title: Cytokine profiles in spontaneously regressing basal cell carcinomas.
abstract: BACKGROUND
  Basal cell carcinomas (BCCs) can cause considerable morbidity due to their ability to enlarge progressively and to destroy underlying tissues. However, some BCCs may undergo spontaneous regression in the absence of therapy capable of inducing antineoplastic effects. Histological criteria for this process have been described, and previous studies have suggested that it may be mediated by infiltrating activated CD4-positive T cells.
  
  
  OBJECTIVE
  The purpose of this study was to compare the expression of cytokines in actively regressing and non-regressing BCCs, to ascertain if active regression is associated with a particular cytokine profile.
  
  
  METHODS
  Reverse transcriptase-polymerase chain reaction, a sensitive, quantitative technique allowing analysis of multiple cytokines from small tumour samples, was used.
  
  
  RESULTS
  Interferon (IFN)-gamma was significantly elevated in actively regressing BCCs compared with non-regressing BCCs. Furthermore, interleukin (IL)-2, tumour necrosis factor (TNF)-beta and CD3 delta tended to be elevated in actively regressing tumours, although not to statistically significant levels. IFN-gamma, IL-2, IL-10, TNF-beta, granulocyte-macrophage colony-stimulating factor and Fas ligand showed strong positive correlations with CD3 delta, indicating an association between infiltrating T cells and these cytokines.
  
  
  CONCLUSIONS
  These findings support a role for T-helper 1 type cytokines in mediating spontaneous regression of BCCs.
authors.affiliation: Department of Medicine (Dermatology), The University of Sydney at Royal Prince Alfred Hospital, Gloucester House, Missenden Road, Camperdown, NSW 2050, Australia.
authors.forename: D A
authors.initials: DA
authors.lastname: Wong
authors.forename: G A
authors.initials: GA
authors.lastname: Bishop
authors.forename: M A
authors.initials: MA
authors.lastname: Lowes
authors.forename: B
authors.initials: B
authors.lastname: Cooke
authors.forename: R S
authors.initials: RS
authors.lastname: Barnetson
authors.forename: G M
authors.initials: GM
authors.lastname: Halliday
mesh_terms: D017252:CD3 Complex / Q000032:analysis; D002280:Basal Cell Carcinoma / Q000276:immunology*; D016207:Cytokines / Q000032:analysis*; D005260:Female; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000032:analysis; D006801:Humans; D007371:Interferon-gamma / Q000032:analysis; D016753:Interleukin-10 / Q000032:analysis; D007376:Interleukin-2 / Q000032:analysis; D008297:Male; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000032:analysis*; D009365:Neoplasm Regression, Spontaneous / Q000276:immunology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012878:Skin Neoplasms / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D019014:fas Receptor / Q000032:analysis
chemical_list: D017252:CD3 Complex; D016207:Cytokines; D007376:Interleukin-2; D009363:Neoplasm Proteins; D014409:Tumor Necrosis Factor-alpha; D019014:fas Receptor; D016753:Interleukin-10; D007371:Interferon-gamma; D016178:Granulocyte-Macrophage Colony-Stimulating Factor