Using a two-stage study design including discovery and replication studies, and stringent Bonferroni correction for multiple statistical analysis, we identified significant genetic interactions between SNPs in <i>RGL1:RAD51B</i> (OR=0.44, <i>p</i> value=3.27x10<sup>-11</sup> in overall lung cancer and OR=0.41, <i>p</i> value=9.71x10<sup>-11</sup> in non-small cell lung cancer), <i>SYNE1:RNF43</i> (OR=0.73, <i>p</i> value=1.01x10<sup>-12</sup> in adenocarcinoma) and <i>FHIT:TSPAN8</i> (OR=1.82, <i>p</i> value=7.62x10<sup>-11</sup> in squamous cell carcinoma) in our analysis.
Further investigation into the role of the FHIT protein in the epidermis is warranted to determine if the reduced/lost expression of FHIT observed in a subset of the cutaneous SCC is contributing to tumorigenesis.
Methylation of FHIT gene was frequently found than HPV infection, therefore methylation of the FHIT gene is suggested to play an important role in the pathogenesis of penile squamous cell carcinoma.
Further investigation into the role of the FHIT protein in the epidermis is warranted to determine if the reduced/lost expression of FHIT observed in a subset of the cutaneous SCC is contributing to tumorigenesis.
These results indicated that the high frequency of FHIT gene disruption was important in the development of both squamous cell carcinomas and adenocarcinomas.
Allele loss and promoter hypermethylation of VHL, RAR-beta, RASSF1A, and FHIT tumor suppressor genes on chromosome 3p in esophageal squamous cell carcinoma.
We evaluated FHIT gene involvement in 39 esophageal carcinomas (18 adenocarcinomas [AC¿, 21 squamous cell carcinomas [SCC]) by both reverse transcriptase-polymerase chain reaction (RT-PCR) amplification and loss of heterozygosity analysis (LOH).
The possibility that three genes, FHIT, VHL, and T beta R-II, recently identified on 3p may be significantly involved in oral SCC development is also discussed.