Background and Objectives : Cancer is a genetic disease in which several genetic events are
required to induce normal cells to convert to malignancy. Functional loss of tumor suppressor
genes is related to these events, but the molecular mechanism is not well known, This study was
designed to identify whether the tumor suppressor genes, Fragile Histidine Triad(FHIT), p16,
Retinoblastoma (Rb), and p53 were involved in the carcinogenesis of laryngeal squamous cell
carcinoma and to determine whether FHIT alterations play a role in laryngeal squamous cell
carcinoma.
Materials and Method : The loss of heterozygosity(LOH) was analysed by using microsatellite
markers D3S1285 and D3S1481 for FHIT, microsatellite marker D9S171 for p16, investigation of
AccⅡ restriction fragment length polymorphism(RELP) and investigation of variable number of
tandem repeat(VNTR) for p53, XbaⅠ RELP and VNTR for Rb. The FHIT gene was examined by
polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP).
Results : The results of LOH analysis by using microsatellite markers D3S1285 and D3S1481 for
FHIT, microsatellite marker D9S171 for p16, investigation of AccⅡ RFLP and investigation of
VNTR for p53, VNTR for Rb were 8％(1/12), 0％(0/13), 18％(2/11), 14％(1/7), 22％(2/9), 17％(1/6),
respectively. As a result of analysis of genomic DNA of FHIT gene by SSCP, two cases showed
that the polymorphic change occurs at exon 8 codon 98(CAT→CAC), and that it is a silent
substitution.
Conclusion : Based on the experimental result of the change in tumor suppressor genes in
laryngeal squamous cell carcinoma, the genetic alterations were most frequently observed in p53
followed by Rb, p16 and FHIT but it is not significant. It is also expected that FHIT has little
influence on the process of carcinogenesis of laryngeal squamous cell carcinoma.
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