Reciprocal expressions of VEGF and the numbers of dendritic cells in arsenic-induced skin cancer: A plausible cause of impaired dendritic cell activation in arsenic carcinogenesis

[[abstract]]Arsenic remains an important environmental hazard that causes several cancers. Arsenic-induced Bowen’s disease (As-BD), a skin carcinoma in situ, is the most common arsenical cancer. Patients with As-BD have an impaired contact hypersensitivity response. We have reported that arsenic paradoxically impairs Dendritic Cell (DC) migration through STAT3 upregulation and VEGF production from epidermal keratinocytes using cell, tissue, and animal models. In this study, we further demonstrated an increased expression of VEGF and decreased numbers of DC in epidermis. More importantly, there are spatial interactions and reciprocal changes in VEGF-DC in epidermis from tissue with As-BD, further validating that immune interactions in the microenvironment play an important role in regulating the disease course of arsenical cancers