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

Research output: Chapter in Book/Report/Conference proceedingConference contributionpeer-review

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.

Original languageEnglish
Title of host publicationArsenic Research and Global Sustainability - Proceedings of the 6th International Congress on Arsenic in the Environment, AS 2016
EditorsProsun Bhattacharya, Gunnar Jacks, Jochen Bundschuh, Prosun Bhattacharya, Marie Vahter, Jerker Jarsjo, Jerker Jarsjo, Jurate Kumpiene, Arslan Ahmad, Charlotte Sparrenbom, Marinus Eric Donselaar, Jochen Bundschuh, Ravi Naidu, Ravi Naidu
PublisherCRC Press/Balkema
Pages434-435
Number of pages2
ISBN (Print)9781138029415
DOIs
StatePublished - 2016
Event6th International Congress on Arsenic in the Environment, AS 2016 - Stockholm, Sweden
Duration: 19 06 201623 06 2016

Publication series

NameArsenic Research and Global Sustainability - Proceedings of the 6th International Congress on Arsenic in the Environment, AS 2016

Conference

Conference6th International Congress on Arsenic in the Environment, AS 2016
Country/TerritorySweden
CityStockholm
Period19/06/1623/06/16

Bibliographical note

Publisher Copyright:
© 2016 Taylor & Francis Group, London.

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