Abstract
Background: The Fragile histidine triad (FHIT) gene is a nucleotide metabolism associated with the Ap3A hydrolase, which may regulate cell cycle and induce cell apoptosis. Phosphate and tensin homolog deleted on chromosome ten (PTEN) had been found to be a dual specificity phosphatase activity (DSP) of the tumor suppressor gene. However, the roles of FHIT and PTEN in patients with non-small-cell lung cancer (NSCLC) is not well established so far.
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