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Immunohistochemical evaluation of Fhit protein expression in oral squamous cell carcinomas
Author(s) -
Heerden W. F. P.,
Swart T. J. P.,
Heerden M. B.,
Rensburg E. J.,
Engelbrecht S.,
Dreyer L.,
Huebner K.
Publication year - 1999
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.1999.tb02102.x
Subject(s) - fhit , immunohistochemistry , stratum spinosum , epithelium , pathology , biology , carcinogenesis , dysplasia , cancer research , cancer , microbiology and biotechnology , medicine , tumor suppressor gene , genetics , stratum corneum
van Heerden WFP, Swart TJP, van Heerden MB, van Rensburg EJ, Engelbrecht S, Dreyer L, Huebner K: Immunohistochemical evaluation of Fhit protein expression in oral squamous cell carcinomas. J Oral Pathol Med 1999; 28: 433–7. © Munksgaard, 1999. The expression of Fhit (fragile histidine triad) protein in oral squamous cell carcinoma (OSCC) and adjacent oral epithelium was evaluated by immunohisto‐chemistry on formalin‐fixed paraffin‐embedded blocks of 32 cases of OSCC. Rabbit polyclonal anti‐GST‐Fhit antiserum at 1:600 was used, after antigen enhancement in a microwave pressure cooker, in a saturated lead thiocyanate solution. This antiserum has been shown specifically to detect human Fhit by immunohistochemistry at dilutions up to 1:10,000. The Fhit protein expression was evaluated using both the intensity and extent of staining. Normal stratified squamous epithelium showed strong positivity, especially in the stratum spinosum and areas of keratinisation. Basal and parabasal cells were negative or expressed low levels of Fhit relative to the squamous epithelium. Mild and moderate epithelial dysplasia showed Fhit expression in the superficial layers, while Fhit expression was absent from severely dysplastic lesions. A reduction or loss of Fhit expression was found in 21 (66%) of the OSCC. The alterations in Fhit protein expression in OSCC, and not in normal tissues, are consistent with the proposal that Fhit inactivation plays a role in oral carcinogenesis.