A pinboard by
George Semango

Assistant Lecturer/ PhD student, Nelson Mandela African Institution of Science and Technology


Search for new cytokine based HIV related malignancy therapy

My research area is on trying to understand how the HIV associated cancer known as Kaposi's sarcoma behaves in order to be able to come up with better treatment modalities for this cancer.


Exploring the Role of IL-32 in human immunodeficiency virus-related Kaposi sarcoma.

Abstract: The intracellular pro-inflammatory mediator interleukin (IL)-32 is associated with tumor progression; however, the mechanisms remain unknown. We studied the IL-32 mRNA expression as well as other pro-inflammatory cytokines and mediators including IL-1α, IL-1β, IL-6, IL-8, tumor necrosis factor (TNF)-α, the pro-angiogenic and anti-apoptotic enzyme COX-2, the IL-8 receptor CXCR1, and the intracellular kinase FAK-1. The interaction of IL-32 expression with expression of IL-6, TNFα, IL-8, and COX-2 was also investigated. Biopsies of 11 human immunodeficiency (HIV)-related, seven non HIV-related Kaposi sarcoma (KS), and seven normal skin tissues of Dutch origin were analyzed. RNA was isolated from the paraffin material and gene expression levels of IL-32α, β, and γ isoforms, IL1a, IL1b, IL6, IL8, TNFA, PTGS2, CXCR1, and PTK2 were determined using quantitative real-time PCR. Significantly higher expression of IL-32β and IL-32γ isoforms was observed in HIV-related KS biopsies compared to non HIV-related KS and normal skin tissue. The splicing ratio of the IL-32 isoforms showed IL-32γ as the highest expressed isoform, followed by IL-32β in HIV-related KS cases compared to non HIV-related KS and normal skin tissue. Our data suggest a possible survival mechanism by the splicing of IL-32γ to IL-32β and also IL-6, IL-8, and CXCR1 signalling pathways to reverse the pro-apoptotic effect of IL-32γ isoform leading to tumor cell survival and thus favoring tumor progression.

Pub.: 19 Oct '17, Pinned: 17 Nov '17