Combined effect of genetic polymorphisms of AURKA and environmental factors on oral cancer development in Taiwan

Oral squamous cell carcinoma (OSCC) is the sixth and fourth most common cause of cancer death in men worldwide and in Taiwan, respectively. AURKA, which encodes a centrosome-related serine/threonine kinase, is frequently amplified and overexpressed in many human cancers, particularly advanced OSCC....

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Published inPLOS ONE Vol. 12; no. 2; p. e0171583
Main Authors Chou, Chia-Hsuan, Chou, Ying-Erh, Chuang, Chun-Yi, Yang, Shun-Fa, Lin, Chiao-Wen
Format Journal Article
LanguageEnglish
Published United States Public Library of Science (PLoS) 02.02.2017
Public Library of Science
Subjects
Alcohol use
Analysis
Areca
Areca - adverse effects
Aurora Kinase A
Aurora Kinase A - genetics
Biology and Life Sciences
Breast cancer
Cancer
Carcinoma, Squamous Cell
Carcinoma, Squamous Cell - etiology
Carcinoma, Squamous Cell - genetics
Case-Control Studies
Chewing
Confidence intervals
Disease susceptibility
Ecological risk assessment
Environmental aspects
Environmental factors
Environmental risk
Gene Frequency
Gene Frequency - genetics
Genetic polymorphisms
Genetic Predisposition to Disease
Genetic Predisposition to Disease - genetics
Haplotypes
Health risk assessment
Health risks
Humans
Male
Mastication
Medical research
Medicine
Medicine and Health Sciences
Middle Aged
Mouth cancer
Mouth Neoplasms
Mouth Neoplasms - etiology
Mouth Neoplasms - genetics
Mutation
Oral cancer
Oral squamous cell carcinoma
Patients
Polymerase chain reaction
Polymorphism
Polymorphism, Single Nucleotide
Polymorphism, Single Nucleotide - genetics
Protein-serine/threonine kinase
Q
R
Real-Time Polymerase Chain Reaction
Research Article
Risk analysis
Risk Factors
Risk management
Science
Single-nucleotide polymorphism
Smoking
Smoking - adverse effects
Squamous cell carcinoma
Taiwan
Taiwan - epidemiology
Threonine
Tumorigenesis
Taiwan
Online AccessGet full text

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Abstract Oral squamous cell carcinoma (OSCC) is the sixth and fourth most common cause of cancer death in men worldwide and in Taiwan, respectively. AURKA, which encodes a centrosome-related serine/threonine kinase, is frequently amplified and overexpressed in many human cancers, particularly advanced OSCC. We conducted a hospital-based case-control study to estimate AURKA single-nucleotide polymorphisms (SNPs) and environmental risk factors to determine OSCC susceptibility and clinicopathological characteristics. We enrolled a total of 876 OSCC patients and 1200 controls. Four SNPs of AURKA, namely rs1047972, rs2273535, rs2064863, and rs6024836, were analyzed using real-time polymerase chain reaction (PCR). Among the 1420 smokers, the AURKA polymorphism carriers with the betel nut chewing habit had a higher risk of oral cancer than AURKA wild-type (WT) carriers without the betel nut chewing habit. Patients with the AURKA rs2064863 gene had a 1.365-fold higher risk of stage III or IV OSCC (95% confidence interval [CI] 1.029-1.811) than those with the rs2064863 WT gene. Furthermore, carriers of the AURKA rs1047972/rs2273535/rs2064863 C-A-T haplotype had a 1.736-fold (95% CI 1.110-2.715) higher risk of OSCC than controls (C-T-T, the most common haplotype). Among patients with the betel quid chewing habit, carriers of other haplotypes (C-T-T, C-A-G, T-A-T, T-A-G, T-T-T, and C-T-G) had a 12.857-fold (95% CI 10.731-15.404) increased risk, and carriers of the C-A-T haplotype had the highest risk (AOR: 31.120; 95% CI 13.864-69.850) of OSCC, compared with those without the betel quid chewing who harbored other haplotypes. In conclusion, betel nut chewing combined with the AURKA C-A-T haplotypes lead to a high risk of OSCC. These findings reveal a novel genetic-environmental predisposition for oral tumorigenesis.
AbstractList Background Oral squamous cell carcinoma (OSCC) is the sixth and fourth most common cause of cancer death in men worldwide and in Taiwan, respectively. AURKA, which encodes a centrosome-related serine/threonine kinase, is frequently amplified and overexpressed in many human cancers, particularly advanced OSCC. We conducted a hospital-based case-control study to estimate AURKA single-nucleotide polymorphisms (SNPs) and environmental risk factors to determine OSCC susceptibility and clinicopathological characteristics. Methodology/Principal findings We enrolled a total of 876 OSCC patients and 1200 controls. Four SNPs of AURKA, namely rs1047972, rs2273535, rs2064863, and rs6024836, were analyzed using real-time polymerase chain reaction (PCR). Among the 1420 smokers, the AURKA polymorphism carriers with the betel nut chewing habit had a higher risk of oral cancer than AURKA wild-type (WT) carriers without the betel nut chewing habit. Patients with the AURKA rs2064863 gene had a 1.365-fold higher risk of stage III or IV OSCC (95% confidence interval [CI] 1.029-1.811) than those with the rs2064863 WT gene. Furthermore, carriers of the AURKA rs1047972/rs2273535/rs2064863 C-A-T haplotype had a 1.736-fold (95% CI 1.110-2.715) higher risk of OSCC than controls (C-T-T, the most common haplotype). Among patients with the betel quid chewing habit, carriers of other haplotypes (C-T-T, C-A-G, T-A-T, T-A-G, T-T-T, and C-T-G) had a 12.857-fold (95% CI 10.731-15.404) increased risk, and carriers of the C-A-T haplotype had the highest risk (AOR: 31.120; 95% CI 13.864-69.850) of OSCC, compared with those without the betel quid chewing who harbored other haplotypes. Conclusions In conclusion, betel nut chewing combined with the AURKA C-A-T haplotypes lead to a high risk of OSCC. These findings reveal a novel genetic-environmental predisposition for oral tumorigenesis.
BACKGROUNDOral squamous cell carcinoma (OSCC) is the sixth and fourth most common cause of cancer death in men worldwide and in Taiwan, respectively. AURKA, which encodes a centrosome-related serine/threonine kinase, is frequently amplified and overexpressed in many human cancers, particularly advanced OSCC. We conducted a hospital-based case-control study to estimate AURKA single-nucleotide polymorphisms (SNPs) and environmental risk factors to determine OSCC susceptibility and clinicopathological characteristics.METHODOLOGY/PRINCIPAL FINDINGSWe enrolled a total of 876 OSCC patients and 1200 controls. Four SNPs of AURKA, namely rs1047972, rs2273535, rs2064863, and rs6024836, were analyzed using real-time polymerase chain reaction (PCR). Among the 1420 smokers, the AURKA polymorphism carriers with the betel nut chewing habit had a higher risk of oral cancer than AURKA wild-type (WT) carriers without the betel nut chewing habit. Patients with the AURKA rs2064863 gene had a 1.365-fold higher risk of stage III or IV OSCC (95% confidence interval [CI] 1.029-1.811) than those with the rs2064863 WT gene. Furthermore, carriers of the AURKA rs1047972/rs2273535/rs2064863 C-A-T haplotype had a 1.736-fold (95% CI 1.110-2.715) higher risk of OSCC than controls (C-T-T, the most common haplotype). Among patients with the betel quid chewing habit, carriers of other haplotypes (C-T-T, C-A-G, T-A-T, T-A-G, T-T-T, and C-T-G) had a 12.857-fold (95% CI 10.731-15.404) increased risk, and carriers of the C-A-T haplotype had the highest risk (AOR: 31.120; 95% CI 13.864-69.850) of OSCC, compared with those without the betel quid chewing who harbored other haplotypes.CONCLUSIONSIn conclusion, betel nut chewing combined with the AURKA C-A-T haplotypes lead to a high risk of OSCC. These findings reveal a novel genetic-environmental predisposition for oral tumorigenesis.
Background Oral squamous cell carcinoma (OSCC) is the sixth and fourth most common cause of cancer death in men worldwide and in Taiwan, respectively. AURKA , which encodes a centrosome-related serine/threonine kinase, is frequently amplified and overexpressed in many human cancers, particularly advanced OSCC. We conducted a hospital-based case-control study to estimate AURKA single-nucleotide polymorphisms (SNPs) and environmental risk factors to determine OSCC susceptibility and clinicopathological characteristics. Methodology/Principal findings We enrolled a total of 876 OSCC patients and 1200 controls. Four SNPs of AURKA , namely rs1047972, rs2273535, rs2064863, and rs6024836, were analyzed using real-time polymerase chain reaction (PCR). Among the 1420 smokers, the AURKA polymorphism carriers with the betel nut chewing habit had a higher risk of oral cancer than AURKA wild-type (WT) carriers without the betel nut chewing habit. Patients with the AURKA rs2064863 gene had a 1.365-fold higher risk of stage III or IV OSCC (95% confidence interval [CI] 1.029–1.811) than those with the rs2064863 WT gene. Furthermore, carriers of the AURKA rs1047972/rs2273535/rs2064863 C-A-T haplotype had a 1.736-fold (95% CI 1.110–2.715) higher risk of OSCC than controls (C-T-T, the most common haplotype). Among patients with the betel quid chewing habit, carriers of other haplotypes (C-T-T, C-A-G, T-A-T, T-A-G, T-T-T, and C-T-G) had a 12.857-fold (95% CI 10.731–15.404) increased risk, and carriers of the C-A-T haplotype had the highest risk (AOR: 31.120; 95% CI 13.864–69.850) of OSCC, compared with those without the betel quid chewing who harbored other haplotypes. Conclusions In conclusion, betel nut chewing combined with the AURKA C-A-T haplotypes lead to a high risk of OSCC. These findings reveal a novel genetic-environmental predisposition for oral tumorigenesis.
Oral squamous cell carcinoma (OSCC) is the sixth and fourth most common cause of cancer death in men worldwide and in Taiwan, respectively. AURKA, which encodes a centrosome-related serine/threonine kinase, is frequently amplified and overexpressed in many human cancers, particularly advanced OSCC. We conducted a hospital-based case-control study to estimate AURKA single-nucleotide polymorphisms (SNPs) and environmental risk factors to determine OSCC susceptibility and clinicopathological characteristics. We enrolled a total of 876 OSCC patients and 1200 controls. Four SNPs of AURKA, namely rs1047972, rs2273535, rs2064863, and rs6024836, were analyzed using real-time polymerase chain reaction (PCR). Among the 1420 smokers, the AURKA polymorphism carriers with the betel nut chewing habit had a higher risk of oral cancer than AURKA wild-type (WT) carriers without the betel nut chewing habit. Patients with the AURKA rs2064863 gene had a 1.365-fold higher risk of stage III or IV OSCC (95% confidence interval [CI] 1.029-1.811) than those with the rs2064863 WT gene. Furthermore, carriers of the AURKA rs1047972/rs2273535/rs2064863 C-A-T haplotype had a 1.736-fold (95% CI 1.110-2.715) higher risk of OSCC than controls (C-T-T, the most common haplotype). Among patients with the betel quid chewing habit, carriers of other haplotypes (C-T-T, C-A-G, T-A-T, T-A-G, T-T-T, and C-T-G) had a 12.857-fold (95% CI 10.731-15.404) increased risk, and carriers of the C-A-T haplotype had the highest risk (AOR: 31.120; 95% CI 13.864-69.850) of OSCC, compared with those without the betel quid chewing who harbored other haplotypes. In conclusion, betel nut chewing combined with the AURKA C-A-T haplotypes lead to a high risk of OSCC. These findings reveal a novel genetic-environmental predisposition for oral tumorigenesis.
Oral squamous cell carcinoma (OSCC) is the sixth and fourth most common cause of cancer death in men worldwide and in Taiwan, respectively. AURKA, which encodes a centrosome-related serine/threonine kinase, is frequently amplified and overexpressed in many human cancers, particularly advanced OSCC. We conducted a hospital-based case-control study to estimate AURKA single-nucleotide polymorphisms (SNPs) and environmental risk factors to determine OSCC susceptibility and clinicopathological characteristics. We enrolled a total of 876 OSCC patients and 1200 controls. Four SNPs of AURKA, namely rs1047972, rs2273535, rs2064863, and rs6024836, were analyzed using real-time polymerase chain reaction (PCR). Among the 1420 smokers, the AURKA polymorphism carriers with the betel nut chewing habit had a higher risk of oral cancer than AURKA wild-type (WT) carriers without the betel nut chewing habit. Patients with the AURKA rs2064863 gene had a 1.365-fold higher risk of stage III or IV OSCC (95% confidence interval [CI] 1.029-1.811) than those with the rs2064863 WT gene. Furthermore, carriers of the AURKA rs1047972/rs2273535/rs2064863 C-A-T haplotype had a 1.736-fold (95% CI 1.110-2.715) higher risk of OSCC than controls (C-T-T, the most common haplotype). Among patients with the betel quid chewing habit, carriers of other haplotypes (C-T-T, C-A-G, T-A-T, T-A-G, T-T-T, and C-T-G) had a 12.857-fold (95% CI 10.731-15.404) increased risk, and carriers of the C-A-T haplotype had the highest risk (AOR: 31.120; 95% CI 13.864-69.850) of OSCC, compared with those without the betel quid chewing who harbored other haplotypes. In conclusion, betel nut chewing combined with the AURKA C-A-T haplotypes lead to a high risk of OSCC. These findings reveal a novel genetic-environmental predisposition for oral tumorigenesis.
Audience Academic
Author Ying-Erh Chou
Shun-Fa Yang
Chiao-Wen Lin
Chun-Yi Chuang
Chia-Hsuan Chou
AuthorAffiliation 2 Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan
5 Institute of Oral Sciences, Chung Shan Medical University, Taichung, Taiwan
3 School of Medicine, Chung Shan Medical University, Taichung, Taiwan
4 Department of Otolaryngology, Chung Shan Medical University Hospital, Taichung, Taiwan
6 Department of Dentistry, Chung Shan Medical University Hospital, Taichung, Taiwan
National Cancer Center, JAPAN
1 Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan
AuthorAffiliation_xml – name: 1 Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan
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– name: 5 Institute of Oral Sciences, Chung Shan Medical University, Taichung, Taiwan
– name: 4 Department of Otolaryngology, Chung Shan Medical University Hospital, Taichung, Taiwan
– name: 6 Department of Dentistry, Chung Shan Medical University Hospital, Taichung, Taiwan
– name: National Cancer Center, JAPAN
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BackLink https://cir.nii.ac.jp/crid/1874242817238873856$$DView record in CiNii
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Conceptualization: CWL.Data curation: CHC.Formal analysis: YEC.Funding acquisition: SFY.Investigation: CWL.Methodology: CYC.Resources: CYC.Validation: CWL.Writing – original draft: CHC CWL.Writing – review & editing: CHC CWL.
Competing Interests: The authors have declared that no competing interests exist.
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Snippet Oral squamous cell carcinoma (OSCC) is the sixth and fourth most common cause of cancer death in men worldwide and in Taiwan, respectively. AURKA, which...
Background Oral squamous cell carcinoma (OSCC) is the sixth and fourth most common cause of cancer death in men worldwide and in Taiwan, respectively. AURKA,...
BACKGROUNDOral squamous cell carcinoma (OSCC) is the sixth and fourth most common cause of cancer death in men worldwide and in Taiwan, respectively. AURKA,...
BackgroundOral squamous cell carcinoma (OSCC) is the sixth and fourth most common cause of cancer death in men worldwide and in Taiwan, respectively. AURKA,...
Background Oral squamous cell carcinoma (OSCC) is the sixth and fourth most common cause of cancer death in men worldwide and in Taiwan, respectively. AURKA ,...
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StartPage e0171583
SubjectTerms Alcohol use
Analysis
Areca
Areca - adverse effects
Aurora Kinase A
Aurora Kinase A - genetics
Biology and Life Sciences
Breast cancer
Cancer
Carcinoma, Squamous Cell
Carcinoma, Squamous Cell - etiology
Carcinoma, Squamous Cell - genetics
Case-Control Studies
Chewing
Confidence intervals
Disease susceptibility
Ecological risk assessment
Environmental aspects
Environmental factors
Environmental risk
Gene Frequency
Gene Frequency - genetics
Genetic polymorphisms
Genetic Predisposition to Disease
Genetic Predisposition to Disease - genetics
Haplotypes
Health risk assessment
Health risks
Humans
Male
Mastication
Medical research
Medicine
Medicine and Health Sciences
Middle Aged
Mouth cancer
Mouth Neoplasms
Mouth Neoplasms - etiology
Mouth Neoplasms - genetics
Mutation
Oral cancer
Oral squamous cell carcinoma
Patients
Polymerase chain reaction
Polymorphism
Polymorphism, Single Nucleotide
Polymorphism, Single Nucleotide - genetics
Protein-serine/threonine kinase
Q
R
Real-Time Polymerase Chain Reaction
Research Article
Risk analysis
Risk Factors
Risk management
Science
Single-nucleotide polymorphism
Smoking
Smoking - adverse effects
Squamous cell carcinoma
Taiwan
Taiwan - epidemiology
Threonine
Tumorigenesis
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Title Combined effect of genetic polymorphisms of AURKA and environmental factors on oral cancer development in Taiwan
URI https://cir.nii.ac.jp/crid/1874242817238873856
https://www.ncbi.nlm.nih.gov/pubmed/28152093
https://www.proquest.com/docview/1864405039
https://www.proquest.com/docview/1865518495
https://www.proquest.com/docview/1868340338
https://pubmed.ncbi.nlm.nih.gov/PMC5289639
https://doaj.org/article/2e84585123624afa8a6fa9e7c9ffe5d2
http://dx.doi.org/10.1371/journal.pone.0171583
Volume 12
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