Germ line polymorphisms of the tumor suppressor gene p53 and lung cancer

Biroš, Erik; Kalina, I; Kohút, A; Stubna, J; Salagovic, J

doi:10.1016/s0169-5002(00)00188-4

Cited by 35 publications

(20 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is not well understood how the common, low-penetrance genes involving cell cycle checkpoints contribute to the lung cancer susceptibility, partly because data on genetic polymorphisms involving cell cycle control genes are sparse. Reports on the association of p53 and Chk2 gene polymorphisms and lung cancer risk are inconsistent (50)(51)(52)(53). SNPs are often considered indicators of genetic risks across individuals.…”

Section: Discussionmentioning

confidence: 99%

Less Efficient G2-M Checkpoint Is Associated with an Increased Risk of Lung Cancer in African Americans

Zheng

Loffredo

Alberg³

et al. 2005

Cancer Research

View full text Add to dashboard Cite

Cell cycle checkpoints play critical roles in the maintenance of genomic integrity. The inactivation of checkpoint genes by genetic and epigenetic mechanisms is frequent in all cancer types, as a less-efficient cell cycle control can lead to genetic instability and tumorigenesis. In an on-going case-control study consisting of 216 patients with non-small cell lung cancer, 226 population-based controls, and 114 hospital-based controls, we investigated the relationship of ;-radiationinduced G 2 -M arrest and lung cancer risk. Peripheral blood lymphocytes were cultured for 90 hours, exposed to 1.0 Gy ;-radiation, and harvested at 3 hours after ;-radiation treatment. ;-Radiation-induced G 2 -M arrest was measured as the percentage of mitotic cells in untreated cultures minus the percentage of mitotic cells in ;-radiation-treated cultures from the same subject. The mean percentage of ;-radiation-induced G 2 -M arrest was significantly lower in cases than in population controls (1.18 versus 1.44, P < 0.01) and hospital controls (1.18 versus 1.40, P = 0.01). When dichotomized at the 50th percentile value in combined controls (population and hospital controls), a lower level of ;-radiation-induced G 2 -M arrest was associated with an increased risk of lung cancer among African Americans after adjusting for baseline mitotic index, age, gender, and pack-years of smoking [adjusted odd ratio (OR), 2.25; 95% confidence interval (95% CI), 0.97-5.20]. A significant trend of an increased risk of lung cancer with a decreased level of G 2 -M arrest was observed (P trend = 0.02) among African Americans, with a lowest-versus-highest quartile adjusted OR of 3.74 (95% CI, 0.98-14.3). This trend was most apparent among African American females (P trend < 0.01), with a lowest-versushighest quartile adjusted OR of 11.75 (95% CI, 1.47-94.04). The results suggest that a less-efficient DNA damage-induced G 2 -M checkpoint is associated with an increased risk of lung cancer among African Americans. Interestingly, we observed a stronger association of DNA damage-induced G 2 -M arrest and lung cancer among African Americans when compared with Caucasians. If replicated, these results may provide clues to the exceedingly high lung cancer incidence experienced by African Americans. (Cancer Res 2005; 65(20): 9566-73)

show abstract

Section: Discussionmentioning

confidence: 99%

Less Efficient G2-M Checkpoint Is Associated with an Increased Risk of Lung Cancer in African Americans

Zheng

Loffredo

Alberg³

et al. 2005

Cancer Research

View full text Add to dashboard Cite

show abstract

“…Other intron 6 base substitutions have been reported, suggesting that this locus represents a potential hot spot region for mutation. Several epidemiological studies have confirmed the correlation between the intron 6 polymorphism and increased risk for the development of various cancer types (Hillebrandt et al, 1997;Biro et al, 2000;Biros et al, 2001;Fiszer-Maliszewska et al, 2003;Buyru et al, 2005).…”

Section: Polymorphism Of Intron 6 (G-c)mentioning

confidence: 89%

Polymorphisms in the p53 pathway

2006

View full text Add to dashboard Cite

“…Of these publications, three (Biros et al 2001a;Fan et al 2000;Murata et al 1996) were excluded because the same data were available in other studies (Biros et al 2001b;Miller et al 2002;Murata et al 1998). In three of the remaining 28 publications (Birgander et al 1995;Biros et al 2001a;Fernandez-Rubio et al 2008;Giuliani et al 2007;Hiraki et al 2003;Honma et al 2008;Irarrazabal et al 2003;Jain et al 2005;Jin et al 1995;Jung et al 2008;Liu et al 2001;Mechanic et al 2007;Miller et al 2002;Murata et al 1998;Nadji et al 2007;Papadakis et al 2002;Pierce et al 2000;Popanda et al 2007;Sakiyama et al 2005;Sreeja et al 2008;Szymanowska et al 2006;To-Figueras et al 1996;Wang et al 1999;Weston et al 1992;Weston et al 1994;Wu et al 2002;Zhang et al 2003;Zhang et al 2006), the ORs were presented separately according to the diVerent ethnicities: Mechanic et al (2007) sorted the data in African and Caucasian, respectively; Pierce et al (2000) presented the data according to Caucasian, Asian, and Mixed descent, respectively; and Jin et al (1995) presented the data according to African-American and Mexican-American, respectively.…”

Section: Main Characteristicsmentioning

confidence: 99%

P53 polymorphism and lung cancer susceptibility: a pooled analysis of 32 case–control studies

et al. 2009

View full text Add to dashboard Cite

To explore the real association between p53 codon 72 polymorphism and lung cancer risk, a pooled analysis of 32 case-control studies involving 19,255 subjects was conducted. When all 32 studies were pooled into the analysis, significantly elevated lung cancer risks were associated with variant genotypes in all genetic models (for Pro/Arg vs. Arg/Arg: OR 1.21, 95% CI 1.01-1.23; for Pro/Pro vs. Arg/Arg: OR 1.20, 95% CI 1.03-1.39; for Pro/Pro + Pro/Arg vs. Arg/Arg: OR 1.14, 95% CI 1.03-1.25; for Pro/Pro vs. Arg/Arg + Pro/Arg: OR 1.06, 95% CI 1.01-1.12). In the subgroup analysis by ethnicity, histological type, or smoking status, significantly increased risks were found in subgroups such as Asians, Caucasians, lung adenocarcinoma patients, or smokers, respectively. In conclusion, our results suggest that the Pro allele at p53 codon 72 is emerging as a low-penetrance susceptibility allele for lung cancer development.

show abstract

Germ line polymorphisms of the tumor suppressor gene p53 and lung cancer

Cited by 35 publications

References 12 publications

Less Efficient G2-M Checkpoint Is Associated with an Increased Risk of Lung Cancer in African Americans

Less Efficient G2-M Checkpoint Is Associated with an Increased Risk of Lung Cancer in African Americans

Polymorphisms in the p53 pathway

P53 polymorphism and lung cancer susceptibility: a pooled analysis of 32 case–control studies

Contact Info

Product

Resources

About