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E-Poster Display

837P - Phase II trial of oncolytic vaccinia virus primed immunochemotherapy in platinum-resistant/refractory ovarian cancer (PRROC) (NCT02759588)


17 Sep 2020


E-Poster Display


Cytotoxic Therapy

Tumour Site

Ovarian Cancer


Robert Holloway


Annals of Oncology (2020) 31 (suppl_4): S551-S589. 10.1016/annonc/annonc276


R.W. Holloway1, A.A. Mendivil2, J.E. Kendrick1, L.N. Abaid2, J.V. Brown2, C.K. Fitzsimmons1, J.A. Kennard1, M. King2, J. LeBlanc1, K. Lopez2, M. Manyam1, N.D. McKenzie1, K.M. Mori2, A.J. Stephens1, S. Ahmad1

Author affiliations

  • 1 Gynecologic Oncology Program, AdventHealth Cancer Institute, 32804 - Orlando/US
  • 2 Gynecologic Oncology, Gynecologic Oncology Associates, 92663 - Newport Beach/US


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Abstract 837P


We evaluated intraperitoneal infusion of Olvi-Vec virus followed by IV carboplatin-doublet (CD) ± bevacizumab (Bev) in heavily pretreated patients (pts) with PRROC. Primary objectives were RECIST overall response rate (ORR) and progression-free survival (PFS). Secondary objectives included overall survival (OS), CA-125 response, safety, and translational studies.


Pts who progressed on most recent therapies received 2 consecutive days of Olvi-Vec followed by CD ± Bev, and then maintenance single agent ± Bev. Pre- & post-virotherapy tumor biopsies and blood were obtained for analyses.


27 pts (median 4 prior lines, 52% platinum-refractory, 48% platinum-resistant) enrolled. Median PFS from last line was 4.6 mos. Mean cycles of CD ± Bev were 6 (±3). Median follow up time is 20.6 mos. RECIST ORR was 54% [95%CI: 33 – 74%; 2 (8%) complete response (CR), 11 (46%) partial response (PR)]. Median duration of response was 8.5 mos (95%CI: 3.7 – NA). Eight (33%) had stable disease. Median PFS was 11.0 mos (95%CI: 6.7 – 13.0) and PFS-6-month was 77%. CA-125 ORR was 85% [95%CI: 65 – 96%; 10 (38%) CR, 12 (46%) PR]. Median OS was 23.2 mos (95%CI: 12.3 – 33.6). Adverse events of virotherapy included pyrexia 58%, abdominal pain 50%, nausea 50%, abdominal distension 46% and fatigue 35%. Translational analyses showed virus-induced infiltration of CD8+ T cells penetrating the tumor islet, upregulation of genes related to inflammation, T-cell activation, and tumor regression in tumors, and activation of tumor-specific T-cells in blood. Table: 837P

Baseline info n = 27 Median (range)
Age 62 (35-78)
Histology High grade serous Intermediate grade serous Mixed 25 (92%) 1 (4%) 1 (4%)
ECOG 0 1 17 (63%) 10 (37%)
Prior # of lines 4 (2-9)
Prior platinum lines 2 (1-5)
Platinum-resistant Platinum-refractory 13 (48%) 14 (52%)
Prior bevacizumab + - 22 (81%) 5 (19%)
Prior PARP inhibitor + - 20 (74%) 7 (26%)
Tumor PD-L1 expression + - Unknown 1 (4%) 25 (92%) 1 (4%)
BRCA1/2 mutations + - 8 (30%) 19 (70%)
Microsatellite instability Stable Unknown 19 (70%) 8 (30%)
Tumor mutational load Low Intermediate Unknown 13 (48%) 4 (15%) 10 (37%)
Response & PFS in last prior line ORR by RECIST ORR by CA-125 PFS (mos), median (95% CI) PFS-6-month 4/27 (15%) 5/24 (21%) 4.5 (2.9 – 5.8) 30%


Despite having PRROC and documented disease progression at enrollment, most pts responded to CD therapies after oncolytic virotherapy, with ORR & PFS exceeding their own last prior therapies. OS exceeds historical comparisons in heavily pretreated PRROC pts. Virus-induced changes in the tumor microenvironment may explain the apparent reversal of platinum resistance.

Clinical trial identification


Editorial acknowledgement


Legal entity responsible for the study

Genelux Corporation, San Diego, CA, USA.


Genelux Corporation, San Diego, CA, USA.


All authors have declared no conflicts of interest.

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