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12 Oncolytic vaccinia (Olvi-Vec) primed immunochemotherapy in platinum-resistant/refractory ovarian cancer
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  1. R Holloway1,
  2. A Mendivil2,
  3. J Kendrick1,
  4. L Abaid2,
  5. J Brown2,
  6. C Fitzsimmons1,
  7. J Kennard1,
  8. M King2,
  9. J LeBlanc1,
  10. K Lopez2,
  11. M Manyam1,
  12. N McKenzie1,
  13. K Mori2,
  14. A Stephens1 and
  15. S Ahmad1
  1. 1AdventHealth Cancer Institute, USA
  2. 2Gynecologic Oncology Associates, USA

Abstract

Introduction Intraperitoneal oncolytic vaccinia virus (Olvi-Vec) was administered to heavily pretreated patients with platinum-resistant/refractory ovarian cancer (PRROC) followed by intravenous carboplatin-doublet (CD) ± bevacizumab (Bev) in a Phase-2 trial (NCT02759588). Primary objectives: RECIST overall response rate (ORR) & progression-free survival (PFS).

Methods Patients with PRROC who progressed after most recent therapies received 2 days of Olvi-Vec followed by CD±Bev, then maintenance with single-agent therapies ± Bev. Pre-&post-virotherapy tumor biopsies were obtained for translational analyses.

Results 27 patients enrolled: median 4 prior regimens, 82% prior Bev, 52% platinum-refractory and 48% platinum-resistant. Mean cycles of CD±Bev were 6(±3). Median follow-up was 26.5 months. RECIST ORR was 54% (95%CI:33–74%): 2(8%) complete response, 11(46%) partial response; 8(33%) stable disease. Median duration of response was 7.6 months (95%CI:3.7–9.6). Clinical benefit rate was 88%. Median PFS was 11.0 months (95%CI:6.7–13.0), and PFS-6-month was 77%. CA-125 ORR was 85% (95%CI:65–96%). There were no Grade 4 adverse events with virotherapy. Performance status was preserved/improved in 24 (89%) patients while on CD±Bev. Post-virotherapy intra-tumoral infiltration of CD8+ T-cells and upregulation of STAT1 expression (p=0.008) were demonstrated.

Abstract 12 Table 1

Baseline characteristics

Conclusions Despite PRROC, prior bevacizumab, and progression on last therapy, the majority of patients achieved RECIST response with median PFS exceeding their prior line of therapy. Virus-induced changes in the tumor microenvironment may explain the apparent clinical reversal of platinum resistance.

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