γ-radiation-induced G2 delay, apoptosis, and p53 response as potential susceptibility markers for lung cancer

摘要: γ-Radiation results in cell cycle arrest and apoptosis a wide variety of cells. Cell provides time for the to repair damaged DNA before entering next phase cycle. If damage is severe cannot be repaired, cells undergo apoptosis. However, if continue grow without or apoptosis, then carcinogenic transformation may occur. We hypothesized that individuals with inherited disruption control and/or susceptible lung cancer development. The from would have shorter G2 period less compared normal upon exposure γ-radiation. To test this hypothesis, following methods were used: (a) fluorescence-activated sorting method was used measure delay; (b) ELISA p53 protein expression levels these lines; (c) γ-radiation-induced chromatid breaks counted as marker repair. Next, delay tested three lymphoblastoid lines determine dose response effect optimal points Finally, assays 30 patients 22 healthy controls. found dose-response relationship detect differential apoptotic index 10 h 48 after γ-radiation, respectively. mean 22.5% ± 10.5% 14.71% 8.8% case (P