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Journal Article•DOI•

Risk genes in head and neck cancer: A systematic review and meta-analysis of last 5 years

Mabel Brunotto1, Ana María Zarate1, Alejandra Bono1, José L. Barra1, Silvina Berra1 •
National University of Cordoba1
01 Mar 2014-Oral Oncology (Pergamon)-Vol. 50, Iss: 3, pp 178-188
TL;DR: The aim of this work was to identify risk genes related to the development and progression of squamous cell carcinoma head and neck (SCCHN) and do a meta-analysis of available estimates, showing no significant association between different allelic variants of Arg72Pro rs1042522 and SCCHN risk.
About: This article is published in Oral Oncology.The article was published on 2014-03-01 and is currently open access. It has received 48 citations till now. The article focuses on the topics: Odds ratio.

Summary (1 min read)

Jump to: [INTRODUCTION] – [METHODS] – [RESULTS] – [DISCUSSION] and [Contributors]

INTRODUCTION

  • Head and Neck Carcinoma (HNC), of which the majority are squamous cell carcinomas of the head and neck , is the sixth most prevalent cancers in mankind and, presents high morbidity and low rates of survival.
  • It is known that the apoptotic and proliferation genes are involved in cancer development and these could be useful as a biomarker of this pathology.
  • Systematic reviews and meta-analysis allow stronger and more generalized conclusions for identifying some models of risk markers.
  • This has led to the production of an enormous number of epidemiologic papers about the relationship between genetic polymorphism and disease.
  • Focused on the microenvironment (focal proliferative lesions precede cancer) or morphostasis theory (morphostatic fields maintain the normal behavior of the cell and its tissue micro-architecture), also known as There are two subtypes.

METHODS

  • This study was made according to the PRISMA reporting items for systematic reviews and metaanalysis guidelines.
  • The search strategy included the following keywords (variably combined): “oral cancer”, “oral cancer polymorphism”, “oncogene”, “tumor suppressor gene”, “squamous cell carcinoma”, “head and neck cancer”.
  • Abstracts and titles of all the identified papers obtained by the electronic search were evaluated.
  • All studies which met the inclusion criteria (presence/absence of mutation and/or polymorphism by PCR, Odd Ratios (OR) adjusted for alcohol and tobacco, 95% Confidence Intervals (CIs) were assessed in order to establish their validity and subsequent data extraction.

RESULTS

  • Nineteen original reports were retrieved from 2285 potential reports that addressed the issue of DNA gene / polymorphisms and risk of SCCHN.
  • Twelve of the studies were of unpaired casecontrol design, 6 studies were matched case-control, and 1 nested case-control (Table 1).
  • TP53, GSTM1, and CYPA1were described in four, three, and two studies respectively, which were considered for meta-analysis.
  • No study reported a significant association between this polymorphism and SCCHN risk.

DISCUSSION

  • There are still numerous points that are unclear or unknown.
  • 57 The ADH7A92G 23 polymorphism has been described as associated with diminished SCCHN risk.
  • As well as smoking, alcohol consumption is another known cancer risk factor.
  • This gene is related to an increase of tumor survival because it promotes angiogenesis and inhibits apoptosis.
  • The model proposed in this work shows the genetic composition of individuals that could be at risk or protected against malignancy transformation.

Contributors

  • MB conceived and coordinated the project, made all the analyses, and wrote the report.
  • All authors contributed individual patient data from trials and commented on the initial surrogate-end point protocol and on drafts of the report.

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Journal Article•DOI•
Interleukin-10 rs1800896 polymorphism is associated with increased head and neck cancer risk but not associated with its clinical stages.

[...]

Wei Huang1, Juan Song2, Xiao-Wei Jia, Yin-Xue Chen1, Jia Shi1, Xun Jiang •
Jinan University1, Hubei University of Medicine2
29 Mar 2017-Oncotarget
TL;DR: It was concluded that interleukin-10 rs1800896 polymorphism was significantly associated with head and neck cancer risk but not with the clinical stages thereof.
Abstract: // Wei Huang 1, * , Juan Song 2, * , Xiao-Wei Jia 3, * , Yin-Xue Chen 1 , Jia Shi 1 , Xun Jiang 3 1 Department of Stomatology, Zhuhai People's Hospital, Zhuhai Hospital Affiliated with Jinan University, Zhuhai 519099, China 2 Department of Clinical Laboratory, Taihe Hospital, Hubei University of Medicine, Shiyan 442000, China 3 Department of Stomatology, Guangzhou Hospital of Integrated Traditional and West Medicine, Guangzhou 510800, China * Co-first authors Correspondence to: Wei Huang, email: hwdentist@163.com Keywords: interleukin-10, polymorphism, head and neck neoplasms, mouth neoplasms, oropharyngeal neoplasms Received: February 13, 2017 Accepted: March 21, 2017 Published: March 29, 2017 ABSTRACT Background: The association of interleukin-10 rs1800896 polymorphism with head and neck cancer risk and its clinical stages has been investigated by many published studies, but the results remain inconsistent. Therefore, we conducted this meta-analysis for further investigation. Results: Six case-control studies involving 1,781 head and neck cancer patients and 1,978 controls were yielded. The results indicated an association between rs1800896 polymorphism and increased head and neck risk [odds ratio (95%confidence interval) for G vs. A, GA vs. AA, GG vs. AA, GA+GG vs. AA, and GG vs. AA + GA were 1.63 (1.30–2.04), 3.17 (2.11–4.76), 1.63 (1.17–2.26), 1.73 (1.25–2.39), and 2.73 (1.82–4.09), respectively]. The subgroup analyses all obtained similar results with overall populations. The results of clinical stages yielded a non-significant association. No publication bias was detected. Materials and Methods: The PubMed and Chinese National Knowledge Infrastructure databases were searched up to December 27, 2016. Two authors independently selected studies, extracted and analyzed the data using the RevMan 5 software. Either a fixed effect or a random effect model was used to estimate pooled odds ratio and its 95% confidence intervals. Conclusions: We concluded that interleukin-10 rs1800896 polymorphism was significantly associated with head and neck cancer risk but not with the clinical stages thereof.

12 citations

Cites background from "Risk genes in head and neck cancer:..."

  • ...HNC is a multifactorial disease [23–24], and genetic background is of great significance in its etiology through involvement in the disease onset and development [7]....

    [...]

  • ...That because genetic background is also responsible for the disease occurrence [7]....

    [...]

Journal Article•
Tooth loss and risk of oral squamous cell carcinoma in Chinese Han population.

[...]

Chenqi Zuo1, Yaqiao Zhu1, Xiayong Wang1, Xian-Tao Zeng2, Cui Huang3 •
Jinan University1, Hubei University of Medicine2, Wuhan University3
15 Nov 2015-International Journal of Clinical and Experimental Medicine
TL;DR: Tooth loss may be not associated with risk of oral cancer in this case-control study, and adjustment for smoking and alcohol showed a non-significant association between tooth loss and OSCC.
Abstract: Objective Association between tooth loss and oral cancer risk was investigated primary studies and meta-analyses, however, the results remain inconsistent. This study is to test the association between tooth loss and oral squamous cell carcinoma (OSCC) in Chinese Han population. Methods Case-control study including histologically confirmed OSCC cases and healthy controls individually matched to the cases for age, sex, and district of residence between May 1, 2010, and Match 31, 2014. Univariate and multiple logistic regression models were used to calculate odds ratios (ORs) and corresponding 95% confidence intervals (CIs) using the STATA 12.0 software. Results Finally included 150 OSCC patients and 167 healthy controls. Cases had a significantly higher mean (SD) number of lost teeth than controls (10.03±6.62 vs. 8.69±5.20; P = 0.045). The results of univariate analysis and adjustment for smoking and alcohol showed a non-significant association between tooth loss and OSCC. After adjustment for age at diagnosis, gender, smoking, alcohol use, body mass index, and history of diabetes mellitus, those in the upper tertiles of lost tooth were significantly more likely to have OSCC (OR = 3.64, 95% CI = 1.15-11.53, P = 0.03; P for trend = 0.11) than in the lower tertiles. The unadjusted and adjusted results of per teeth also revealed non-significant association. Conclusions Tooth loss may be not associated with risk of oral cancer in this case-control study. The relevant large-scale studies in Chinese are suggested to perform.

10 citations

Cites background from "Risk genes in head and neck cancer:..."

  • ...Genetic factors are also play an important role in the development of oral cancer [28, 29]....

    [...]

Journal Article•DOI•
COX-2 rs689466, rs5275, and rs20417 polymorphisms and risk of head and neck squamous cell carcinoma: a meta-analysis of adjusted and unadjusted data.

[...]

Wei-Dong Leng1, Xiu-Jie Wen2, Joey S.W. Kwong3, Wei Huang4, Jian-Gang Chen5, Xian-Tao Zeng1, Xian-Tao Zeng5 •
Hubei University of Medicine1, Third Military Medical University2, Sichuan University3, Jinan University4, Wuhan University5
13 Jul 2016-BMC Cancer
TL;DR: Current results suggest that COX-2 rs689466, rs5275, and rs20417 polymorphisms are not associated with HNSCC.
Abstract: Numerous case–control studies have been performed to investigate the association between three cyclooxygenase-2 (COX-2) polymorphisms (rs20417 (−765G > C), rs689466 (−1195G > A), and rs5275 (8473 T > C)) and the risk of head and neck squamous cell carcinoma (HNSCC). However, the results were inconsistent. Therefore, we conducted this meta-analysis to investigate the association. We searched in PubMed, Embase, and Web of Science up to January 20, 2015 (last updated on May 12, 2016). Two independent reviewers extracted the data. Odds ratios (ORs) with their 95 % confidence intervals (CIs) were used to assess the association. All statistical analyses were performed using the Review Manager (RevMan) 5.2 software. Finally 8 case–control studies were included in this meta-analysis. For unadjusted data, an association with increased risk was observed in three genetic models in COX-2 rs689466 polymorphism; however, COX-2 rs5275 and rs20417 polymorphisms were not related to HNSCC risk in this study. The pooled results from adjusted data all revealed non-significant association between these three polymorphisms and risk of HNSCC. We also found a similar result in the subgroup analyses, based on both unadjusted data and adjusted data. Current results suggest that COX-2 rs689466, rs5275, and rs20417 polymorphisms are not associated with HNSCC. Further large and well-designed studies are necessary to validate this association.

9 citations

Cites background from "Risk genes in head and neck cancer:..."

  • ...Besides environmental risk factors, such as tooth loss [1], alcohol consumption [2], periodontal diseases [3], smoking [4], tooth brushing [5], and human papillomavirus (HPV) [6], genetic factors [7, 8] also play an significant role in the onset and development of HNSCC....

    [...]

Journal Article•DOI•
Association between TGF-β1 Polymorphisms and Head and Neck Cancer Risk: A Meta-Analysis.

[...]

Quan Shi1, Xing Wang2, Chuan Cai1, Shuo Yang1, Na Huo1, Hongchen Liu1 •
Chinese PLA General Hospital1, Shanxi Medical University2
03 Nov 2017-Frontiers in Genetics
TL;DR: It was found that TGF-β1 869C/T polymorphism may be involved in susceptibility to HNC, especially in Asian patients, however, given the limitations of this meta-analysis, further well-designed studies are required in the future.
Abstract: Background and Objective: Studies have been conducted to explore the association between the single nucleotide polymorphisms (SNPs) in transforming growth factor beta 1 (TGF-β1) and head and neck cancer (HNC) susceptibility, however the findings are still inconclusive. Therefore, we conduct this meta-analysis to quantitatively assess the association. Methods: Embase and PubMed were searched for all eligible clinical studies. The odds ratio (OR) and 95% confidence interval (CI) of each study were pooled to estimate the association between SNPs in the TGF-β1 and the HNC risk. Subgroup analysis was used to explore whether particular characteristics were related to the value of overall ORs and 95% CIs. Results: Seven case-control studies, including three SNPs (-509C/T, 869T/C, and 915G/C), were examined. Overall, this meta-analysis failed to identify a significant association between TGF-β1-509C/T, 915G/C polymorphism and HNC risk in any models. As for the 869T/C polymorphism, significant associations were observed in the allelic model (C vs. T: OR = 1.351, 95%CI: 1.030-1.772), the homozygote model (CC vs. TT: OR = 1.585, 95%CI: 1.026-2.449) and the dominant model (CT/CC vs. TT: OR = 1.398, 95%CI: 1.008-1.937). This polymorphism was also found in the Asian group as well (C vs. T: OR = 1.400, 95%CI: 1.003-1.956, CC vs. TT: OR = 1.814, 95%CI: 1.018-3.233). Conclusion: Meta-analysis failed to show a statistical association between TGF-β1-509C/T, 915G/C polymorphism, and HNC risk in any genetic models. However, it was found that TGF-β1 869C/T polymorphism may be involved in susceptibility to HNC, especially in Asian patients. However, given the limitations of this meta-analysis, further well-designed studies are required in the future.

8 citations

Cites background from "Risk genes in head and neck cancer:..."

  • ...…common cancer and ninth most frequent cause of cancer-related death, HNC affected more than 4.6 million people worldwide in 2013, and it has a high morbidity and a low survival rate (Petersen, 2009; Brunotto et al., 2014; Chai et al., 2015; Global Burden of Disease Study 2013 Collaborators, 2015)....

    [...]

  • ...…with Epstein-Barr virus (EBV) or human papillomavirus (HPV), and environmental exposure are the primary etiologic factors contributing to HNC. Likewise, genetic susceptibility also plays a critical role in the development of HNC (Brunotto et al., 2014; Lacko et al., 2014; Munshi et al., 2015)....

    [...]

Book Chapter•DOI•
Folate-Decorated Polyamidoamine Dendrimer Nanoparticles for Head and Neck Cancer Gene Therapy.

[...]

Leyuan Xu1, Hu Yang2•
Yale University1, Virginia Commonwealth University2
01 Jan 2019-Methods of Molecular Biology
TL;DR: In a mouse xenograft model of HNSCC, the design and synthesis of fluorescently labeled, folic acid-decorated polyamidoamine generation 4 (G4) dendrimer conjugates for H NSCC-targeted gene delivery significantly enhances gene transfection or knockdown efficiency in HNS CC cells.
Abstract: Gene delivery systems have been developed on the basis of dendrimers and many other types of nanoparticle carriers, but few have been developed for head and neck squamous cell carcinomas (HNSCC). Herein, we describe the design and synthesis of fluorescently labeled, folic acid-decorated polyamidoamine (PAMAM) generation 4 (G4) dendrimer conjugates for HNSCC-targeted gene delivery. This delivery system comprises a dendrimer as the carrier that is conjugated with folic acid (FA) as HNSCC targeting moiety and imaging agents fluorescein isothiocyanate (FITC) or IRDye 800CW (NIR) for in vitro trafficking or bioimaging, respectively. By complexing with plasmid or siRNA, G4-FA/plasmid (or siRNA) significantly enhances gene transfection or knockdown efficiency in HNSCC cells. In a mouse xenograft model of HNSCC, this versatile G4-FA vector shows high biocompatibility, tumor targeting, high uptake, and sustained retention, making it a suitable platform for HNSCC gene therapy.

8 citations

References
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Cochrane Handbook for Systematic Reviews of Interventions, Version 5.1.0. The Cochrane Collaboration

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Journal Article•DOI•
Signaling to NF-kappaB.

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Matthew S. Hayden1, Sankar Ghosh•
Yale University1
15 Sep 2004-Genes & Development
TL;DR: An overview of established NF-kappaB signaling pathways is provided with focus on the current state of research into the mechanisms that regulate IKK activation and NF- kappaB transcriptional activity.
Abstract: The transcription factor NF-kappaB has been the focus of intense investigation for nearly two decades. Over this period, considerable progress has been made in determining the function and regulation of NF-kappaB, although there are nuances in this important signaling pathway that still remain to be understood. The challenge now is to reconcile the regulatory complexity in this pathway with the complexity of responses in which NF-kappaB family members play important roles. In this review, we provide an overview of established NF-kappaB signaling pathways with focus on the current state of research into the mechanisms that regulate IKK activation and NF-kappaB transcriptional activity.

3,829 citations

Journal Article•DOI•
Human DNA Repair Genes

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Richard D. Wood1, Michael Mitchell2, John Sgouros2, Tomas Lindahl1•
University of Cambridge1, Lincoln's Inn2
16 Feb 2001-Science
TL;DR: Modulation of DNA repair should lead to clinical applications including improvement of radiotherapy and treatment with anticancer drugs and an advanced understanding of the cellular aging process.
Abstract: Cellular DNA is subjected to continual attack, both by reactive species inside cells and by environmental agents. Toxic and mutagenic consequences are minimized by distinct pathways of repair, and 130 known human DNA repair genes are described here. Notable features presently include four enzymes that can remove uracil from DNA, seven recombination genes related to RAD51, and many recently discovered DNA polymerases that bypass damage, but only one system to remove the main DNA lesions induced by ultraviolet light. More human DNA repair genes will be found by comparison with model organisms and as common folds in three-dimensional protein structures are determined. Modulation of DNA repair should lead to clinical applications including improvement of radiotherapy and treatment with anticancer drugs and an advanced understanding of the cellular aging process.

1,581 citations

"Risk genes in head and neck cancer:..." refers methods in this paper

  • ...This study was about 8-oxiguanineDNA glycosylase gene (OGG1), which is involved in DNA repair mechanisms [50,51]....

    [...]

Journal Article•DOI•
MicroRNA: Biogenesis, Function and Role in Cancer.

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Leigh Ann MacFarlane1, Paul R. Murphy•
Dalhousie University1
31 Oct 2010-Current Genomics
TL;DR: The P-body model outlines microRNA sorting and shuttling between specialized P- body compartments that house enzymes required for slicer –dependent and –independent silencing, addressing the reversibility of these silencing mechanisms.
Abstract: MicroRNAs are small, highly conserved non-coding RNA molecules involved in the regulation of gene expression. MicroRNAs are transcribed by RNA polymerases II and III, generating precursors that undergo a series of cleavage events to form mature microRNA. The conventional biogenesis pathway consists of two cleavage events, one nuclear and one cytoplasmic. However, alternative biogenesis pathways exist that differ in the number of cleavage events and enzymes responsible. How microRNA precursors are sorted to the different pathways is unclear but appears to be determined by the site of origin of the microRNA, its sequence and thermodynamic stability. The regulatory functions of microRNAs are accomplished through the RNA-induced silencing complex (RISC). MicroRNA assembles into RISC, activating the complex to target messenger RNA (mRNA) specified by the microRNA. Various RISC assembly models have been proposed and research continues to explore the mechanism(s) of RISC loading and activation. The degree and nature of the complementarity between the microRNA and target determine the gene silencing mechanism, slicer-dependent mRNA degradation or slicer-independent translation inhibition. Recent evidence indicates that P-bodies are essential for microRNA-mediated gene silencing and that RISC assembly and silencing occurs primarily within P-bodies. The P-body model outlines microRNA sorting and shuttling between specialized P-body compartments that house enzymes required for slicer –dependent and –independent silencing, addressing the reversibility of these silencing mechanisms. Detailed knowledge of the microRNA pathways is essential for understanding their physiological role and the implications associated with dysfunction and dysregulation.

1,328 citations

"Risk genes in head and neck cancer:..." refers background in this paper

  • ...The miRNA are small portions of RNA, approximately 20–22 nucleotides, which may target a specific messenger RNA and generate feedback of its translation efficiency and stability [41–45]....

    [...]

Journal Article•DOI•
The codon 72 polymorphic variants of p53 have markedly different apoptotic potential.

[...]

Patrick Dumont1, J. I-Ju Leu2, Anthony Della Pietra1, Donna L. George2, Maureen E. Murphy1 •
Fox Chase Cancer Center1, University of Pennsylvania2
03 Feb 2003-Nature Genetics
TL;DR: It is found that in cell lines containing inducible versions of alleles encoding the Pro72 and Arg72 variants, and in cells with endogenous p53, the Arg72 variant induces apoptosis markedly better than does the Pro 72 variant.
Abstract: The gene TP53, encoding p53, has a common sequence polymorphism that results in either proline or arginine at amino-acid position 72. This polymorphism occurs in the proline-rich domain of p53, which is necessary for the protein to fully induce apoptosis. We found that in cell lines containing inducible versions of alleles encoding the Pro72 and Arg72 variants, and in cells with endogenous p53, the Arg72 variant induces apoptosis markedly better than does the Pro72 variant. Our data indicate that at least one source of this enhanced apoptotic potential is the greater ability of the Arg72 variant to localize to the mitochondria; this localization is accompanied by release of cytochrome c into the cytosol. These data indicate that the two polymorphic variants of p53 are functionally distinct, and these differences may influence cancer risk or treatment.

1,234 citations

"Risk genes in head and neck cancer:..." refers background in this paper

  • ...Cellular functions of this polymorphism were studied in in vitro culture, and it was observed that the protein variant codon72 arginine (R72) has a suppressor function of malignancy and induces an increase in apoptotic activity in relation to the variant 72 proline (P72) [36,37]....

    [...]

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Frequently Asked Questions (14)
Q1. What are the contributions mentioned in the paper "Risk genes in head and neck cancer: a systematic review and meta-analysis of last 5 years" ?

The case-control studies guidelines of the Scottish Intercollegiate Guidelines Network and MOOSE are followed. Two members of the team ( AB, AMZ ) evaluated complete articles independently and double-blinded, to establish their quality. The papers were encoded and delivered independently to each reviewer. 

It is known that the p53 suppressor tumor gene has a key role in stress cellular response, to preserve genome stability, and it is universally recognized as a human cancer marker when it is mutated. 

Overexpression of the DEC1 Protein InducesSenescence In Vitro and Is Related to Better Survival in Esophageal Squamous Cell Carcinoma. 

59 The AA genotype of the ADH1B R48H gene encodes an enzyme that is about 40 times more active than the enzyme encoded by AG and GG genotypes. 

The evaluation of diagnostic markers such as symptoms and genetic tests helps to increase the sensitivity or specificity of the determination of the presence/absence of malignancy. 

Authors such as Piva et al. 48 have observed inflammatory infiltrate in epithelial dysplasia with overexpression of NFKB and TNF-α, establishing a connection between the cancer and inflammation. 

61,62 Research by Su et al. 62 showed that allele G of CRYAB C-802G is correlated to breast cancer risk, and could be useful as a clinical marker for its early detection. 

the model proposed in this paper could fit models 1, 2, and 3 because it considers such epigenetic events as inflammation, mutational compounds such as tobacco and alcohol, and genomic stability and the cell cycle regulation process. 

The authors conducted a systematic review and meta-analysis of case-control studies from the MEDLINE, Scopus, Cochrane, and CancerLit databases between January 2007 and January 2013. 

3,29 Cancer is a complex pathology, and its incidence and survival index are closely related to social, cultural and socio-economic determinants of health. 

Pradhan S, Nagashri MN, Gopinath KS, Kumar A.Expression profiling of CYP1B1 in oral squamous cell carcinoma: counter intuitive down regulation in tumors. 

This gene encodes glutathioneStransferase Mu 1, which is critical to detoxification and the removal of electrophilic carcinogens. 

The identification of a predictive model of risk polymorphisms could help in early diagnosis, and in understanding disease recurrence and/or progression in the subset of patients. 

A search was made of combined electronic databases, and the bibliographies of all selected papers were searched to identify grey literature.