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Basal cell carcinoma is associated with high TNF‐α release but not with TNF‐α polymorphism at position − 308
Author(s) -
Skov Lone,
Allen Michael H.,
Bang Bo,
Francis David,
Barker Jonathan N. W. N.,
Baadsgaard Ole
Publication year - 2003
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.0906-6705.2003.00085.x
Subject(s) - tumor necrosis factor alpha , allele , peripheral blood mononuclear cell , genotype , lipopolysaccharide , secretion , biology , immunology , basal (medicine) , endocrinology , medicine , gene , genetics , in vitro , insulin
The mechanisms underlying induction of UVB‐induced immunosuppression are not fully understood, but tumour necrosis factor alpha (TNF‐α) is suggested to play a central role. A single base pair polymorphism at position − 308 in the promoter region of the TNF‐α gene associated with an enhanced secretion of TNF‐α has been identified in humans. We have therefore investigated the association of the − 308 polymorphism with the risk of basal cell carcinoma (BCC) in humans. The frequency of TNF G and TNF A alleles among Caucasian patients with a previous BCC ( n = 191) and healthy adults ( n = 107) were compared. For the TNF − 308 polymorphism there was no significant association between the genotype or allele frequencies and having a BCC. To determine whether patients with a previous BCC had an increased capacity to secrete TNF‐α, mononuclear cells were stimulated with lipopolysaccharide. Mononuclear cells from patients with a previous BCC ( n = 15) demonstrated a significantly increased release of TNF‐α upon stimulation with lipopolysaccharide ( P < 0.03) compared with mononuclear cells from age‐matched control subjects ( n = 16). Further studies of other polymorphisms of the TNF‐α gene associated with increased TNF‐α production and BCC are necessary.