title: Bcl-2 expression in oral squamous cell carcinoma.
abstract: Apoptosis is a genetically regulated process involved in tissue size regulation, morphogenesis, and elimination of genetically damaged cells. A pallet of genes is involved in the control of apoptosis, such as bcl-2 family whose oncogenic potential has been demonstrated in oral tumorigenesis. Different members of bcl-2 family may promote or inhibit apoptosis by synthesizing anti- and proapoptotic proteins. One of antiapoptotic proteins, bcl-2, with a crucial role in apoptosis regulation was the object of our study. By means of immunohistochemistry we estimated the level of overexpression of bcl-2 proteins in a series of the 26 formalin fixed, paraffin-embedded samples of oral squamous cell carcinoma (OSCC). Analyzed tumors originated from different sites of oral cavity; 7/26 belonged to stage II, 14/26 to stage III, and 5/26 to stage IV. Immunoreactivity was scored according to the percentage and intensity of positive cytoplasmic bcl-2 staining. All tumors had low percentage of positively stained bcl-2 cells, with mean values for lower/higher intensity of 8.3 +/- 2.5/34.4 +/- 7, 7.5 +/- 1.1/31.9 +/- 4.3, and 8.4 +/- 5.8/31.5 +/- 5.8 within stages II, III, and IV, respectively. Low level of bcl-2 expression in our sample seems to be associated with higher survival rate: 77% for the 5-year follow-up period. Comparing clinicopathologic and risk factors data within each and between three groups of analyzed tumors (lip-tongue P = 0.58, tongue-floor of the mouth, P = 0.21, lip-floor of the mouth, P = 0.50) there was no significant difference. However, our results suggest that the level of bcl-2 expression could be a valuable predictor of tumor behavior and disease outcome.
authors.affiliation: Institute of Biology and Human Genetics, School of Dentistry, University of Belgrade, Dr Subotica 8, 11000 Belgrade, Serbia and Montenegro. brankapo@verat.net
authors.forename: B
authors.initials: B
authors.lastname: Popović
authors.forename: B
authors.initials: B
authors.lastname: Jekić
authors.forename: I
authors.initials: I
authors.lastname: Novaković
authors.forename: L J
authors.initials: LJ
authors.lastname: Luković
authors.forename: Z
authors.initials: Z
authors.lastname: Tepavcević
authors.forename: V
authors.initials: V
authors.lastname: Jurisić
authors.forename: M
authors.initials: M
authors.lastname: Vukadinović
authors.forename: J
authors.initials: J
authors.lastname: Milasin
mesh_terms: D000328:Adult; D000368:Aged; D017209:Apoptosis / Q000235:genetics; D002294:Carcinoma, Squamous Cell / Q000737:chemistry / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006801:Humans; D008048:Lip Neoplasms / Q000737:chemistry / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009062:Mouth Neoplasms / Q000737:chemistry / Q000378:metabolism* / Q000473:pathology; D011379:Prognosis; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis* / Q000235:genetics*; D014062:Tongue Neoplasms / Q000737:chemistry / Q000378:metabolism / Q000473:pathology
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2