Abstract
Cancer outcomes in people living with human immunodeficiency virus (PWH) may be driven in part by a distinct tumor microenvironment (TME) for cancers that develop in the setting of persistent immune dysfunction.
Tumor samples from PWH were retrospectively obtained from the AIDS Cancer Specimen Resource, Moffitt Cancer Center, and Huntsman Cancer Institute. Staining of 22 different tumor immune markers was compared between PWH and cancer and patients diagnosed with the same cancer type but without human immunodeficiency virus.
A total of 292 samples were analyzed, with 51 samples obtained from PWH (lung cancer = 17; breast cancer = 14; and prostate cancer = 20). Cells positive for PD-1 were observed more frequently in PWH and lung cancer [OR, 1.88; 95% confidence interval (CI), 1.02–3.45], whereas CD11b+ cells were observed less frequently (OR, 0.4; 95% CI, 0.17–0.93). Three immune markers showed higher abundance in PWH and breast cancer, including PD-L1 (OR, 3.24; 95% CI, 1.52–6.91), CD14 (OR, 3.37; 95% CI, 1.14–10.0), and FOXP3 (OR, 1.91; 95% CI, 1.03–3.53). In PWH and prostate cancer, the abundance of five immune markers was higher, including PD-L1 (OR, 5.94; 95% CI, 3.77–9.34), whereas three markers had lower abundance including CD14 (OR, 0.40; 95% CI, 0.22–0.74), as well as CD16 and CD11c.
This pilot study showed that differences in the TME exist for PWH diagnosed with age-related non-AIDS–defining cancers. Future work evaluating TME differences in relation to clinical endpoints is needed.
Findings are consistent with the hypothesis of altered tumorigenesis for cancers developing in an environment of immunosuppression.
RSS Feeds