Infection of Human Papillomavirus Type 18 and p53 Codon 72 Polymorphism in Lung Cancer Patients From India*

Jain, Neeraj; Singh, Vikram; Hedau, Suresh; Kumar, Suresh; Daga, Mradul Kumar; Dewan, Richa; Murthy, N S; Husain, Syed Akhtar; Das, Bhudev C.

doi:10.1378/chest.128.6.3999

Cited by 55 publications

(37 citation statements)

References 58 publications

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“…However, Li et al [19] and Hu et al [20] revealed that there was no significant relationship between TP53 codon 72 polymorphism and susceptibility in NSCLC. Our finding confirmed the results of Papadakis et al [16] and Jain et al [17], as well as the data of those that detected a higher prevalence of homozygosity for GG genotype in patients with NSCLC. According to these reports, there are conflicting consequences between TP53 codon 72 polymorphism and the risk of lung cancer.…”

Section: Discussionsupporting

confidence: 93%

“…Papadakis et al [16] studied Greek Caucasian people, finding that TP53 GG homozygosity was associated with advanced lung cancer, and significantly increased the risk of lung cancer. Jain et al [17] reported that a significantly increased frequency of GG homozygotes was observed in Indian patients with advanced lung cancer when compared with control subjects. Piao et al [18] found that the CG and CC genotypes were associated with increased risk of lung cancer compared with the GG genotype in a South Korean population.…”

Section: Discussionmentioning

confidence: 99%

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Association of miR-502-binding site single nucleotide polymorphism in the 3′-untranslated region of SET8 and TP53 codon 72 polymorphism with non-small cell lung cancer in Chinese population

Yang¹,

Guo²,

Wei³

et al. 2014

ABBS

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The objective of this study was to identify whether the miR-502-binding site single nucleotide polymorphism (SNP) in the 3 0 -untranslated region (3 0 -UTR) of set domain-containing protein 8 (SET8) and the tumor protein p53 (TP53) codon 72 polymorphism were associated with the risk for non-small cell lung cancer (NSCLC), either independently or jointly, among Chinese people from southern Han. The genotypes of SET8 and TP53 codon 72 polymorphisms of peripheral blood DNA were detected using polymerase chain reaction-restriction fragment length polymorphism and direct DNA sequencing in a case -control study on 164 NSCLC cases and 199 controls. The SET8 TT (odds ratio, OR 5 2.173, 95% confidence interval, CI 5 1.0454.517) or TP53 GG (OR 5 2.579, 95% CI 5 1.366 -4.870) genotype was associated with an increased risk of NSCLC by comparing with the SET8 CC or TP53 CC genotype, respectively. Similar results were obtained in SET8 recessive model (OR 5 2.074, 95% CI 5 1.019 -4.221, P < 0.05), and the dominant and recessive model of TP53 codon 72 were performed, respectively (OR 5 1.809, 95% CI 5 1.159 -2.825, P < 0.05; OR 5 1.933, 95% CI 5 1.096 -3.409, P < 0.05). In addition, interaction between the SET8 and TP53 polymorphisms increased the risk of NSCLC in a multiply manner, with the OR being 3.032 (95%CI 5 1.580 -5.816) for subjects carrying both SET8 TT and TP53 GG genotypes. Therefore, the miR-502-binding site SNP in the 3 0 -UTR of SET8 and the TP53 codon 72 polymorphism may be markers of genetic susceptibility to NSCLC in Chinese population, and there is a possible gene-gene interaction in the incidence of NSCLC.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Association of miR-502-binding site single nucleotide polymorphism in the 3′-untranslated region of SET8 and TP53 codon 72 polymorphism with non-small cell lung cancer in Chinese population

Yang¹,

Guo²,

Wei³

et al. 2014

ABBS

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“…A recent Korean study using PCR methods for detecting HPV 16, 18 and 33 showed low prevalence of the high-risk genotypes averaging 10% and no association with smoking status or sex (30). A study from India that looked at 40 patients with lung cancer showed again low prevalence (5%) of HPV 18 and absence of HPV 16 (31). Several recent well conducted studies from Europe using fresh frozen tissue and modern methodologies have similarly shown the absence or low prevalence of HPV DNA and associated E6/E7 mRNA in lung cancer tissues (32)(33)(34).…”

Section: %) --------------------------------------------------------mentioning

confidence: 99%

Assessment of human papillomavirus and Epstein-Barr virus in lung adenocarcinoma

Lim

2009

Oncol Rep

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Abstract. The association of human papillomavirus (HPV) and Epstein-Barr virus (EBV) infection with non-small cell lung cancer is controversial. HPV and EBV prevalence in a uniform population of lung adenocarcinoma was investigated, hypothesizing that there would be differences seen between smokers and non-smokers and between sexes. Patients involved in this study were selected from a single institution database of lung cancer. In total 497 patients with adenocarcinoma were identified and 110 patients had sufficient tissue for analysis with an in situ hybridization method that probed for high-risk and low-risk HPV and EBV. There were 65 males and 45 females, 78 patients with stage I-IIIA disease and 32 patients with stage IIIB-IV disease. There were similar number of smokers and non-smokers. Across all stages HPV and EBV staining was absent from all tissues examined. It is unlikely that HPV or EBV is an important etiological agent in adenocarcinoma of the lung, even among the neversmokers. IntroductionCigarette smoke is strongly associated with the development of lung cancer (1). While the epidemic of smoking has reduced through public health awareness programs and education, the incidence of lung cancer remains unabated. There has been a demographic change in the global pandemic with a global realignment of histological subtypes. Adenocarcinoma incidence is rising globally among both smokers and nonsmokers. Up to 30% of all diagnosed non-small cell lung cancer (NSCLC) among various Asian countries, including Singapore, do not have a history of exposure to cigarette smoking. These patients tend to be predominantly female and have adenocarcinoma (2). This has given rise to different postulates as to the possible etiologies of NSCLC in this distinct of patients, ranging from exposure to cooking oil fumes (3,4), as well as diet and cancer susceptibility genotypes among Asians (5-7). Human papillomavirus (HPV) and Epstein-Barr virus (EBV) have been variously described to be associated and causative with several cancers. HPV is likely to be causal in cervical carcinoma and head and neck squamous cell carcinoma (HNSCC), and EBV in nasopharyngeal carcinoma. There have been various reports of association between HPV and EBV with lung cancer but results have not been conclusive (8). Leveraging on the excess of non-tobacco related lung cancer in our patients we investigated HPV and EBV prevalence in a uniform population of adenocarcinoma of the lung, hypothesizing that there would be differences seen between smokers and nonsmokers and between sexes. Patients and methodsPatients. Patients involved in this study were selected from a database of NSCLC patients, diagnosed in a single institution (SGH) from 1999 to 2002. The study had the approval of the Institutional Review Board of National Cancer Centre Singapore. The main selection criterion was a diagnosis of adenocarcinoma. Four hundred and ninety-seven patients were identified and among them, 110 patients had sufficient tissue blocks available for our analysis using in ...

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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%

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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Infection of Human Papillomavirus Type 18 and p53 Codon 72 Polymorphism in Lung Cancer Patients From India*

Cited by 55 publications

References 58 publications

Association of miR-502-binding site single nucleotide polymorphism in the 3′-untranslated region of SET8 and TP53 codon 72 polymorphism with non-small cell lung cancer in Chinese population

Association of miR-502-binding site single nucleotide polymorphism in the 3′-untranslated region of SET8 and TP53 codon 72 polymorphism with non-small cell lung cancer in Chinese population

Assessment of human papillomavirus and Epstein-Barr virus in lung adenocarcinoma

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

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Infection of Human Papillomavirus Type 18 and p53 Codon 72 Polymorphism in Lung Cancer Patients From India*

Cited by 55 publications

References 58 publications

Association of miR-502-binding site single nucleotide polymorphism in the 3&prime;-untranslated region of SET8 and TP53 codon 72 polymorphism with non-small cell lung cancer in Chinese population

Association of miR-502-binding site single nucleotide polymorphism in the 3&prime;-untranslated region of SET8 and TP53 codon 72 polymorphism with non-small cell lung cancer in Chinese population

Assessment of human papillomavirus and Epstein-Barr virus in lung adenocarcinoma

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

Contact Info

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Association of miR-502-binding site single nucleotide polymorphism in the 3′-untranslated region of SET8 and TP53 codon 72 polymorphism with non-small cell lung cancer in Chinese population

Association of miR-502-binding site single nucleotide polymorphism in the 3′-untranslated region of SET8 and TP53 codon 72 polymorphism with non-small cell lung cancer in Chinese population