples were taken both before and after virotherapy for analysis.
After a median follow-up of 20.6 months, the objective response rate was 54%, including 2 patients with a complete response, 11 with a partial response, and 8 with stable disease. The median duration of response was 8.5 months. The 6-month progression-free survival rate was 77%, and the median progression-free survival was 11 months. The objective response rate as measured by CA-125 levels was 85%, with 10 complete responses and 12 partial responses. In addition, median overall survival was 23.2 months.
Common adverse effects associated with the virotherapy were pyrexia (58%), abdominal pain (50%), nausea (50%), abdominal distention (46%), and fatigue (35%).
Analysis of tumor and blood samples indicated that the virus induced infiltration of CD8-positive T cells into the tumor islet, upregulation of inflammatory genes, T-cell activation, and activation of tumor-specific T cells in the blood.
Disclosure: The authors reported no conflicts of interest.
