Fragile Histidine Triad Gene

Genomic instability has been found in cervical neoplasia and commonly involves the short arm of chromosome 3 in the fragile histidine triad (FHIT) gene (3p14.2). The presence of aberrant FHIT transcripts was found to be generated by alternative splicing of exons 5, 7, and 10 and of introns 5 and 7 (26).

LOH at 3p14.2 region was found to be progressive with increasing cervical lesions from CIN to invasive cancer, suggesting that loss of FHIT could represent an early event in the pathogenesis of cervical carcinoma (27). However, the prognostic role of loss of FHIT expression in this tumor is still controversial (28,29). Recent evidence suggests that FHIT instability may play a synergistic role with HR-HPV in the patho-genesis of high-grade cervical lesions. In fact HPV can integrate into FRA3B, the most active chromosome breakage site contained in the 3p14.2 region (30).

Other risk factors, as cigaret smoking (31), alcohol consumption, or concurrent chronic inflammation can target FHIT locus, accounting for the development of those high-grade cervical lesions, which are not associated with HR-HPV. Thus, suggesting that the presence of abnormal fragile histidine triad transcripts could itself be an independent risk factor associated with an alternative carcinogenic pathway (32).

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