The TP53 Arg72Pro polymorphism and lung cancer risk in a population of Northern Spain

Fernández-Rubio, Aida; López-Cima, María Felicitas; González-Arriaga, Patricia; García-Castro, Laura; Pascual, Teresa; Marrón, Manuel G.; Tardón, Adonina

doi:10.1016/j.lungcan.2008.01.017

Cited by 34 publications

(32 citation statements)

References 27 publications

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“…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. Therefore, each cohort in one publication was considered for pooling anal...…”

Section: Main Characteristicsmentioning

confidence: 99%

“…A common one at codon 72 of exon 4, which encodes proline (Pro) or arginine (Arg), has been reported to aVect the risks of many types of cancer especially of lung cancer (Agorastos et al 2004;Belyavskaya et al 2006;Chen et al 2000;Lee et al 2000;Weston et al 1992;Zehbe et al 2001). Although many studies have reported the Pro allele at codon 72 was a risk factor for developing lung cancer (Fernandez-Rubio et al 2008;Liu et al 2001;Mechanic et al 2007;Popanda et al 2007;Sreeja et al 2008;Szymanowska et al 2006), the results are inconclusive. Since single study may have been underpowered in clarifying this polymorphism with lung cancer susceptibility, in the present study we performed a meta-analysis of the published studies to increase statistical power to address this controversy.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2009

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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.

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Section: Main Characteristicsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

et al. 2009

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“…TP53 polymorphisms have widely been studied in NSCLC, but the results are contradictory. Three studies reported a significantly increased risk (23)(24)(25), one (26) reported an insignificant risk increase, and three (9,17,27) (25), we, however, believe to be on the right track, since this TP53 variant has lower activity in apoptosis and its association with an increased NSCLC risk is plausible.…”

Section: Discussionmentioning

confidence: 88%

Association between the TP53 and CYP2E1*5B gene polymorphisms and non-small cell lung cancer

Ada

Bilgen

Volkan

et al. 2016

Archives of Industrial Hygiene and Toxicology

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Non-small cell lung cancer (NSCLC) is the most common form of lung cancer. Genetic polymorphisms in tumour suppressor genes and genes encoding xenobiotic metabolising enzymes alter the activity of their corresponding enzymes and are important individual susceptibility factors for NSCLC. Because of the lack of information in literature, the aim of our study was to investigate the role of the tumour suppressor gene TP53 (Arg72Pro) and the xenobiotic metabolising CYP2E1*5B gene polymorphisms on the risk of NSCLC development. The study population consisted of 172 patients and 172 controls (156 men and 16 women in each group). Genetic polymorphisms were determined with real-time polymerase chain reaction (PCR) and PCR restriction fragment length polymorphism (PCR-RFLP). Multivariate analysis showed a significant association with NSCLC for the combination between the TP53 codon72 Arg/Pro and the Pro/Pro genotypes (OR 2.21, 95 % CI 1.39-3.51; p=0.001). We also analysed whether combinations of these gene variants with GSTM1, GSTT1, GSTP1 exon 5 (Ile105Val), and GSTP1 exon 6 (Ala114Val) gene polymorphisms were associated with the NSCLC risk. A significant increase in the risk was observed for the following combinations: TP53 codon72 variant with GSTM1 null (OR 2.22, 95 % CI 1.23-4.04; p=0.009), GSTT1 null (OR 2.98, 95 % CI 1.49-5.94; p=0.002), and GSTP1 (Ala114Val) variant genotypes (OR 3.38, p=0.002). Further studies with larger samples are needed to verify these findings. KEY WORDS: carcinogen metabolism; CYP2E1; genetic polymorphism; GST; NSCLCLung cancer is the most common cancer type in the world, which affects men in particular. It is also the leading cause of death among cancers (1). Histologically, about 80 % of lung cancers are non-small cell lung carcinomas (NSCLC). The inbuilt phase I and II biotransformation enzyme systems inactivate environmental carcinogens, especially those present in tobacco smoke, depending on the regulating polymorphisms. Epidemiological studies show that genetic differences and interactions among genetic variants might modify lung cancer susceptibility (2, 3). Therefore, it is important to identify individual genetic and acquired factors that modify lung cancer risk in order to develop preventive strategies based on this information. This is particularly true for identifying polymorphisms of tumour suppressor genes and xenobiotic metabolising enzyme genes. The TP53 tumour suppressor gene is an essential regulator of the cell-cycle arrest, DNA repair, and apoptosis (4). An important single nucleotide polymorphism detected in TP53 is Arg72Pro. This allele has been shown to decrease the activity of the corresponding protein, which is crucial for the apoptotic function of TP53 (5, 6). Recent studies have reported the association between this polymorphism and lung cancer (7-11).CYP2E1 is an important phase I biotransformation enzyme that transforms N-nitrosamines, vinyl chloride, and benzene in tobacco smoke into mutagenic and carcinogenic metabolites (12). In NSCLC patients it has been fou...

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“…No interactions (additive and multiplicative) of smoking and the TP53 Arg72Pro or TP53BP1 Asp353Glu SNP with lung cancer were observed in this study. Some studies have found no evidence for any interaction between the TP53 Arg72Pro polymorphism and smoking (48)(49)(50) while other studies indicated that the interaction was probable (51,52). However, these studies did not indicate P-values for the interaction measures (additive or multiplicative) (51,52).…”

Section: ------------------------------------------------------------mentioning

confidence: 93%

Cigarette smoking, TP53 Arg72Pro, TP53BP1 Asp353Glu and the risk of lung cancer in a Japanese population

Kiyohara¹

2010

Oncol Rep

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Abstract. The tumor suppressor protein p53 (TP53) plays a central role in directing cellular responses to DNA damage. Tumor protein 53-binding protein 1 (TP53BP1) binds to TP53 and has a potential role in DNA damage responses. DNA damage-dependent interaction between TP53 and TP53BP1 may contribute to lung cancer risk. We aimed to assess whether or not TP53 and TP53BP1 genetic polymorphisms modulate lung cancer susceptibility in a Japanese population. We investigated the relationship of the TP53 Arg72Pro and TP53BP1 Asp353Glu polymorphisms to lung cancer risk with special reference to polymorphism-polymorphism and polymorphism-smoking interactions among 462 lung cancer cases and 379 controls. The Glu/Glu genotype of TP53BP1 Asp353Glu polymorphism was associated with a decreased risk of lung cancer [odds ratio (OR) = 0.46, 95% confidence interval (CI) = 0.29-0.74]. There was no polymorphism-smoking interaction. A combination of the Pro allele carriage of the TP53 Arg72Pro polymorphism and the Glu/Glu genotype of the TP53BP1 Asp353Glu polymorphism was associated with a decreased risk of lung cancer (OR=0.38, 95% CI=0.17-0.83). The multiplicative interaction measure was statistically significant (OR for interaction = 2.93, 95% CI=1.24-6.93). The relative excess risk due to interaction and attributable proportion due to interaction were 0.74 (95% CI=0.38-1.20) and 0.63 (95% CI=0.05-1.21), respectively. Both the additive interaction measures were not equal to zero, suggesting that the existence of a biological interaction. Our findings indicate the possible association of the Glu allele of the TP53BP1 Asp353Glu polymorphism with lower risk of lung cancer especially among the Pro allele carriers of the TP53 Arg72Pro polymorphism.

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The TP53 Arg72Pro polymorphism and lung cancer risk in a population of Northern Spain

Cited by 34 publications

References 27 publications

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

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

Association between the TP53 and CYP2E1*5B gene polymorphisms and non-small cell lung cancer

Cigarette smoking, TP53 Arg72Pro, TP53BP1 Asp353Glu and the risk of lung cancer in a Japanese population

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