Joint effect among p53, CYP1A1, GSTM1 polymorphism combinations and smoking on prostate cancer risk: an exploratory genotype-environment interaction study

Quiñones, Luis A.; Irarrázabal, Carlos E.; Rojas, Claudio R.; Orellana, Cristian E.; Acevedo, Cristián; Huidobro, Christian; Varela, Nelson; Cáceres, Dante

doi:10.1111/j.1745-7262.2006.00135.x

Cited by 56 publications

(28 citation statements)

References 22 publications

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“…Numerous reports have shown that p53 is one of the most frequently mutated genes in smoking-associated lung cancers (44,45). Moreover, interactions and joint effects between p53 genetic variations and smoking status on the risk of various types of cancer have also been well documented (46,47). Consistently, the finding in our CART analysis that p53 intron 6 and p27 5 ¶ UTR SNPs characterize different risk groups in heavy smokers confirmed the essential role of both genes in smoking-related lung carcinogenesis.…”

Section: Discussionsupporting

confidence: 79%

Genetic Variants in Cell Cycle Control Pathway Confer Susceptibility to Lung Cancer

Wang¹,

Spitz²,

Yang³

et al. 2007

Clinical Cancer Research

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Purpose: To test the hypothesis that common sequence variants of cell cycle control genes may affect lung cancer predisposition. Experimental Design: We explored lung cancer risk associations of 11polymorphisms in seven cell cycle genes in a large case-control study including 1,518 Caucasian lung cancer patients and 1,518 controls. Results: When individuals with variant-containing genotypes were compared with homozygous wild-type carriers, a significantly increased lung cancer risk was identified for polymorphisms in p53 intron 6 [rs1625895; odds ratio (OR), 1.29; 95% confidence interval (95% CI), 1.08-1.55] and in p27 5 ¶ untranslated region (UTR; rs34330; OR, 1.27; 95% CI, 1.01-1.60). Compared with homozygous wild-types, the homozygous variant genotypes of STK15 F31I and CCND1 G870A were associated with a significantly altered lung cancer risk with ORs of 0.58 (95 % CI, 0.37-0.90) and 1.26 (95% CI, 1.03-1.53), respectively. To assess the cumulative effects of all the investigated polymorphisms on lung carcinogenesis, we conducted a combined analysis and found that compared with low-risk individuals with few adverse alleles, individuals with more adverse alleles had an increased risk in a significant dose-dependent manner (P trend = 0.041). This pattern was more evident in ever smokers (P trend = 0.037), heavy smokers (P trend = 0.020), and older subjects (P trend = 0.011). Higher-order gene-gene interactions were evaluated using the classification and regression tree analysis, which indicated that STK15 F31I and p53 intron 6 polymorphisms might be associated with lung carcinogenesis in never/light-smokers and heavy smokers, respectively. Conclusions: Our results suggest that cell cycle gene polymorphisms and smoking may function collectively to modulate the risk of lung cancer.

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Section: Discussionsupporting

confidence: 79%

Genetic Variants in Cell Cycle Control Pathway Confer Susceptibility to Lung Cancer

Wang¹,

Spitz²,

Yang³

et al. 2007

Clinical Cancer Research

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“…By contrast, another study of a Caucasian population performed by Quiñones et al (21) identified a positive association of the Pro/Pro genotype with prostate cancer risk (OR=2.89; 95% CI, 1.17-7.10). Studies carried out in Japan (22), China (23) and Northern India (24) reported the same increased association of the Pro allele with prostate cancer risk as the study by Quiñones et al (21), however, the studies of men in Argentina (27) and Iran (28) did not. One study by Ricks-Santi et al (26) found a significant association of the Arg allele with the prevalence of prostate cancer in populations of men of African descent.…”

Section: P21 C98a P21 C70t ------------------------------------------mentioning

confidence: 70%

“…The two variants were considered wild-type, resulting in a non-conservative change (6,15). In certain studies the Pro allele was associated with increased prostate cancer risk (21)(22)(23)(24)(25), while in others the Arg allele was associated with prostate cancer predisposition (26). Other studies, mainly larger studies and meta-analyses, did not detect any association of the p53 codon 72 polymorphism with prostate cancer risk (27)(28)(29)(30).…”

Section: Introductionmentioning

confidence: 99%

Association of p53 and p21 polymorphisms with prostate cancer

Sivoňová¹,

Vilčková²,

Kliment³

et al. 2015

Biomedical Reports

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Abstract. Cell cycle deregulation is common in human cancer. Alterations of the tumor-suppressor gene p53 and its downstream effector p21 have been indicated in the development of numerous human malignancies. Therefore, we hypothesize that the p53 codon 72 polymorphism, either on its own or in combination with p21 (C98A and C70T) polymorphisms, modifies the risk of prostate cancer within the Slovak population, and no previous studies have investigated these gene-gene interactions in the pathogenesis of prostate cancer in the Slovak population. Polymerase chain reaction-restriction fragment length polymorphism was used to determine the p53 and p21 genotypes in subjects comprising 300 prostate cancer patients and 446 healthy individuals. These 3 polymorphisms individually did not correlate with the prostate cancer risk. Conversely, the interaction between the p53 and p21 polymorphisms significantly decreased the risk of prostate cancer, with the odds ratio (OR) being 0.49 [95% confidence interval (CI), 0.27-0.86; P<0.05] for subjects carrying the p53 codon 72 arginine (Arg)/proline (Pro)+Pro/Pro and p21 C98A CA genotypes compared to the combined reference genotypes p53 codon 72 Arg/Arg and p21 C98A CC. Neither the p53 genotypes nor the p21 genotypes showed statistically significant differences in Gleason score or serum prostate-specific antigen levels (P>0.05). A decreased risk of prostate cancer association with the p21 C98A CA genotype (OR=0.58; 95% CI, 0.36-0.93; P<0.05) in non-smokers compared to the non-smokers with the p21 C98A CC genotype was observed. Smokers carrying the p53 codon 72 Pro/Pro genotype were not at any significant risk of prostate cancer (OR=2.97; 95% CI, 0.51-17.15) compared to the non-smokers with the Arg/Arg genotype. Taken together, to the best of our knowledge this is the first study to show that a combination of the variant genotypes of p53 codon 72 and p21 C98A may modify the prostate cancer risk within the Slovak population.

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“…significant role in the etiology of this disease (Quinones et al, 2006). Given the multicausal etiology of prostate cancer, synergistic interactions among genetic and other risk factors might have significant effects on prostate cancer risk, especially gene-gene (G×G) and geneenvironment (G×E) interactions (Quinones et al, 2006 However, for men who have a father or brother with prostate cancer, their risk is known to be higher. The risk is higher again if more than one member of your family has prostate cancer.…”

Section: Introductionmentioning

confidence: 99%

The p53 codon 72 polymorphism and association to prostate cancer in Iranian patients

Doosti¹,

Dehkordi²

2011

Afr. J. Biotechnol.

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Tp53 is an important tumor suppressor gene, which induces cell growth arrest or apoptosis when subjected to cytotoxic stimuli. Association has been reported between various cancers and p53 codon 72 polymorphism. Our objective was to investigate the possible association between p53 at codon 72 for Arg/Arg, Arg/Pro and Pro/Pro allele polymorphisms in blood samples from 187 prostate cancer patients and 185 controls in southwest Iran by nested-polymerase chain reaction (PCR) of p53 exon 4 and digestion with BstUI restriction enzyme and the DNA fragments were then resolved by electrophoresis in 2% agarose gel. The frequencies of Arg/Arg, Arg/Pro and Pro/Pro genotypes were 39.57% (74/187), 52.41% (98/187) and 8.02% (15/187), respectively, in the cases with prostate cancer, and 27.03% (50/185), 60% (111/185) and 12.97% (24/185), respectively in the healthy controls. Statistically, analyzed and combined results showed there was a significant difference in the frequency of the Arg/Arg genotype and Arg allele between prostate cancer cases and control (p>0.001). These findings suggest that p53 Arg/Arg genotype could be a risk factor for the development of prostate cancer among patients in southwest Iran.

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Joint effect among p53, CYP1A1, GSTM1 polymorphism combinations and smoking on prostate cancer risk: an exploratory genotype-environment interaction study

Cited by 56 publications

References 22 publications

Genetic Variants in Cell Cycle Control Pathway Confer Susceptibility to Lung Cancer

Genetic Variants in Cell Cycle Control Pathway Confer Susceptibility to Lung Cancer

Association of p53 and p21 polymorphisms with prostate cancer

The p53 codon 72 polymorphism and association to prostate cancer in Iranian patients

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