title: Cutaneous basal cell carcinomas: distinct host factors are associated with the development of tumors on the trunk and on the head and neck.
abstract: BACKGROUND
  Patients with basal cell carcinoma (BCC) demonstrate marked variation in clinical phenotype, suggesting the presence of distinct subgroups. Patients with truncal lesions comprise an interesting subgroup, because, although the pathogenesis of these tumors is unclear, there is evidence to suggest that their development is mediated by different mechanisms than the mechanisms that mediate the development of BCC on other sites. The authors now speculate that some patients inherit a predisposition to truncal BCC and develop disproportionately more BCC on this site than other patients.
  
  
  METHODS
  The authors studied 100 patients who, at the time of initial presentation, had a truncal BCC lesion and 493 patients who had a lesion on the head and neck. The 493 patients with head and neck lesions included 36 patients who subsequently developed a truncal BCC and 457 patients who do not.
  
  
  RESULTS
  Initial presentation with a truncal tumor was associated with significantly more subsequent BCC lesions on this site compared with patients who presented initially with a head and neck lesion. The mean truncal tumor accrual after initial presentation in patients who presented with an initial truncal BCC lesion was 0.13 BCC lesions per year compared with 0.03 BCC lesions per year in patients who presented with an initial head and neck lesion (P < 0.001). Patients with truncal lesions were significantly younger at the time of initial presentation and developed more clusters of BCC lesions (2--10 new tumors at any presentation) compared with patients who did not develop tumors on the trunk.
  
  
  CONCLUSIONS
  These data suggest that the development of a truncal BCC is not random but, rather, is associated with a predisposition. In contrast, the accrual of nontruncal BCC lesions was similar in patients with and without initial truncal lesions, suggesting that different mechanisms determine the development of truncal BCC and nontruncal BCC.
authors.affiliation: Center for Cell and Molecular Medicine, School of Postgraduate Medicine, North Staffordshire Hospital, Keele University, Staffordshire, England.
authors.forename: S
authors.initials: S
authors.lastname: Ramachandran
authors.forename: A A
authors.initials: AA
authors.lastname: Fryer
authors.forename: A
authors.initials: A
authors.lastname: Smith
authors.forename: J
authors.initials: J
authors.lastname: Lear
authors.forename: B
authors.initials: B
authors.lastname: Bowers
authors.forename: P W
authors.initials: PW
authors.lastname: Jones
authors.forename: R C
authors.initials: RC
authors.lastname: Strange
mesh_terms: D000328:Adult; D000368:Aged; D002280:Basal Cell Carcinoma / Q000235:genetics / Q000473:pathology*; D004273:DNA, Neoplasm; D005260:Female; D020022:Genetic Predisposition to Disease; D006258:Head and Neck Neoplasms / Q000235:genetics / Q000473:pathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D012189:Retrospective Studies; D012307:Risk Factors; D012878:Skin Neoplasms / Q000235:genetics / Q000473:pathology*
chemical_list: D004273:DNA, Neoplasm