title: Oral leukoplakias with different degrees of dysplasia: comparative study of hMLH1, p53, and AgNOR.
abstract: BACKGROUND
  hMLH1 is one of the major proteins of the mammalian mismatch repair system. It has been suggested that the mismatch repair machinery could be linked to p53, a tumor suppressor protein. The AgNOR technique is used to assess cell proliferation. The aim was to compare the immunoexpression of hMLH1 and p53, and AgNOR number in oral leukoplakias with different degrees of dysplasia.
  
  
  METHODS
  Sixty-two samples were evaluated by immunohistochemistry for hMLH1 and p53, and AgNOR technique, being 17 without dysplasia, 19 with mild dysplasia, 16 with moderate dysplasia, and 10 with severe dysplasia.
  
  
  RESULTS
  hMLH1 immunoexpression showed decreasing indexes, while p53 and AgNOR showed increasing indexes from lesions with lower degrees of dysplasia to lesions with more severe dysplasia. An inverse correlation between hMLH1 and both p53 and AgNOR, and a direct correlation between p53 and AgNOR were observed.
  
  
  CONCLUSIONS
  Alterations in the immunoexpression pattern of hMLH1 and p53 seemed to be early events in oral carcinogenesis. During acquisition of a more dysplastic phenotype, keratinocytes may show diminished capacity of DNA repair and tumor suppression, as well as higher cellular proliferation, and these pathways can be somehow interconnected.
authors.affiliation: Department of Oral Pathology and Surgery, School of Dentistry, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
authors.forename: Patrícia Carlos
authors.initials: PC
authors.lastname: Caldeira
authors.forename: Maria Cássia Ferreira
authors.initials: MC
authors.lastname: Aguiar
authors.forename: Ricardo Alves
authors.initials: RA
authors.lastname: Mesquita
authors.forename: Maria Auxiliadora Vieira
authors.initials: MA
authors.lastname: do Carmo
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000096:biosynthesis*; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000704:Analysis of Variance; D034961:Antigens, Nuclear / Q000096:biosynthesis*; D016022:Case-Control Studies; D049109:Cell Proliferation; D053843:DNA Mismatch Repair; D005260:Female; D006801:Humans; D015603:Keratinocytes / Q000378:metabolism / Q000473:pathology; D007972:Leukoplakia, Oral / Q000378:metabolism / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D009061:Mouth Mucosa / Q000166:cytology / Q000378:metabolism / Q000473:pathology; D009062:Mouth Neoplasms / Q000378:metabolism / Q000473:pathology*; D000070957:MutL Protein Homolog 1; D009687:Nuclear Proteins / Q000096:biosynthesis*; D018709:Statistics, Nonparametric; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis*
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D034961:Antigens, Nuclear; C501486:MLH1 protein, human; D009687:Nuclear Proteins; D016159:Tumor Suppressor Protein p53; C051963:nucleolar organizer region associated proteins; D000070957:MutL Protein Homolog 1