Gene–environment interaction and susceptibility in head and neck cancer patients and in their first‐degree relatives: a study of <scp>N</scp>ortheast <scp>I</scp>ndian population

Choudhury, Joydeep; Ghosh, Sankar Kumar

doi:10.1111/jop.12249

Cited by 20 publications

(13 citation statements)

References 32 publications

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“…Approximately 550,000 cases of HNSCC are newly diagnosed each year in the world, and only 40-50% of patients with HNSCC survive for 5 years [1]. It is well known that HNSCC is a multifactorial disease with contributing etiologies including tobacco smoking, alcohol consumption, and infection with the human papillomavirus (HPV) [2,3]. In addition, some reports have shown the importance of epigenetic mechanisms in the development and progression of HNSCC and other cancers [4,5].…”

Section: Introductionmentioning

confidence: 99%

Associations among smoking, MGMT hypermethylation, TP53-mutations, and relapse in head and neck squamous cell carcinoma

et al. 2020

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Background Epigenetic silencing of the O 6-methylguanine-DNA methyltransferase (MGMT) DNA repair enzyme via promoter hypermethylation (hmMGMT) may increase mutations in the TP53 oncosuppressor gene and contribute to carcinogenesis. The effects of smoking, which is a risk factor for head and neck squamous cell carcinoma (HNSCC), were investigated to determine whether they up-or down-regulate hmMGMT. Additionally, the impact of hmMGMT and disruptive TP53-mutations on relapse was investigated in patients with HNSCC. Methods This study included 164 patients with HNSCC who were negative for both p16 protein expression and human papilloma virus infection. The association of smoking and hmMGMT was investigated using multiple logistic regression analysis. Competing risk regression was used to evaluate the effects of hmMGMT and TP53-mutations in exon 2 to 11 on relapse of HNSCC. Results hmMGMT was observed in 84% of the 164 patients. TP53-mutations, specifically, G:C>A: T transition, were more frequent in patients with hmMGMT (32%) than in those without hmMGMT (8%). The frequency of disruptive TP53-mutations was not significantly different between groups. Compared with nonsmoking, heavy smoking of 20 pack-years or more was significantly associated with decreased hmMGMT (adjusted odds ratio, 0.08; 95% CI, 0.01 to 0.56; P = 0.01). Patients who had both hmMGMT and disruptive TP53-mutations

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Section: Introductionmentioning

confidence: 99%

Associations among smoking, MGMT hypermethylation, TP53-mutations, and relapse in head and neck squamous cell carcinoma

et al. 2020

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“…However, interactions between rs11536896 and other environmental factors were not found. Further, environmental factors and SNPs were pooled into two groups (high-and low-risk group) in MDR models, falling off the multifactor criterion predictors from impactive n dimensions to one dimension (Choudhury & Ghosh, 2015), which was a new method to investigate potential interactions of gene-environment models in human genetics and biological studies. The model overwhelms the others by reducing change of type 1 error better than traditional account methods in the multiple testing (Milne et al 2008;Motsinger-Reif et al 2008;Xu et al 2014).…”

Section: Discussionmentioning

confidence: 99%

Research Article Association between polymorphisms in TLR4 gene targeted by microRNA-140 and cervical precancerous lesion in south Chinese women: a case control study

Huang¹,

Li²,

Zhong³

et al. 2017

Genet. Mol. Res.

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Toll-like receptor 4 (TLR4), one of the key immune system effectors, plays a main role in immune recognition of cervical cancer. Micro-RNAs are involved in regulation of multiple important genes in the progression of cervical cancer. A case-control study of 592 people was conducted from Yun'an County, Yunfu City, Guangdong Province, China. Cervical fall off epithelia were collected to detect human papilloma virus (HPV), followed by Thin Prep cytology test (TCT). Moreover, extraction of DNA from peripheral blood were performed for genotyping from the 296 patients and another 296 age-matched healthy control subjects.

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“…Epidemiological studies from the northeast India reported tobacco smoking as one of the strongest risk factor for HNC (Yadav et al, 2010;Talukdar et al, 2013;Choudhury and Ghosh, 2014;Ghosh et al, 2014a) . Moreover, it was seen that tobacco-betel quid chewing also had a very high impact on HNC risk (Sharan et al, 2012;Choudhury et al, 2014) .…”

Section: Discussionmentioning

confidence: 99%

Influence of the CYP1A1 T3801C Polymorphism on Tobacco and Alcohol-Associated Head and Neck Cancer Susceptibility in Northeast India

Singh

Choudhury²,

Kapfo³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Gene–environment interaction and susceptibility in head and neck cancer patients and in their first‐degree relatives: a study of Northeast Indian population

Abstract: GSTM1 and GSTT1 null genotypes may act as markers to determine the genetic susceptibility in HNSCC patients and in their first-degree relatives. Furthermore, tobacco chewing and GSTM1 null genotype interaction identified as the strongest gene-environment model to predict HNSCC.

Cited by 20 publications

References 32 publications

Associations among smoking, MGMT hypermethylation, TP53-mutations, and relapse in head and neck squamous cell carcinoma

Associations among smoking, MGMT hypermethylation, TP53-mutations, and relapse in head and neck squamous cell carcinoma

Research Article Association between polymorphisms in TLR4 gene targeted by microRNA-140 and cervical precancerous lesion in south Chinese women: a case control study

Influence of the CYP1A1 T3801C Polymorphism on Tobacco and Alcohol-Associated Head and Neck Cancer Susceptibility in Northeast India

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