Fhit expression is absent or reduced in a subset of primary head and neck cancer

Anticancer Res. Mar-Apr 2000;20(2A):1057-60.


Background: The inactivation of the FHIT gene at 3p14.2 by various mechanisms might be of importance in head and neck squamous cell carcinoma (HNSCC). Most reports are based on DNA and RNA findings of intragenic deletions and abnormal transcripts.

Material and methods: To study the protein expression of this putative tumour suppressor gene, we analysed 48 HNSCCs by immunohistochemistry using a polyclonal antibody (ZR44). The results were compared with mutation analysis, clinical data and loss of heterozygosity (LOH) data at 3p14.2.

Results: Complete absence of Fhit expression was detected in 8 out of 48 of tumours (17%) and 3 tumours (6%) showed heterogenous staining. The overall frequency of LOH for microsatellite D3S1234 was 64% and 5/7 of Fhit negative tumours exhibited LOH.

Conclusion: Our findings provide further evidence that FHIT is inactivated in a subtype of HNSCC; however, the incidence of lack of Fhit expression compared to the high frequency of LOH on chromosome 3p supports the notion of additional tumour suppressor genes at 3p14.

Publication types

  • Comparative Study

MeSH terms

  • Acid Anhydride Hydrolases*
  • Antibodies
  • Carcinoma, Squamous Cell / genetics*
  • Carcinoma, Squamous Cell / pathology*
  • Carcinoma, Squamous Cell / surgery
  • Chromosome Mapping
  • Chromosomes, Human, Pair 3*
  • Cytoplasm / pathology
  • DNA Mutational Analysis
  • Exons
  • Head and Neck Neoplasms / genetics*
  • Head and Neck Neoplasms / pathology*
  • Head and Neck Neoplasms / surgery
  • Humans
  • Immunohistochemistry
  • Loss of Heterozygosity*
  • Neoplasm Proteins / analysis*
  • Polymorphism, Single-Stranded Conformational
  • Proteins / analysis*
  • Proteins / genetics*


  • Antibodies
  • Neoplasm Proteins
  • Proteins
  • fragile histidine triad protein
  • Acid Anhydride Hydrolases