title: Mast cells in basal cell carcinoma express VEGF, IL-8 and RANTES.
abstract: BACKGROUND
  Basal cell carcinoma (BCC) is the most common malignant tumor of the skin. Although an increase in mast cell infiltration was observed in BCC lesions, definite evidence of an active role of mast cells in the pathogenesis of BCC is still lacking. BCC is accompanied by cellular infiltrates. Moreover, the stroma in the BCC lesions is characterized by an increased number of mast cells and increased vascularity. The aim of this study was to elucidate the probable role of mast cells in BCC, especially focusing on the relationship between mast cells and lymphocytic infiltration as well as angiogenesis.
  
  
  METHODS
  We examined the expression and distribution of VEGF, IL-8 and RANTES in 16 nodular BCC lesions by immunohistochemistry. We also examined the lymphocyte subset, and the correlation between VEGF expression and microvessel density in the BCC lesion. mRNA expression of IL-8 and RANTES was examined by the reverse transcriptase-polymerase chain reaction.
  
  
  RESULTS
  T cells, especially CD4+/CD45RO+ memory T cells were the predominant infiltrating lymphocyte population in BCC lesions. An increased number of tryptase+ cells (mast cells) was found in the stroma. VEGF+/IL-8+/RANTES+ cells were also found abundantly in the stroma of all BCC lesions. The number of VEGF+, IL-8+ and RANTES+ cells was significantly higher than that in controls. By immunohistochemistry of serial sections, tryptase+ cells were found to express VEGF, IL-8 or RANTES. Messenger RNA expression of IL-8 and RANTES was also observed in the BCC lesions.
  
  
  CONCLUSIONS
  This study suggests that mast cells may play an active role in the angiogenesis of BCC through the production of VEGF and IL-8. Furthermore, mast cells may also regulate lymphocytic infiltration through the production of IL-8 and RANTES.
authors.affiliation: Department of Dermatology, Nippon Medical School, Tokyo, Japan.
authors.forename: Mikako
authors.initials: M
authors.lastname: Aoki
authors.forename: Ruby
authors.initials: R
authors.lastname: Pawankar
authors.forename: Yayoi
authors.initials: Y
authors.lastname: Niimi
authors.forename: Seiji
authors.initials: S
authors.lastname: Kawana
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D002280:Basal Cell Carcinoma / Q000098:blood supply / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D018946:Chemokine CCL5 / Q000235:genetics / Q000378:metabolism*; D016228:Endothelial Growth Factors / Q000378:metabolism*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism*; D016209:Interleukin-8 / Q000235:genetics / Q000378:metabolism*; D016131:Lymphocyte Subsets / Q000276:immunology / Q000473:pathology; D008222:Lymphokines / Q000378:metabolism*; D008297:Male; D008407:Mast Cells / Q000276:immunology* / Q000473:pathology; D008833:Microcirculation / Q000473:pathology; D008875:Middle Aged; D009389:Neovascularization, Pathologic; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012334:RNA, Neoplasm / Q000235:genetics / Q000378:metabolism; D012878:Skin Neoplasms / Q000098:blood supply / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
chemical_list: D018946:Chemokine CCL5; D016228:Endothelial Growth Factors; D036341:Intercellular Signaling Peptides and Proteins; D016209:Interleukin-8; D008222:Lymphokines; D012333:RNA, Messenger; D012334:RNA, Neoplasm; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors