Lunch & Poster Display session Poster Display session

96P - Clearance of HPV anal premalignant lesions and modulation of systemic immune responses to HPV oncogenes with low dose pomalidomide

Presentation Number
96P
Lecture Time
12:15 - 12:15
Speakers
  • M. Polizzotto (Sydney, Australia)
Session Name
Lunch & Poster Display session
Location
Room B, Geneva Palexpo, Geneva, Switzerland
Date
12.12.2019
Time
12:15 - 13:15
Authors
  • M. Polizzotto (Sydney, Australia)
  • D. Van Bockel (Surry Hills, Austria)
  • C. Law (Sydney, NSW, Australia)
  • J. Roberts (Sydney, NSW, Australia)
  • G. Buckland (Surry Hills, Austria)
  • S. Just (Sydney, NSW, Australia)
  • S. Comben (Sydney, NSW, Australia)
  • R. Hillman (Sydney, NSW, Australia)
  • R. Gilson (London, United Kingdom)
  • S. Pett (London, United Kingdom)
  • M. Poynten (Sydney, NSW, Australia)
  • M. Law (Sydney, NSW, Australia)
  • A. Kelleher (Sydney, NSW, Australia)
  • S. Emery (Sydney, NSW, Australia)

Abstract

Background

Anal high-grade intraepithelial lesions (HSIL) precede the development of HPV-associated anal cancer and so present a target for early intervention and cancer prevention. Spontaneous HSIL clearance is associated with systemic CD4 T-cell response to the HPV oncogene E6. Pomalidomide may enhance immune responses to HPV and be therapeutic in HSIL.

Methods

This phase II single centre study (NCT3113942) recruited participants with persistent (>12 months) biopsy-proven anal HSIL. Therapy was oral pomalidomide, 2mg for 21 of 28 days for up to 6 months. Primary outcome was response at end therapy (CR defined as histological clearance; PR as ≥ 50% reduction in area); secondary included response after 6 further months observation. Immune activation markers (CD38, HLA DR) were assessed with flow cytometry and antigen-specific CD4+ T-cell responses to HPV E6 and E7 with OX40 immunoassay.

Results

26 participants were enrolled, 24 were evaluable for response. All male; median age 54 (range 41-74). All AIN3 HSIL, median duration HSIL 37 months (15-86), median octants 2 (0.5-5); HPV16 in 55%; multiple high risk HPV types in 50%. Overall response (CR+PR) was 52% (CI: 31-73) at end therapy, increasing to 63% (95% CI 40-81) after 6 further months observation. Adverse events (AEs) were mild and self-limited, including cytopenias, constipation, and rash. Over 137 cycles (c), attributable grade 3/4 events were grade 3 neutropenia (4 c) and grade 3 angina (1 c). Systemic CD4 T-cell responses to HPV E6 but not E7 increased significantly during therapy, peaking day 14 of therapy: baseline 0.06%, (IQR 0.01 – 0.12%), median increase day 14 0.13% (IQR: 0.02 – 0.26%), p = 0.001. Activation of CD4 and CD8 cells increased significantly during therapy. Parameters returned to baseline after therapy.

Conclusion

Low dose oral pomalidomide was well tolerated and induced durable continuing clearance of anal HSIL of multiple genotypes in even in chronic extensive disease. Induction of HPV-specific CD4+ responses and immune activation support an immunological mechanism of action. Immunotherapy with pomalidomide is a promising approach to prevention of anal cancer and potentially other HPV cancers.

Clinical trial identification

NCT3113942.

Legal entity responsible for the study

Kirby Institute, University of New South Wales, Sydney, Australia.

Funding

Cancer Institute of New South Wales.

Disclosure

All authors have declared no conflicts of interest.

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