title: Interaction between bcl-2 and P53 in neoplastic progression of basal cell carcinoma of the head and neck.
abstract: BACKGROUND
  Basal cell carcinoma (BCC) is the most frequent tumor of the human skin and generally shows a favourable clinical behaviour. However, a percentage of BCC grows aggressively, infiltrating contiguous structures, sometimes giving distant metastases.
  
  
  METHODS
  Bcl-2 and p53 protein expression was studied immunohistochemically in 60 cases of BCC (30 non-aggressive, BCC1 and 30 aggressive cases, BCC2) of the head and neck region with a complete clinical follow-up.
  
  
  RESULTS
  All the BCC1 showed distinct cytoplasmic staining for bcl-2. The intensity of staining ranged from intermediate to high, with only three cases showing low positivity. Among BCC2, none of the 30 cases showed positivity for bcl-2. Bcl-2 expression was directly correlated with the BCC1 sub-type and a favourable clinical follow-up (p<0.01). Among BCC1, 27 cases were found negative for p53 protein expression while 3 exhibited only a low immunoreactivity. Among BCC2, 11 out of 30 cases showed an intermediate immunoreactivity, and 18 out of 30 exhibited high positivity for p53 protein. The expression of p53 protein correlated inversely with cellular differentiation (p<0.01).
  
  
  CONCLUSIONS
  From the analysis of these results it is reasonable to consider bcl-2 and p53 protein expression as useful discriminating prognostic factors in the evaluation of BCCs of the head and neck region. In fact, the finding of clones expressing bcl-2 in a case of BCC may be indicative of an "indolent" cellular neoplastic phenotype. In other words, bcl-2 could be used as a "clonal marker" of a still favourable clinical behaviour. Conversely, the partial or complete loss of bcl-2-bearing neoplastic clones during histological transformation, with the appearance of clones expressing p53 protein in a BCC could be considered a hallmark of transition from a low-to high-grade malignancy, characterized by the emergence of cellular clones with a more aggressive phenotype, responsible for worse clinical behaviour.
authors.affiliation: Department of Biomorphological and Functional Sciences, University of Naples Federico II, Italy.
authors.forename: S
authors.initials: S
authors.lastname: Staibano
authors.forename: L
authors.initials: L
authors.lastname: Lo Muzio
authors.forename: G
authors.initials: G
authors.lastname: Pannone
authors.forename: M
authors.initials: M
authors.lastname: Scalvenzi
authors.forename: G
authors.initials: G
authors.lastname: Salvatore
authors.forename: M E
authors.initials: ME
authors.lastname: Errico
authors.forename: S
authors.initials: S
authors.lastname: Fanali
authors.forename: G
authors.initials: G
authors.lastname: De Rosa
authors.forename: A
authors.initials: A
authors.lastname: Piattelli
mesh_terms: D000328:Adult; D000368:Aged; D002280:Basal Cell Carcinoma / Q000378:metabolism* / Q000473:pathology*; D018450:Disease Progression; D005260:Female; D006258:Head and Neck Neoplasms / Q000378:metabolism* / Q000473:pathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis*; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis*
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53