569. Immune Microenvironments of Anal Cancer Precursors Differ by HIV-Serostatus and are Associated with Ablation Outcomes
Session: Poster Abstract Session: HIV: Cancer and Dysplasia
Thursday, October 5, 2017
Room: Poster Hall CD
  • IDweek poster-final 2017.pdf (322.3 kB)
  • Background: HPV-associated anal cancer precursors (high-grade squamous intraepithelial lesions, HSIL) follow a more virulent course in HIV+ patients than in their HIV- counterparts. This study aims to characterize the subpopulations of mucosa-infiltrating T lymphocytes in HSIL microenvironments, correlating them with HIV-serostatus and electrocautery ablation (EA) outcomes.

    Methods: Using immunohistochemistry, we quantified mucosa-infiltrating CD4+ and CD8+ T lymphocytes in 115 HSIL (from 70 HIV+ and 45 HIV- patients) and 20 benign anal mucosa samples (from 10 HIV+ and 10 HIV- patients). Clinicopathological parameters were collected and compared by HIV status.

    Results: Patients’ age, cytology diagnoses, and HPV types were comparable between HIV+ and HIV- groups. In benign controls, T lymphocytes were sparse in both HIV+ and HIV- anal mucosa. The number of total mucosa-infiltrating T lymphocytes and the CD8+ subset were significantly higher in anal HSIL from HIV+ subjects than in those from HIV- subjects (mean 71 vs. 47; 46.5 vs. 22/HPF, p<0.001) whereas the CD4+ subset was similar between groups (24.5 vs. 25/HPF, p=0.4). Among patients who underwent EA, subsequent anoscopy and biopsy detected persistent anal HSIL in 21/51 (41%) HIV+ and 5/27 (19%) HIV- patients (p=0.04, mean 12-month follow-up, range 3-36). Unadjusted analysis showed a trend towards EA failures associated with HIV seropositivity (OR 2.0; 95% CI 0.80-4.9) and increased number of mucosa-infiltrating CD8+ T cells (OR 2.3; 95% CI 0.9-5.3).

    Conclusion: Anal HSIL immune microenvironments differ significantly by HIV serostatus. HSIL in HIV+ subjects with increased mucosa-infiltrating CD8+ T cells tended to persist after EA. Therapies that target mucosal immunity may improve treatment outcomes of those lesions.

    Michael Gaisa, MD, PhD1, Yuxin Liu, MD PhD2, Yotam Arens, MD3 and Keith Sigel, MD, PhD1, (1)Dept. of Medicine, Division of Infectious Disease, Icahn School of Medicine at Mount Sinai, New York, NY, (2)Pathology, Icahn School of Medicine at Mount Sinai, New York, NY, (3)Icahn School of Medicine at Mount Sinai, New York, NY


    M. Gaisa, None

    Y. Liu, None

    Y. Arens, None

    K. Sigel, None

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