Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
gamma-radiation-induced G(2) delay, apoptosis, and p53 response as potential susceptibility markers for lung cancer
Autore:
Zhao, H; Spitz, MR; Tomlinson, GE; Zhang, HF; Minna, JD; Wu, XF;
Indirizzi:
Univ Texas, MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA Univ Texas Houston TX USA 77030 tr, Dept Epidemiol, Houston, TX 77030 USA Univ Texas, Hlth Sci Ctr, Sch Publ Hlth, Houston, TX 77030 USA Univ TexasHouston TX USA 77030 Ctr, Sch Publ Hlth, Houston, TX 77030 USA Univ Texas, SW Med Ctr, Hamon Canc Therapeut Oncol Res, Dallas, TX 75390 USA Univ Texas Dallas TX USA 75390 Therapeut Oncol Res, Dallas, TX 75390 USA
Titolo Testata:
CANCER RESEARCH
fascicolo: 21, volume: 61, anno: 2001,
pagine: 7819 - 7824
SICI:
0008-5472(20011101)61:21<7819:GGDAAP>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELL-CYCLE CHECKPOINTS; DNA-DAMAGE; BREAST-CANCER; REPAIR; PHOSPHORYLATION; INHIBITION; DEFECTS; ARREST; DEATH;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Zhao, H Univ Texas, MD Anderson Canc Ctr, Dept Epidemiol, Box 189,1515 Holcombe Blvd, Houston, TX 77030 USA Univ Texas Box 189,1515 Holcombe Blvd Houston TX USA 77030 030 USA
Citazione:
H. Zhao et al., "gamma-radiation-induced G(2) delay, apoptosis, and p53 response as potential susceptibility markers for lung cancer", CANCER RES, 61(21), 2001, pp. 7819-7824

Abstract

gamma -Radiation results in cell cycle arrest and apoptosis in a wide variety of cells. Cell cycle arrest provides time for the cell to repair damaged DNA before entering the next phase of the cycle. If the damage is severe and cannot be repaired, the cells undergo apoptosis. However, if the damaged cells continue to grow without repair or apoptosis, then carcinogenic transformation may occur. We hypothesized that individuals with inherited disruption in cell cycle control and/or apoptosis and/or DNA repair may be susceptible to lung cancer development. The cells from susceptible individuals would have a shorter G(2) period and less apoptosis compared with cells from normal individuals upon exposure to gamma -radiation. To test this hypothesis, the following methods were used: (a) fluorescence-activated cell sorting method was used to measure apoptosis and G(2) cell cycle delay; (b) theELISA method was used to measure p53 protein expression levels in these cell lines; and (c) gamma -radiation-induced chromatid breaks were counted asa marker for DNA damage or repair. Next, gamma -radiation-induced G(2) delay and apoptosis were tested in three lymphoblastoid cell lines to determine the dose response effect and optimal time points of gamma -radiation. Finally, these assays were tested in lymphoblastoid cell tines from 30 lung cancer patients and 22 healthy controls. We found a dose-response relationship for gamma -radiation-induced G(2) delay and apoptosis. The optimal time points to detect differential G(2) delay and apoptotic index were 10 h and 48 h after gamma -radiation, respectively. The mean G(2) delay was 22.5 % +/- 10.5 % for the control cell tines and 14.71 % +/- 8.8 % for case cell lines (P < 0.01). The mean apoptotic index was 20.4% +/- 11.7% for the controls and 14.3% +/- 7.8% for the cases (P < 0.05). The controls had a significantly higher p53 response ratio and fewer chromatid breaks than the cases. We also found that a p53 increasing ratio was strongly related to cell cycleG(2) delay (gamma = 0.413; P = 0.002) and chromatid breaks (gamma = 0.384;P = 0.028). Therefore, we concluded that gamma -radiation-induced G(2) delay, apoptosis, p53 increasing ratio, and chromatid breaks might potentiallybe used as susceptibility markers for lung cancer risk. A large epidemiology study is in progress to confirm these findings.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/10/20 alle ore 15:14:45