Submitted Successfully!
Thank you for your contribution! You can also upload a video entry related to this topic through the link below:
https://encyclopedia.pub/user/video_add?id=15280
Check Note
2000/2000
Ver. Summary Created by Modification Content Size Created at Operation
1 + 1231 word(s) 1231 2021-10-21 05:11:40 |
2 format corrected. + 537 word(s) 1768 2021-10-22 10:03:48 |
Susceptibility to Head and Neck Cancers

HNC involves a series of tumors originating in the oropharynx, hypopharynx, oral cavity, lip, larynx, or nasopharynx. Smoking, alcohol consumption, and high-risk human papillomaviruses have been related to HNC. In connection with the role of genetics in HNC, several recent meta-analyses have reported the association of polymorphisms with the risk of HNCs.

  • head and neck carcinoma
  • oral carcinoma
  • polymorphism
  • N-acetyltransferases
  • meta-analysis

1. Introduction

Cellular inflammation and immunity can play a significant role in various stages of carcinogenesis [1] such as head and neck cancers (HNCs). HNC mortality rates are elevating and disproportionately affect people in low- and middle-income countries and areas with restricted resources [2]. Global Burden of Disease Study (GBD) in 2016 estimated 512,492 deaths due to HNC (a minimum of 15,018 deaths in North Africa and the Middle East to a maximum of 199,280 in South Asia) and predicted the death count to reach 705,901 in 2030 [3][4]. HNC involves a series of tumors originating in the oropharynx, hypopharynx, oral cavity, lip, larynx, or nasopharynx [5]. Smoking, alcohol consumption, and high-risk human papillomaviruses have been related to HNC [5][6][7]. In connection with the role of genetics in HNC, several recent meta-analyses have reported the association of polymorphisms with the risk of HNCs [8][9][10][11].

A number of heterocyclic and aromatic amines are the main carcinogenic compounds of tobacco smoke [12][13] that their metabolism in humans is complex and includes acetylation as a main pathway for DNA mutation and the onset of carcinogenesis [14]. In particular, two N-acetyltransferases, NAT1 and NAT2 perform a role in catalyzing the deactivation and activation of several carcinogenic amines through N- and O-acetylation, respectively [14][15]. Both NAT genes ( NAT1 and NAT2 ) have polymorphisms in humans and in accordance with slow and rapid acetylator phenotypes [16]. The NAT2 metabolized gene is located in region 10 of chromosome 8p21, which contains two exons with a long intron of about 8.6 kb [17]. Exon 1 is very short (100 bp) and the entire protein-coding region in Exon 2 is 870 bp [18]. Also, the NAT1 gene is located on the short arm of chromosome 8 (8p21) [19][20]. NAT1 accelerates acetylation specifically for arylamine receptor structures such as p-aminosalicylic and p-aminobenzoic acids [21] and NAT2 acetylates other arylamine-acceptor structures, such as isoniazid, sulfasalazine, procainamide, and caffeine [19].

Evidence from the published articles on the relationship between NAT1 and NAT2 polymorphisms and HNC susceptibility is conflicting [22][23]. The association between the polymorphisms ( NAT1 and NAT2 ) and the HNC risk has been evaluated by one [24] and four [25][26][27][28] meta-analyses, respectively. However, these studies were published several years ago with the most recent one being published in 2015. Therefore, through this meta-analysis, we intend to update the evidence on the association between the polymorphisms and the HNC risk by including more studies. In addition, we aim to conduct trial sequential analysis (TSA) and meta-regression.

2. Analysis on Results

Twenty-eight studies included in the analysis were published between 1998 and 2014 ( Table 1 ). Fourteen articles [22][23][29][30][31][32][33][34][35][36][37][38][39][40] reported the results in Caucasians, nine [41][42][43][44][45][46][47][48][49] in Asians, and five [50][51][52][53][54] among participants of mixed ethnicity. The control source in eighteen articles [22][23][41][30][32][33][36][37][38][39][42][43][45][46][47][51][52][54] was hospitals and ten [29][31][34][35][40][44][48][49][50][53] recruited the controls from a general population. In total, the articles included 5154 HNC cases and 6194 controls. Age, gender distribution, sample size, tumor type, genotyping method, and the quality score are shown in Table 1 .

Table 1. Characteristics of the articles included in the meta-analysis.
The First Author, Publication Year Country Ethnicity Control Source Number Mean Year Male Percentage Type of Tumor Genotyping Method Quality Score
Case Control Case Control Case Control
Gonzalez, 1998 [34] Spain Caucasian PB 75 200 58.7 45 100 75 Oral, pharyngeal, laryngeal PCR-RFLP 7
Katoh, 1998 [41] Japan Asian HB 62 122 61.7 62.4 64.5 61.5 Oral PCR-RFLP 7
Henning, 1999 [23] Germany Caucasian HB 255 510 61.4 NA 90.6 NA Laryngeal PCR 7
Jourenkova-Mironova, 1999 [37] France Caucasian HB 250 172 54.4 54.9 96 94.8 Oral, pharyngeal, laryngeal PCR-RFLP 7
Morita, 1999 [48] Japan Asian PB 145 164 59.0 49.8 86.9 62.2 Oral, pharyngeal, laryngeal PCR 7
Olshan, 2000 [54] USA Mixed HB 171 193 59.5 56.8 81.3 59.1 Oral, pharyngeal, laryngeal PCR 7
Chen, 2001 [29] USA Caucasian PB 341 552 NA NA 70.4 71.6 Oral PCR-RFLP 9
Fronhoffs, 2001 [32] Germany Caucasian HB 291 300 59.8 47.1 80.1 58 Oral, pharyngeal, laryngeal RT-PCR 6
Hahn, 2002 [35] Germany Caucasian PB 94 92 61.5 45.1 65.9 51.1 Oral PCR-RFLP 7
Lei, 2002 [45] China Asian HB 62 56 60.2 58.2 NA NA Laryngeal PCR-RFLP 7
Varzim, 2002 [40] Portugal Caucasian PB 88 172 62.8 43.0 94.3 72.7 Laryngeal PCR-RFLP 7
Cheng, 2003 [43] Taiwan Asian HB 279 325 NA NA NA NA Pharyngeal PCR-RFLP 6
Gajecka, 2005 [33] Poland Caucasian HB 289 311 57.9 45.9 100 100 Laryngeal PCR-RFLP 8
Rydzanicz, 2005 [38] Poland Caucasian HB 266 143 61.6 53.1 95.1 100 Oral, pharyngeal, laryngeal PCR-RFLP 8
Unal, 2005 [39] Turkey Caucasian HB 45 104 53.5 50.0 93.3 65.4 Laryngeal PCR-RFLP 7
Marques, 2006 [52] Brazil Mixed HB 231 212 56.6 55.3 83.5 79.2 Oral PCR-RFLP 8
Gara, 2007 [51] Tunisia Mixed HB 64 160 50.7 53.6 65.6 45 Oral, pharyngeal, laryngeal PCR-RFLP 7
Majumder, 2007 [47] India Asian HB 297 342 NA NA NA NA Oral PCR-RFLP 6
Boccia, 2008 [22] Italy Caucasian HB 210 245 63.6 63.3 71.4 72.2 Oral, pharyngeal, laryngeal PCR-RFLP 8
Buch, 2008 [50] USA Mixed PB 182 399 58.7 58.7 87.4 75.7 Oral PCR-RFLP 9
Harth, 2008 [36] Germany Caucasian HB 312 300 59.7 47.2 80.4 58.7 Oral, pharyngeal, laryngeal PCR-RFLP 6
Chatzimichalis, 2010 [30] Greece Caucasian HB 88 102 66.5 62.5 87.5 74.5 Laryngeal PCR-RFLP 8
Demokan, 2010 [31] Turkey Caucasian PB 95 93 59.6 53.3 86.3 52.7 Oral, pharyngeal, laryngeal PCR 8
Hou, 2011 [44] China Asian PB 172 170 49.6 49.6 100 100 Oral, pharyngeal PCR-RFLP and Taqman 9
Balaji, 2012 [42] India Asian HB 157 132 53.1 55.1 54.8 34.8 Oral Taqman 7
Majumder, 2012 [46] India Asian HB 299 381 NA NA NA NA Oral PCR 6
Tian, 2013 [49] China Asian PB 233 102 60.0 60.0 NA NA Laryngeal PCR 8
Marques, 2014 [53] Brazil Mixed PB 101 141 NA NA NA NA Oral, pharyngeal, laryngeal PCR-RFLP 7
Abbreviations: HB, hospital-based; PB, Population-based; PCR, Polymerase Chain Reaction; RT, Real Time; RFLP, Restriction Fragment Length Polymorphism; NA, Not Available. Taqman: The 5′ Nuclease Assay.

Table 2 shows the prevalence of slow and rapid acetylators of NAT1 and NAT2 polymorphisms. Eight studies [23][41][31][32][37][40][46][54] included NAT1 polymorphism with 1509 HNC cases and 1829 controls and twenty-five studies [22][23][41][29][30][31][33][34][35][36][37][38][39][40][42][43][44][45][47][48][49][50][51][52][53] included NAT2 polymorphism with 4393 HNC cases and 5321 controls.

Table 2. Prevalence of the polymorphisms of N-acetyltransferases 1 and 2 (NAT1 and NAT2), (slow vs. rapid acetylators).
Author, Year NAT1
Case Control
Slow Rapid Slow Rapid
Katoh, 1998 [41] 9 53 46 76
Henning, 1999 [23] 144 109 232 164
Jourenkova-Mironova, 1999 [37] 141 109 98 74
Olshan, 2000 [54] 83 88 108 85
Fronhoffs, 2001 [32] 195 96 206 94
Varzim, 2002 [40] 48 40 107 65
Demokan, 2010 [31] 53 42 42 51
Majumder, 2012 [46] 128 171 168 213
Author, Year NAT2
Case Control
Slow Rapid Slow Rapid
Gonzalez, 1998 [34] 28 47 37 163
Katoh, 1998 [41] 7 55 7 115
Henning, 1999 [23] 138 117 286 224
Jourenkova-Mironova, 1999 [37] 142 108 91 81
Morita, 1999 [48] 18 127 17 147
Chen, 2001 [29] 198 143 302 250
Hahn, 2002 [35] 59 35 57 35
Lei, 2002 [45] 50 12 34 22
Varzim, 2002 [40] 47 41 76 96
Cheng, 2003 [43] 39 240 54 271
Gajecka, 2005 [33] 127 162 165 146
Rydzanicz, 2005 [38] 131 135 72 71
Unal, 2005 [39] 15 30 7 97
Marques, 2006 [52] 29 202 38 174
Gara, 2007 [51] 33 31 59 101
Majumder, 2007 [47] 190 107 205 137
Boccia, 2008 [22] 109 101 128 117
Buch, 2008 [50] 84 98 224 175
Harth, 2008 [36] 189 123 181 119
Chatzimichalis, 2010 [30] 39 49 65 37
Demokan, 2010 [31] 50 45 45 48
Hou, 2011 [44] 46 126 33 137
Balaji, 2012 [42] 100 57 67 65
Tian, 2013 [49] 189 44 56 46
Marques, 2014 [53] 48 53 51 90

When there was one study for a subgroup, we could delete it [55]. Subgroup analyses were performed based on ethnicity, sample size, control source, genotyping method, and tumor type ( Table 3 ). With regards to NAT1 polymorphism, no subgroup differences were observed. For NAT2 polymorphism, significant subgroup effects were observed for ethnicity and the control source. Slow acetylators among Asians and also the population-based studies could be effective factors on the pooled result of the association between NAT2 polymorphism and the HNC risk.

Table 3. Subgroup analyses of association between N-acetyltransferases 1 and 2 (NAT1 and NAT2) polymorphisms and the risk of head and neck cancer (slow vs. rapid acetylators).
Polymorphism Variable (N) OR 95% CI p-Value I2 Pheterogeneity
NAT1 Overall (8) 0.89 0.77, 1.02 0.09 48% 0.06
Ethnicity          
Caucasian (5) 0.96 0.80, 1.15 0.64 0% 0.45
Asian (2) 0.55 0.17, 1.80 0.32 87% 0.005
Control source          
Hospital-based (6) 0.87 0.74, 1.01 0.06 46% 0.10
Population-based (2) 1.05 0.51, 2.17 0.90 72% 0.06
Sample size          
≥200 (6) 0.90 0.77, 1.04 0.15 0% 0.87
<200 (2) 0.67 0.13, 3.56 0.64 91% 0.0007
Genotyping method          
PCR (4) 0.94 0.79, 1.14 0.54 26% 0.26
PCR-RFLP (3) 0.64 0.34, 1.18 0.15 74% 0.02
Tumor type          
Oral (2) 0.55 0.17, 1.80 0.32 87% 0.005
Laryngeal (2) 0.87 0.67, 1.15 0.33 0% 0.43
NAT2 Overall (25) 1.22 1.02, 1.46 0.03 74% <0.00001
Ethnicity          
Caucasian (13) 1.10 0.89, 1.37 0.38 71% <0.0001
Asian (8) 1.60 1.13, 2.26 0.008 69% 0.002
Mixed (4) 1.04 0.61, 1.77 0.89 79% 0.003
Control source          
Hospital-based (15) 1.10 0.88, 1.37 0.39 71% <0.0001
Population-based (10) 1.41 1.04, 1.92 0.03 75% <0.0001
Sample size          
≥200 (20) 1.19 1.00, 1.42 0.05 70% <0.00001
<200 (5) 1.49 0.68, 3.29 0.32 85% <0.0001
Genotyping method          
PCR (4) 1.47 0.77, 2.78 0.24 85% 0.0002
PCR-RFLP (19) 1.14 0.93, 1.39 0.21 72% <0.00001
Tumor type          
Oral (7) 1.05 0.80,1.38 0.72 62% 0.01
Pharyngeal (2) 0.82 0.54, 1.24 0.35 0% 0.96
Laryngeal (8) 1.48 0.88, 2.51 0.14 88% <0.00001
Abbreviations: PCR, Polymerase Chain Reaction; RFLP, Restriction Fragment Length Polymorphism.

The meta-regression analyses assessing the effect of publication year, the sample size, and the mean age and gender distribution of cases and controls on the risk of HNC in NAT1 and NAT2 polymorphisms are shown in Table 4 . Sample size, the mean age of cases, and the percentage of males in the controls were confounding factors for the pooled result of the association between NAT2 polymorphism and the HNC susceptibility. With an increase in sample size, age of the cases, and percentage of males in the controls, the OR decreased.

Table 4. Meta-regression analysis of association between N-acetyltransferases 1 and 2 (NAT1 and NAT2) polymorphisms and the risk of head and neck cancer (slow vs. rapid acetylators).
Polymorphism Variable   Point Estimate Standard Error Lower Limit Upper Limit Z-Value p-Value
NAT1 Publication year Slope 0.01830 0.01361 −0.00837 0.04497 1.34462 0.17875
Intercept −36.77098 27.26207 −90.20365 16.66169 −1.34880 0.17740
Sample size Slope 0.00027 0.00045 −0.00060 0.00115 0.61240 0.54027
Intercept −0.25993 0.24912 −0.74819 0.22833 −1.04340 0.29676
Mean age of cases Slope −0.01179 0.03248 −0.07546 0.05186 −0.36300 0.71660
Intercept 0.57037 1.93376 −3.21972 4.36047 0.29496 0.76803
Mean age of controls Slope −0.02263 0.03624 −0.09365 0.04839 −0.62459 0.53224
Intercept 1.17938 2.13386 −3.00290 5.36167 0.55270 0.58047
Male percentage of cases Slope −0.01131 0.01256 −0.03593 0.01331 −0.90074 0.36773
Intercept 0.86738 1.11137 −1.31087 3.04562 0.78046 0.43512
Male percentage of controls Slope −0.00268 0.00617 −0.01478 0.00942 −0.43474 0.066375
Intercept 0.03230 0.43459 −0.81948 0.88409 0.07433 0.94074
NAT2 Publication year Slope 0.00944 0.01016 −0.01047 0.02934 0.092942 0.35267
Intercept −18.82284 20.36308 −58.73373 21.08806 −0.92436 0.35530
Sample size Slope −0.00080 0.00020 −0.00120 −0.00040 −3.91239 0.00009
Intercept 0.50882 0.11300 0.28733 0.73030 4.50265 0.00001
Mean age of cases Slope −0.04050 0.01356 −0.06706 −0.01393 −2.098776 0.00281
Intercept 2.47888 0.80007 0.91077 4.04699 3.09832 0.00195
Mean age of controls Slope −0.00438 0.00889 −0.02180 0.01305 −0.49203 0.62270
Intercept 0.34691 0.47403 −0.58217 1.27600 0.73184 0.46427
Male percentage of cases Slope −0.0629 0.00393 −0.01399 0.00141 −1.60201 0.10915
Intercept 0.57366 0.33428 −0.08152 1.22884 1.71610 0.08614
Male percentage of controls Slope −0.00785 0.00289 −0.01351 −0.00219 −2.71989 0.00653
Intercept 0.64373 0.22152 0.20956 1.07790 2.90598 0.00366

3. Current Insights

This meta-analysis showed a significant relationship between NAT2 polymorphisms and the HNC susceptibility with slow acetylators being at higher risk for HNC than rapid acetylators. For NAT2 polymorphism, the ethnicity, the control source, and genotyping methods could modify the association of this polymorphism and the HNC risk. In addition, TSA showed the amount of information for the association between the polymorphisms (NAT1 and NAT2) and the HNC risk was not large enough.
The findings from studies exploring the association of NAT1 polymorphism with other cancers and HNC are different. One meta-analysis [24] found NAT1 polymorphism to be related to the risk of lung, colorectal, head and neck, bladder, and gastric carcinomas, but not with prostate, breast, and pancreatic carcinomas and non-Hodgkin’s lymphoma. Varzim et al. [40] checked the association between NAT1 polymorphism and the laryngeal cancer risk and found that the association depends on tumor location. Among the eight studies included in our meta-analyses [23][41][31][32][37][40][46][54] which evaluated the association between NAT1 polymorphism and the HNC risk, just one study [41] reported a protective role of NAT1 slow acetylators in the HNC patients while the rest of the studies did not find any association.
Comparing the individual studies included in the meta-analysis, differences were observed between the studies. For example, five studies [34][39][42][49] found an elevated risk of HNC for NAT2 slow acetylators, one found a protective role of these acetylators in HNC patients, and three did not find any association between NAT2 polymorphism and the HNC risk [23][38][43].
Effective factors on the association between NAT polymorphisms and the risk of HNC were not included in our analysis due to low numbers of studies, including smoking, gene combination, and the linkage disequilibrium. One study [34] found an elevated frequency of the NAT2 slow acetylator genotypes among HNC patients who smoked less than those who smoked more frequently. Another study reported an association in cases with a smoking history ≤30 years in duration [41]. These contradictory results [41][34][39] suggest the need to evaluate the effect of NAT polymorphisms independent of the history of smoking. In addition, assessing the frequencies of gene-gene combination (NAT2 with GSTM1, XPD, and CYP1A1) between cases with laryngeal cancer and the controls, the frequency of combinations was superior to cases than in controls where the numbers of combinations had an increased risk of laryngeal cancer and the numbers of other combinations had a protective role [33]. The linkage disequilibrium between the genes of NAT1 and NAT2 has been observed in HNC [23][31][56] and other cancers [57][58][59]. Research [60] showed the highest level of carcinogen-DNA adducts formation in cases with acetylation activity of NAT1 rapid and NAT2 slow. Therefore, future studies should consider the linkage between these polymorphisms.

4. Conclusions

There was no association between NAT1 polymorphism and susceptibility to HNC, whereas an association between and NAT2 polymorphism and the HNC risk was found. Slow acetylators of NAT2 polymorphism were at greater risk for HNC than the rapid acetylators. Despite the stability of the results, the presence of high heterogeneity, publication bias, and confounding factors warrant the need for more studies to confirm the results of the present meta-analysis as well as TSA.

This entry is adapted from 10.3390/medicina57101095

References

  1. Rezaei, F.; Mohammadi, H.; Heydari, M.; Sadeghi, M.; Mozaffari, H.R.; Khavid, A.; Godiny, M.; Brand, S.; M Dürsteler, K.; Brühl, A.B.; et al. Association between IL-8 (-251T/A) and IL-6 (-174G/C) Polymorphisms and Oral Cancer Susceptibility: A Systematic Review and Meta-Analysis. Medicina 2021, 57, 405.
  2. Patterson, R.H.; Fischman, V.G.; Wasserman, I.; Siu, J.; Shrime, M.G.; Fagan, J.J.; Koch, W.; Alkire, B.C. Global burden of head and neck cancer: Economic consequences, health, and the role of surgery. Otolaryngol.–Head Neck Surg. 2020, 162, 296–303.
  3. Vos, T.; Abajobir, A.A.; Abate, K.H.; Abbafati, C.; Abbas, K.M.; Abd-Allah, F.; Abdulkader, R.S.; Abdulle, A.M.; Abebo, T.A.; Abera, S.F. Global, regional, and national incidence, prevalence, and years lived with disability for 328 diseases and injuries for 195 countries, 1990–2016: A systematic analysis for the Global Burden of Disease Study 2016. Lancet 2017, 390, 1211–1259.
  4. Foreman, K.J.; Marquez, N.; Dolgert, A.; Fukutaki, K.; Fullman, N.; McGaughey, M.; Pletcher, M.A.; Smith, A.E.; Tang, K.; Yuan, C.-W. Forecasting life expectancy, years of life lost, and all-cause and cause-specific mortality for 250 causes of death: Reference and alternative scenarios for 2016—40 for 195 countries and territories. Lancet 2018, 392, 2052–2090.
  5. Nigro, C.L.; Denaro, N.; Merlotti, A.; Merlano, M. Head and neck cancer: Improving outcomes with a multidisciplinary approach. Cancer Manag. Res. 2017, 9, 363.
  6. Weinberger, P.M.; Yu, Z.; Haffty, B.G.; Kowalski, D.; Harigopal, M.; Brandsma, J.; Sasaki, C.; Joe, J.; Camp, R.L.; Rimm, D.L. Molecular classification identifies a subset of human papillomavirus–associated oropharyngeal cancers with favorable prognosis. J. Clin. Oncol. 2006, 24, 736–747.
  7. Johnson, D.E.; Burtness, B.; Leemans, C.R.; Lui, V.W.Y.; Bauman, J.E.; Grandis, J.R. Head and neck squamous cell carcinoma. Nat. Rev. Dis. Primers 2020, 6, 1–22.
  8. Mozaffari, H.R.; Rostamnia, M.; Sharifi, R.; Safaei, M.; Zavattaro, E.; Tadakamadla, S.K.; Imani, M.M.; Sadeghi, M.; Golshah, A.; Moradpoor, H. A PRISMA-compliant meta-analysis on association between X-ray repair cross complementing (XRCC1, XRCC2, and XRCC3) polymorphisms and oral cancer susceptibility. Gene 2021, 781, 145524.
  9. Rezaei, F.; Doulatparast, D.; Sadeghi, M. Common polymorphisms of Interleukin-10 (-1082A/G,-592A/C, and-819C/T) in oral cancers: An updated meta-analysis. J. Interferon Cytokine Res. 2020, 40, 357–369.
  10. Xia, S.; Wu, S.; Wang, M. The Association Between the XRCC1 Arg399Gln Polymorphism and the Risk of Head and Neck Cancer: An Updated Meta-Analysis Including 14586 Subjects. Technol. Cancer Res. Treat. 2021, 20, 15330338211033060.
  11. Wu, T.; Zhang, Z.T.; Li, L.; Liu, R.Y.; Bei, B.T. Correlation between hypoxia-inducible factor-1α C1772T/G1790A polymorphisms and head and neck cancer risk: A meta-analysis. World J. Surg. Oncol. 2021, 19, 210.
  12. Vineis, P. Epidemiology of cancer from exposure to arylamines. Environ. Health Perspect. 1994, 102, 7–10.
  13. Bartsch, H.; Malaveille, C.; Friesen, M.; Kadlubar, F.; Vineis, P. Black (air-cured) and blond (flue-cured) tobacco cancer risk IV: Molecular dosimetry studies implicate aromatic amines as bladder carcinogens. Eur. J. Cancer 1993, 29, 1199–1207.
  14. Hein, D.W.; Doll, M.A.; Rustan, T.D.; Gray, K.; Feng, Y.; Ferguson, R.J.; Grant, D.M. Metabolic activation and deactivation of arylamine carcinogens by recombinant human NAT1 and polymorphic NAT2 acetyltransferases. Carcinogenesis 1993, 14, 1633–1638.
  15. Hein, D.W.; Doll, M.A.; Fretland, A.J.; Leff, M.A.; Webb, S.J.; Xiao, G.H.; Devanaboyina, U.-S.; Nangju, N.A.; Feng, Y. Molecular genetics and epidemiology of the NAT1 and NAT2 acetylation polymorphisms. Cancer Epidemiol. Prev. Biomark. 2000, 9, 29–42.
  16. Vatsis, K.P.; Weber, W.W. Structural heterogeneity of Caucasian N-acetyltransferase at the NAT1 gene locus. Arch. Biochem. Biophys. 1993, 301, 71–76.
  17. Feki-Tounsi, M.; Khlifi, R.; Louati, I.; Fourati, M.; Mhiri, M.-N.; Hamza-Chaffai, A.; Rebai, A. Polymorphisms in XRCC1, ERCC2, and ERCC3 DNA repair genes, CYP1A1 xenobiotic metabolism gene, and tobacco are associated with bladder cancer susceptibility in Tunisian population. Environ. Sci. Pollut. Res. 2017, 24, 22476–22484.
  18. Imam, H.; Imam, T.; Abbas, S.Z.; Ismail, M.; Muhammad, S.A. Association study of NAT2 gene polymorphism and risk of oral cancer in Southern Punjab, Pakistan. J. Pak. Med Assoc. 2021, 71, 1954–1958.
  19. Sabbagh, N.; Delaporte, E.; Marez, D.; Lo-Guidice, J.-M.; Piette, F.; Broly, F. NAT2 genotyping and efficacy of sulfasalazine in patients with chronic discoid lupus erythematosus. Pharmacogenetics 1997, 7, 131–135.
  20. Wang, L.; Minchin, R.F.; Butcher, N.J. Arylamine N-acetyltransferase 1 protects against reactive oxygen species during glucose starvation: Role in the regulation of p53 stability. PLoS ONE 2018, 13, e0193560.
  21. Minchin, R.F. Acetylation of p-aminobenzoylglutamate, a folic acid catabolite, by recombinant human arylamine N-acetyltransferase and U937 cells. Biochem. J. 1995, 307, 1–3.
  22. Boccia, S.; Cadoni, G.; Sayed-Tabatabaei, F.A.; Volante, M.; Arzani, D.; De Lauretis, A.; Cattel, C.; Almadori, G.; Van Duijn, C.M.; Paludetti, G. CYP1A1, CYP2E1, GSTM1, GSTT1, EPHX1 exons 3 and 4, and NAT2 polymorphisms, smoking, consumption of alcohol and fruit and vegetables and risk of head and neck cancer. J. Cancer Res. Clin. Oncol. 2008, 134, 93–100.
  23. Henning, S.; Cascorbi, I.; Münchow, B.; Jahnke, V.; Roots, I. Association of arylamine N-acetyltransferases NAT1 and NAT2 genotypes to laryngeal cancer risk. Pharmacogenetics 1999, 9, 103–111.
  24. Zhang, K.; Gao, L.; Wu, Y.; Chen, J.; Lin, C.; Liang, S.; Su, J.; Ye, J.; He, X. NAT1 polymorphisms and cancer risk: A systematic review and meta-analysis. Int. J. Clin. Exp. Med. 2015, 8, 9177.
  25. Zheng, Y.; Li, Y.; Teng, Y.; Zhang, Z.; Cao, X. Association of NAT2 phenotype with risk of head and neck carcinoma: A meta-analysis. Oncol. Lett. 2012, 3, 429–434.
  26. Zhuo, X.-L.; Ling, J.-J.; Zhou, Y.; Zhao, H.-Y.; Song, Y.-F.; Tan, Y.-H. NAT2 polymorphisms with oral carcinoma susceptibility: A meta-analysis. Mol. Biol. Rep. 2012, 39, 8813–8819.
  27. Ying, X.-J.; Dong, P.; Shen, B.; Wang, J.; Wang, S.; Wang, G. Possible association of NAT2 polymorphism with laryngeal cancer risk: An evidence-based meta-analysis. J. Cancer Res. Clin. Oncol. 2011, 137, 1661–1667.
  28. Zhang, L.; Xiang, Z.; Hao, R.; Li, R.; Zhu, Y. N-acetyltransferase 2 genetic variants confer the susceptibility to head and neck carcinoma: Evidence from 23 case–control studies. Tumor Biol. 2014, 35, 3585–3595.
  29. Chen, C.; Ricks, S.; Doody, D.R.; Fitzgibbons, E.D.; Porter, P.L.; Schwartz, S.M. N-Acetyltransferase 2 polymorphisms, cigarette smoking and alcohol consumption, and oral squamous cell cancer risk. Carcinogenesis 2001, 22, 1993–1999.
  30. Chatzimichalis, M.; Xenellis, J.; Tzagaroulakis, A.; Sarof, P.; Banis, K.; Gazouli, M.; Bibas, A. GSTT1, GSTM1, GSTM3 and NAT2 polymorphisms in laryngeal squamous cell carcinoma in a Greek population. J. Laryngol. Otol. 2010, 124, 318–323.
  31. Demokan, S.; Suoglu, Y.; Gözeler, M.; Demir, D.; Dalay, N. N-acetyltransferase 1 and 2 gene sequence variants and risk of head and neck cancer. Mol. Biol. Rep. 2010, 37, 3217–3226.
  32. Fronhoffs, S.; Brüning, T.; Ortiz-Pallardo, E.; Bröde, P.; Koch, B.; Harth, V.; Sachinidis, A.; Bolt, H.M.; Herberhold, C.; Vetter, H. Real-time PCR analysis of the N-acetyltransferase NAT1 allele* 3,* 4,* 10,* 11,* 14 and* 17 polymorphism in squamous cell cancer of head and neck. Carcinogenesis 2001, 22, 1405–1412.
  33. Gajecka, M.; Rydzanicz, M.; Jaskula-Sztul, R.; Kujawski, M.; Szyfter, W.; Szyfter, K. CYP1A1, CYP2D6, CYP2E1, NAT2, GSTM1 and GSTT1 polymorphisms or their combinations are associated with the increased risk of the laryngeal squamous cell carcinoma. Mutat. Res. Fundam. Mol. Mech. Mutagenesis 2005, 574, 112–123.
  34. Gonzalez, M.; Alvarez, V.; Pello, M.; Menendez, M.; Suarez, C.; Coto, E. Genetic polymorphism of N-acetyltransferase-2, glutathione S-transferase-M1, and cytochromes P450IIE1 and P450IID6 in the susceptibility to head and neck cancer. J. Clin. Pathol. 1998, 51, 294–298.
  35. Hahn, M.; Hagedorn, G.; Kuhlisch, E.; Schackert, H.K.; Eckelt, U. Genetic polymorphisms of drug-metabolizing enzymes and susceptibility to oral cavity cancer. Oral Oncol. 2002, 38, 486–490.
  36. Harth, V.; Schäfer, M.; Abel, J.; Maintz, L.; Neuhaus, T.; Besuden, M.; Primke, R.; Wilkesmann, A.; Thier, R.; Vetter, H. Head and neck squamous-cell cancer and its association with polymorphic enzymes of xenobiotic metabolism and repair. J. Toxicol. Environ. Health Part A 2008, 71, 887–897.
  37. Jourenkova-Mironova, N.; Wikman, H.; Bouchardy, C.; Mitrunen, K.; Dayer, P.; Benhamou, S.; Hirvonen, A. Role of arylamine N-acetyltransferase 1 and 2 (NAT1 and NAT2) genotypes in susceptibility to oral/pharyngeal and laryngeal cancers. Pharm. Genom. 1999, 9, 533–537.
  38. Rydzanicz, M.; Wierzbicka, M.; Gajęcka, M.; Szyfter, W.; Szyfter, K. The impact of genetic factors on the incidence of multiple primary tumors (MPT) of the head and neck. Cancer Lett. 2005, 224, 263–278.
  39. Ünal, M.; Tamer, L.; Akbaş, Y.; Pata, Y.S.; Vayisoǧlu, Y.; Deǧirmenci, U.; Çamdeviren, H. Genetic polymorphism of N-acetyltransferase 2 in the susceptibility to laryngeal squamous cell carcinoma. Head Neck J. Sci. Spec. Head Neck 2005, 27, 1056–1060.
  40. Varzim, G.; Monteiro, E.; Silva, R.; Pinheiro, C.; Lopes, C. Polymorphisms of arylamine N-acetyltransferase (NAT1 and NAT2) and larynx cancer susceptibility. ORL 2002, 64, 206–212.
  41. Katoh, T.; Kaneko, S.; Boissy, R.; Watson, M.; Ikemura, K.; Bell, D.A. A pilot study testing the association between N-acetyltransferases 1 and 2 and risk of oral squamous cell carcinoma in Japanese people. Carcinogenesis 1998, 19, 1803–1807.
  42. Balaji, L.; Krishna, B.S.; Bhaskar, L. An unlikely role for the NAT2 genotypes and haplotypes in the oral cancer of south Indians. Arch. Oral Biol. 2012, 57, 513–518.
  43. Cheng, Y.-J.; Chien, Y.-C.; Hildesheim, A.; Hsu, M.-M.; Chen, I.-H.; Chuang, J.; Chang, J.; Ma, Y.D.; Luo, C.-T.; Hsu, W.-L. No association between genetic polymorphisms of CYP1A1, GSTM1, GSTT1, GSTP1, NAT2, and nasopharyngeal carcinoma in Taiwan. Cancer Epidemiol. Prev. Biomark. 2003, 12, 179–180.
  44. Hou, Y.-Y.; Ou, H.-L.; Chu, S.-T.; Wu, P.-C.; Lu, P.-J.; Chi, C.-C.; Leung, K.-W.; Lee, C.-Y.; Wu, P.-H.; Hsiao, M. NAT2 slow acetylation haplotypes are associated with the increased risk of betel quid–related oral and pharyngeal squamous cell carcinoma. Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endodontol. 2011, 112, 484–492.
  45. Lei, D.; Pan, X.; Guo, C.; Xu, F.; Zhang, L.; Liu, D.; Luan, X. Relationship between polymorphism of N-acetyltransferase 2 and genetic susceptibility to laryngeal carcinoma. Zhonghua Zhong Liu Za Zhi 2002, 24, 154–156.
  46. Majumder, M.; Ghosh, S.; Roy, B. Association between polymorphisms at N-acetyltransferase 1 (NAT1) & risk of oral leukoplakia & cancer. Indian J. Med Res. 2012, 136, 605.
  47. Majumder, M.; Sikdar, N.; Ghosh, S.; Roy, B. Polymorphisms at XPD and XRCC1 DNA repair loci and increased risk of oral leukoplakia and cancer among NAT2 slow acetylators. Int. J. Cancer 2007, 120, 2148–2156.
  48. Morita, S.; Yano, M.; Tsujinaka, T.; Akiyama, Y.; Taniguchi, M.; Kaneko, K.; Miki, H.; Fujii, T.; Yoshino, K.; Kusuoka, H. Genetic polymorphisms of drug-metabolizing enzymes and susceptibility to head-and-neck squamous-cell carcinoma. Int. J. Cancer 1999, 80, 685–688.
  49. Tian, S.; Zhang, J.; Yuan, X.; Huang, M.; Guo, Z.; Chen, F.; Li, Q.; Guan, Z. The association between genetic polymorphisms of NAT1, NAT2 and susceptibility to laryngeal squamous carcinoma (LSCC) in Han population in Guangdong China. J. Modern Oncol. 2013, 6, 1213–1218.
  50. Buch, S.C.; Nazar-Stewart, V.; Weissfeld, J.L.; Romkes, M. Case–control study of oral and oropharyngeal cancer in whites and genetic variation in eight metabolic enzymes. Head Neck J. Sci. Spec. Head Neck 2008, 30, 1139–1147.
  51. Gara, S.; Abdennebi, M.; Chatti, S.; Touati, S.; Ladgham, A.; Guemira, F. Association of NAT2 gene substitution mutation T341C with increased risk for head and neck cancer in Tunisia. Acta Oncol. 2007, 46, 834–837.
  52. Marques, C.F.; Koifman, S.; Koifman, R.J.; Boffetta, P.; Brennan, P.; Hatagima, A. Influence of CYP1A1, CYP2E1, GSTM3 and NAT2 genetic polymorphisms in oral cancer susceptibility: Results from a case-control study in Rio de Janeiro. Oral Oncol. 2006, 42, 632–637.
  53. Marques, C.R.; Da Silva, T.M.; De Albuquerque, D.M.; Chaves, M.S.; Marques Filho, M.F.; Oliveira, J.S.; Di Pietro, G.; Sousa, S.M.B.; Simoes, A.L.; Rios-Santos, F. NAT2, XRCC1 and hOGG1 polymorphisms, cigarette smoking, alcohol consumption and risk of upper aerodigestive tract cancer. Anticancer. Res. 2014, 34, 3217–3224.
  54. Olshan, A.F.; Weissler, M.C.; Watson, M.A.; Bell, D.A. GSTM1, GSTT1, GSTP1, CYP1A1, and NAT1 polymorphisms, tobacco use, and the risk of head and neck cancer. Cancer Epidemiol. Prev. Biomark. 2000, 9, 185–191.
  55. Richardson, M.; Garner, P.; Donegan, S. Interpretation of subgroup analyses in systematic reviews: A tutorial. Clin. Epidemiol. Glob. Health 2019, 7, 192–198.
  56. Hickman, D.; Risch, A.; Buckle, V.; Spurr, N.; Jeremiah, S.; McCarthy, A.; Sim, E. Chromosomal localization of human genes for arylamine N-acetyltransferase. Biochem. J. 1994, 297, 441–445.
  57. Moslehi, R.; Chatterjee, N.; Church, T.R.; Chen, J.; Yeager, M.; Weissfeld, J.; Hein, D.W.; Hayes, R.B. Cigarette smoking, N-acetyltransferase genes and the risk of advanced colorectal adenoma. Future Med. 2006, 7, 819–829.
  58. Cascorbi, I.; Roots, I.; Brockmöller, J. Association of NAT1 and NAT2 polymorphisms to urinary bladder cancer: Significantly reduced risk in subjects with NAT1* 10. Cancer Res. 2001, 61, 5051–5056.
  59. Chen, J.; Stampfer, M.J.; Hough, H.L.; Garcia-Closas, M.; Willett, W.C.; Hennekens, C.H.; Kelsey, K.T.; Hunter, D.J. A prospective study of N-acetyltransferase genotype, red meat intake, and risk of colorectal cancer. Cancer Res. 1998, 58, 3307–3311.
  60. Badawi, A.F.; Hirvonen, A.; Bell, D.A.; Lang, N.P.; Kadlubar, F.F. Role of aromatic amine acetyltransferases, NAT1 and NAT2, in carcinogen-DNA adduct formation in the human urinary bladder. Cancer Res. 1995, 55, 5230–5237.
More
Information
Subjects: Biology
Contributor:
View Times: 16
Revisions: 2 times (View History)
Update Time: 22 Oct 2021
Table of Contents

    Confirm

    Are you sure to Delete?

    Video Upload Options

    Do you have a full video?
    Cite
    If you have any further questions, please contact Encyclopedia Editorial Office.
    Sadeghi, M. Susceptibility to Head and Neck Cancers. Encyclopedia. Available online: https://encyclopedia.pub/entry/15280 (accessed on 23 May 2022).
    Sadeghi M. Susceptibility to Head and Neck Cancers. Encyclopedia. Available at: https://encyclopedia.pub/entry/15280. Accessed May 23, 2022.
    Sadeghi, Masoud. "Susceptibility to Head and Neck Cancers," Encyclopedia, https://encyclopedia.pub/entry/15280 (accessed May 23, 2022).
    Sadeghi, M. (2021, October 22). Susceptibility to Head and Neck Cancers. In Encyclopedia. https://encyclopedia.pub/entry/15280
    Sadeghi, Masoud. ''Susceptibility to Head and Neck Cancers.'' Encyclopedia. Web. 22 October, 2021.
    Share
    Download
    Cite
    Top