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Journal articles on the topic 'ADH1C'

Author: Grafiati

Published: 4 June 2021

Last updated: 14 February 2022

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1

Ayuso, Pedro, Elena García-Martín, José A. Cornejo-García, José A. G. Agúndez, and José María Ladero. "Genetic Variants of Alcohol Metabolizing Enzymes and Alcohol-Related Liver Cirrhosis Risk." Journal of Personalized Medicine 11, no. 5 (2021): 409. http://dx.doi.org/10.3390/jpm11050409.

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Alcohol-related liver disease (ARLD) is a major public health issue caused by excessive alcohol consumption. ARLD encompasses a wide range of chronic liver lesions, alcohol-related liver cirrhosis being the most severe and harmful state. Variations in the genes encoding the enzymes, which play an active role in ethanol metabolism, might influence alcohol exposure and hence be considered as risk factors of developing cirrhosis. We conducted a case-control study in which 164 alcohol-related liver cirrhosis patients and 272 healthy controls were genotyped for the following functional single nucleotide variations (SNVs): ADH1B gene, rs1229984, rs1041969, rs6413413, and rs2066702; ADH1C gene, rs35385902, rs283413, rs34195308, rs1693482, and rs35719513; CYP2E1 gene, rs3813867. Furthermore, copy number variations (CNVs) for ADH1A, ADH1B, ADH1C, and CYP2E1 genes were analyzed. A significant protective association with the risk of developing alcohol-related liver cirrhosis was observed between the mutant alleles of SNVs ADH1B rs1229984 (Pc value = 0.037) and ADH1C rs283413 (Pc value = 0.037). We identified CNVs in all genes studied, ADH1A gene deletions being more common in alcohol-related liver cirrhosis patients than in control subjects, although the association lost statistical significance after multivariate analyses. Our findings support that susceptibility to alcohol-related liver cirrhosis is related to variations in alcohol metabolism genes.

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2

Tóth, Réka, Szilvia Fiatal, Beáta Petrovski, Martin McKee, and Róza Ádány. "Combined Effect of ADH1B RS1229984, RS2066702 and ADH1C RS1693482/ RS698 Alleles on Alcoholism and Chronic Liver Diseases." Disease Markers 31, no. 5 (2011): 267–77. http://dx.doi.org/10.1155/2011/350528.

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The aim of this study was to analyze the combined effect of the most frequent alcohol dehydrogenase polymorphisms (Arg48His and Arg370Cys in ADH1B, Arg272Gln and Ile350Val in ADH1C) on the alcohol use habits, alcohol dependence and chronic liver diseases in Hungary.The study included men, aged 45–64 years. Altogether, 241 cases with chronic liver disease (CLD) and 666 randomly selected controls without CLD were analysed for all four polymorphisms. Associations between the polymorphisms, individually, and in combination, and excessive and problem drinking and CLD, were assessed using logistic regression.In this study we have identified a novel mutation, called ADH1B Arg370His. The ADH1C Arg272Gln and Ile350Val showed almost complete linkage. The 272Gln/350Val allele increased the risk of excessive and problem drinking in homozygous form (OR = 1.582,p= 0.035, CI = 1.034–2.421, OR = 1.780,p= 0.016, CI = 1.113–2.848, respectively). The joint analysis showed that when combined with the wild type ADH1C Arg272/Ile350 allele, the ADH1B 48His is protective against CLD (OR = 0.368,p= 0.019, CI = 0.159–0.851).The results obtained in the study help not only to clarify the effects of different ADH SNPs but to better understand how these polymorphisms modify each other’s effects in the development of alcoholism and related diseases.

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3

Cleveland, H. Harrington, Gabriel L. Schlomer, David J. Vandenbergh, et al. "Associations between alcohol dehydrogenase genes and alcohol use across early and middle adolescence: Moderation × Preventive intervention." Development and Psychopathology 30, no. 1 (2017): 297–313. http://dx.doi.org/10.1017/s0954579417000633.

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AbstractData from the in-school sample of the PROSPER preventive intervention dissemination trial were used to investigate associations between alcohol dehydrogenase genes and alcohol use across adolescence, and whether substance misuse interventions in the 6th and 7th grades (targeting parenting, family functioning, social norms, youth decision making, and peer group affiliations) modified associations between these genes and adolescent use. Primary analyses were run on a sample of 1,885 individuals and included three steps. First, we estimated unconditional growth curve models with separate slopes for alcohol use from 6th to 9th grade and from 9th to 12th grade, as well as the intercept at Grade 9. Second, we used intervention condition and three alcohol dehydrogenase genes, 1B (ADH1B), 1C (ADH1C), and 4 (ADH4) to predict variance in slopes and intercept. Third, we examined whether genetic influences on model slopes and intercepts were moderated by intervention condition. The results indicated that the increase in alcohol use was greater in early adolescence than in middle adolescence; two of the genes, ADH1B and ADH1C, significantly predicted early adolescent slope and Grade 9 intercept, and associations between ADH1C and both early adolescent slope and intercept were significantly different across control and intervention conditions.

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4

Mohelnikova-Duchonova, Beatrice, David Vrana, Ivana Holcatova, Miroslav Ryska, Zdenek Smerhovsky, and Pavel Soucek. "CYP2A13, ADH1B, and ADH1C Gene Polymorphisms and Pancreatic Cancer Risk." Pancreas 39, no. 2 (2010): 144–48. http://dx.doi.org/10.1097/mpa.0b013e3181bab6c2.

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5

Ji, Yong Bae, Seung Hwan Lee, Kyung Rae Kim, et al. "Association between ADH1B and ADH1C polymorphisms and the risk of head and neck squamous cell carcinoma." Tumor Biology 36, no. 6 (2015): 4387–96. http://dx.doi.org/10.1007/s13277-015-3078-y.

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6

Rebello, André Soares, and Maria da Glória Da Costa Carvalho. "Metodologia para estudo do polimorfismo do gene da enzima álcool desidrogenase." Revista de Ciências Médicas e Biológicas 7, no. 2 (2008): 163. http://dx.doi.org/10.9771/cmbio.v7i2.4445.

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As principais enzimas responsáveis pelo metabolismo do álcool são a álcool desidrogenase (ADH) e aldeído desidrogenase (ALDH). EsSas enzimas estão presentes em várias formas e são codificadas por diferentes genes. Alguns desses genes apresentam polimorfismos, e as enzimas codificadas por eles podem apresentar diferenças quanto à eficiência metabólica em relação ao álcool e ao aldeído acético. EsSa variação tem se mostrado um fator que influencia a quantidade de álcool ingerido e o risco no aumento de abuso e dependência ao álcool. Neste trabalho, nós descrevemos um método que permite estudar o polimorfismo de um dos genes da enzima álcool desidrogenase, o gene ADH1C. O DNA foi isolado de doadores e o polimorfismo foi determinado pela reação em cadeia pela polimerase (PCR). Nossos resultados confirmam a viabilidade da técnica por nós descrita para o estudo do polimorfismo do gene ADH1C.

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7

Dannenberg, Luke O., Hui-Ju Chen, Huijun Tian, and Howard J. Edenberg. "Differential Regulation of the Alcohol Dehydrogenase 1B (ADH1B) and ADH1C Genes by DNA Methylation and Histone Deacetylation." Alcoholism: Clinical and Experimental Research 30, no. 6 (2006): 928–37. http://dx.doi.org/10.1111/j.1530-0277.2006.00107.x.

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8

Wang, Jiwen, Jinyu Wei, Xiaoling Xu, et al. "Replication Study of ESCC Susceptibility Genetic Polymorphisms Locating in the ADH1B-ADH1C-ADH7 Cluster Identified by GWAS." PLoS ONE 9, no. 4 (2014): e94096. http://dx.doi.org/10.1371/journal.pone.0094096.

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9

Mulligan, Connie J., Robert W. Robin, Michael V. Osier, et al. "Allelic variation at alcohol metabolism genes ( ADH1B , ADH1C , ALDH2 ) and alcohol dependence in an American Indian population." Human Genetics 113, no. 4 (2003): 325–36. http://dx.doi.org/10.1007/s00439-003-0971-z.

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10

van Beek, Jenny H. D. A., Gonneke Willemsen, Marleen H. M. de Moor, Jouke Jan Hottenga, and Dorret I. Boomsma. "Associations Between ADH Gene Variants and Alcohol Phenotypes in Dutch Adults." Twin Research and Human Genetics 13, no. 1 (2010): 30–42. http://dx.doi.org/10.1375/twin.13.1.30.

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AbstractRecently, Macgregor et al. (2009) demonstrated significant associations of ADH polymorphisms with reactions to alcohol and alcohol consumption measures in an Australian sample. The aim of the present study was to replicate these findings in a Dutch sample. Survey data on alcohol phenotypes came from 1,754 unrelated individuals registered with the Netherlands Twin Register. SNPs in the ADH gene cluster located on chromosome 4q (n= 491) were subdivided in seven gene sets: ADH5, ADH4, ADH6, ADH1A, ADH1B, ADH1C and ADH7. Within these sets associations of SNPs with alcohol consumption measures, age at onset variables, reactions to alcohol and problem drinking liability were examined. Of the original 38 SNPs studied by Macgregor et al. (2009), six SNPs were not available in our dataset, because one of them had a minor allele frequency < .01 (rs1229984) and five could not be imputed. The remaining SNP associations with alcohol phenotypes as identified by Macgregor et al. (2009) were not replicated in the Dutch sample, after correcting for multiple genotype and phenotype testing. Significant associations were found however, for reactions to alcohol with a SNP in ADH5 (rs6827292,p= .001) and a SNP just upstream of ADH5 (rs6819724,p= .0007) that is in strong LD with rs6827292. Furthermore, an association between age at onset of regular alcohol use and a SNP just upstream of ADH7 (rs2654849,p= .003) was observed. No significant associations were found for alcohol consumption and problem drinking liability. Although these findings do not replicate the earlier findings at the SNP level, the results confirm the role of the ADH gene cluster in alcohol phenotypes.

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11

Rebello, André Soares, Rodrigo Moura-Neto, and Maria da Glória da Costa Carvalho. "Association study of the Ile349val polymorphism of the gene ADH1C and alcohol dependence." Jornal Brasileiro de Psiquiatria 60, no. 1 (2011): 7–10. http://dx.doi.org/10.1590/s0047-20852011000100002.

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OBJECTIVE: The aim of this study was to investigate the polymorphism Ile349Val of the enzyme alcohol dehydrogenase ADH1C gene among individuals with alcohol dependence syndrome (ADS) attending Alcoholics Anonymous (AA) meetings. METHODS: A total of 120 subjects residing in Rio de Janeiro city participated in this study. Subjects were divided into two groups: a group consisting of 54 individuals from the ADS group and 66 individuals that declared not having any alcohol dependence (control group). DNA was extracted from mouth epithelial cells by phenol-chloroform method and further submitted to amplification by polymerase chain reaction (PCR). RESULTS: Our results did not show differences between the genotypes of control individuals and ADS subjects. Nevertheless, we found increased rates of alcoholism in families of ADS subjects as compared to controls. CONCLUSIONS: Our results did not show any genotype difference on the ADH1C gene when control and AA genotypes are compared.

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12

Ueta, Mayumi, Chie Sotozono, Hiromi Nishigaki, et al. "Gene expression analysis of conjunctival epithelium of patients with Stevens-Johnson syndrome in the chronic stage." BMJ Open Ophthalmology 4, no. 1 (2019): e000254. http://dx.doi.org/10.1136/bmjophth-2018-000254.

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ObjectiveTo investigate the pathology underlying the ocular surface complications of patients with Stevens-Johnson syndrome (SJS) in the chronic stage.Methods and analysisUsing oligonucleotide microarrays, we performed comprehensive gene expression analysis of the conjunctival epithelium of patients with SJS in the chronic stage (n=3). The controls were patients with conjunctival chalasis (n=3). We confirmed the downregulation and upregulation of transcripts of interest by quantitative real-time PCR (RT-PCR) assay. The expression of ocular surface protein with significantly upregulated transcripts was assessed immunohistochemically.ResultsCompared with the controls, in the conjunctival epithelium of patients with SJS, 50 transcripts were downregulated by less than one-tenth (analysis of variance (ANOVA) p<0.05). Transcripts MUC7, PIGR, HEPACAM2, ADH1C and SMR3A were downregulated by less than one-fiftieth. 65 transcripts were upregulated more than 10- fold; the difference between patients with SJS and the controls was significant (ANOVA p<0.05). There were 14 transcripts that were upregulated more than 50-fold; they were SERPINB4, KRT1, KRTDAP, S100A7, SBSN, KLK6, SERPINB12, PNLIPRP3, CASP14, ODZ2, CA2, CRCT1, CWH43 and FLG. Quantitative RT-PCR of conjunctival epithelium samples from 11 patients with SJS and 26 controls showed that the gene expression of PIGR, HEPACAM2 and ADH1C was significantly downregulated while the gene expression of ODZ2 (teneurin-2) was significantly upregulated in patients with SJS. We document that teneurin-2 protein can be expressed in human conjunctival epithelium.ConclusionOur results suggest that the downregulation of PIGR, HEPACAM2 and ADH1C and upregulation of teneurin-2 expression contribute to the pathology of the ocular surface in patients with SJS in the chronic stage.

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13

Høiseth, Gudrun, Per Magnus, Gun Peggy Knudsen, et al. "Is ADH1C genotype relevant for the cardioprotective effect of alcohol?" Alcohol 47, no. 2 (2013): 81–84. http://dx.doi.org/10.1016/j.alcohol.2012.12.005.

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14

Duell, E. J., N. Sala, N. Travier, et al. "Genetic variation in alcohol dehydrogenase (ADH1A, ADH1B, ADH1C, ADH7) and aldehyde dehydrogenase (ALDH2), alcohol consumption and gastric cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort." Carcinogenesis 33, no. 2 (2011): 361–67. http://dx.doi.org/10.1093/carcin/bgr285.

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15

Chang, J. S., K. Straif, and N. Guha. "The role of alcohol dehydrogenase genes in head and neck cancers: a systematic review and meta-analysis of ADH1B and ADH1C." Mutagenesis 27, no. 3 (2011): 275–86. http://dx.doi.org/10.1093/mutage/ger073.

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16

Offermans, Nadine S. M., Shannon M. Ketcham, Piet A. van den Brandt, Matty P. Weijenberg, and Colinda C. J. M. Simons. "Alcohol intake, ADH1B and ADH1C genotypes, and the risk of colorectal cancer by sex and subsite in the Netherlands Cohort Study." Carcinogenesis 39, no. 3 (2018): 375–88. http://dx.doi.org/10.1093/carcin/bgy011.

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17

Lawlor, Debbie A., Marianne Benn, Luisa Zuccolo, et al. "ADH1B and ADH1C Genotype, Alcohol Consumption and Biomarkers of Liver Function: Findings from a Mendelian Randomization Study in 58,313 European Origin Danes." PLoS ONE 9, no. 12 (2014): e114294. http://dx.doi.org/10.1371/journal.pone.0114294.

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18

Konishi, Tamiko, Huai-Rong Luo, Maria Calvillo, Matthew S. Mayo, Keh-Ming Lin, and Yu-Jui Yvonne Wan. "ADH1B*1, ADH1C*2, DRD2 (???141C Ins), and 5-HTTLPR Are Associated With Alcoholism in Mexican American Men Living in Los Angeles." Alcoholism: Clinical & Experimental Research 28, no. 8 (2004): 1145–52. http://dx.doi.org/10.1097/01.alc.0000134231.48395.42.

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19

Filopanti, M., A. M. Barbieri, G. Mantovani, et al. "Role of UGT1A1 and ADH gene polymorphisms in pegvisomant-induced liver toxicity in acromegalic patients." European Journal of Endocrinology 170, no. 2 (2014): 247–54. http://dx.doi.org/10.1530/eje-13-0657.

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ContextHepatotoxicity is one of the most serious adverse effects in acromegalic patients treated with pegvisomant (PEG-V). Recent studies have found an association between this adverse event and the UGT1A1 allele 28 polymorphism associated with Gilbert's syndrome.ObjectiveTo determine whether UGT1A1*28 and alcohol dehydrogenase (ADH) polymorphisms influence liver toxicity during PEG-V treatment.Design and settingMulticenter observational retrospective study conducted in 13 tertiary care endocrinology units in Italy.PatientsA total of 112 patients with active disease resistant to somatostatin analogs (SSTa) and 108 controls were enrolled.InterventionsClinical and biochemical data were recorded by electronic clinical reporting forms. Blood or DNA samples were sent to the coordinating center for genotyping.ResultsNo differences in genotypes between patients and controls were found. During PEG-V therapy liver function tests (LFT), abnormalities and overt hepatotoxicity developed in 17 and 4.5% of patients respectively. Logistic and linear regression analyses showed an association between LFT abnormalities during the follow-up visit and prior events of LFT abnormalities in medical history (odds ratio=1.25;P=0.04) and the number of concomitant medications, other than SSTa (B=3.9;P=0.03). No correlation between LFT alterations and UGT1A1 allele 28 as well as ADH1C and B polymorphisms was found.ConclusionsUGT1A1 allele 28 and ADH1C and B polymorphisms do not predict increased risk of hepatotoxicity during PEG-V therapy. Conversely, patients with multi-therapies and with previous episodes of liver disease should be carefully managed, due to the observed association between these conditions and LFT abnormalities during PEG-V therapy.

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20

Ayhan, Yavuz, Şeref Can Gürel, Özgür Karaca, et al. "Association between ADH1C and ALDH2 polymorphisms and alcoholism in a Turkish sample." Nordic Journal of Psychiatry 69, no. 3 (2014): 233–39. http://dx.doi.org/10.3109/08039488.2014.972450.

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21

Xue, Yao, Meilin Wang, Dongyan Zhong, et al. "ADH1C Ile350Val Polymorphism and Cancer Risk: Evidence from 35 Case–Control Studies." PLoS ONE 7, no. 5 (2012): e37227. http://dx.doi.org/10.1371/journal.pone.0037227.

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22

Hidaka, Akihisa, Shizuka Sasazuki, Keitaro Matsuo, et al. "Genetic polymorphisms of ADH1B, ADH1C and ALDH2, alcohol consumption, and the risk of gastric cancer: the Japan Public Health Center-based prospective study." Carcinogenesis 36, no. 2 (2014): 223–31. http://dx.doi.org/10.1093/carcin/bgu244.

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23

Sun, Leimin, Inke R. K??nig, Arne Jacobs, et al. "Mean Corpuscular Volume and ADH1C Genotype in White Patients With Alcohol-Associated Diseases." Alcoholism: Clinical & Experimental Research 29, no. 5 (2005): 788–93. http://dx.doi.org/10.1097/01.alc.0000163500.81691.74.

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24

Ward, A. K., J. J. McKinnon, S. Hendrick, and F. C. Buchanan. "The impact of vitamin A restriction and ADH1C genotype on marbling in feedlot steers1." Journal of Animal Science 90, no. 8 (2012): 2476–83. http://dx.doi.org/10.2527/jas.2011-4404.

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25

Kortunay, S., A. Koseler, C. O. Kara, B. Topuz, and E. O. Atalay. "Frequencies of ADH1C alleles and genotypes in a Turkish head and neck cancer population." Methods and Findings in Experimental and Clinical Pharmacology 32, no. 3 (2010): 187. http://dx.doi.org/10.1358/mf.2010.32.3.1440739.

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Osier, Michael V., Andrew J. Pakstis, David Goldman, Howard J. Edenberg, Judith R. Kidd, and Kenneth K. Kidd. "A Proline-Threonine Substitution in Codon 351 of ADH1C Is Common in Native Americans." Alcoholism: Clinical and Experimental Research 26, no. 12 (2002): 1759–63. http://dx.doi.org/10.1111/j.1530-0277.2002.tb02481.x.

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27

Chen, Hui‐Ju, Huijun Tian, and Howard J. Edenberg. "Natural haplotypes in the regulatory sequences affect human alcohol dehydrogenase 1C ( ADH1C ) gene expression." Human Mutation 25, no. 2 (2005): 150–55. http://dx.doi.org/10.1002/humu.20127.

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Krone, K. G., A. K. Ward, K. M. Madder, S. Hendrick, J. J. McKinnon, and F. C. Buchanan. "Interaction of vitamin A supplementation level with ADH1C genotype on intramuscular fat in beef steers." Animal 10, no. 3 (2016): 403–9. http://dx.doi.org/10.1017/s1751731115002153.

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29

Kohlenberg-M??ller, K., and A. Wolf. "POLYMORPHISM AT THE ADH1C LOCI, ALCOHOL CONSUMPTION PATTERNS AND SENSITITVITY TO ALCOHOL IN HEALTHY VOLUNTEERS." Alcoholism: Clinical & Experimental Research 28, Supplement (2004): 30A. http://dx.doi.org/10.1097/00000374-200408002-00141.

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30

Chen, Hui-Ju, Kristie Carr, Ronald E. Jerome, and Howard J. Edenberg. "A Retroviral Repetitive Element Confers Tissue-Specificity to the Human Alcohol Dehydrogenase 1C (ADH1C) Gene." DNA and Cell Biology 21, no. 11 (2002): 793–801. http://dx.doi.org/10.1089/104454902320908441.

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Zimta, Alina-Andreea, Diana Cenariu, Alexandru Irimie, et al. "The Role of Nrf2 Activity in Cancer Development and Progression." Cancers 11, no. 11 (2019): 1755. http://dx.doi.org/10.3390/cancers11111755.

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Nrf2 is a transcription factor that stimulates the expression of genes which have antioxidant response element-like sequences in their promoter. Nrf2 is a cellular protector, and this principle applies to both normal cells and malignant cells. While healthy cells are protected from DNA damage induced by reactive oxygen species, malignant cells are defended against chemo- or radiotherapy. Through our literature search, we found that Nrf2 activates several oncogenes unrelated to the antioxidant activity, such as Matrix metallopeptidase 9 (MMP-9), B-cell lymphoma 2 (BCL-2), B-cell lymphoma-extra large (BCL-xL), Tumour Necrosis Factor α (TNF-α), and Vascular endothelial growth factor A (VEGF-A). We also did a brief analysis of The Cancer Genome Atlas (TCGA) data of lung adenocarcinoma concerning the effects of radiation therapy and found that the therapy-induced Nrf2 activation is not universal. For instance, in the case of recurrent disease and radiotherapy, we observed that, for the majority of Nrf2-targeted genes, there is no change in expression level. This proves that the universal, axiomatic rationale that Nrf2 is activated as a response to chemo- and radiation therapy is wrong, and that each scenario should be carefully evaluated with the help of Nrf2-targeted genes. Moreover, there were nine genes involved in lipid peroxidation, which showed underexpression in the case of new radiation therapy: ADH1A, ALDH3A1, ALDH3A2, ADH1B, GPX2, ADH1C, ALDH6A1, AKR1C3, and NQO1. This may relate to the fact that, while some studies reported the co-activation of Nrf2 and other oncogenic signaling pathways such as Phosphoinositide 3-kinases (PI3K), mitogen-activated protein kinase (MAPK), and Notch1, other reported the inverse correlation between Nrf2 and the tumor-promoter Transcription Factor (TF), Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). Lastly, Nrf2 establishes its activity through interactions at multiple levels with various microRNAs. MiR-155, miR-144, miR-28, miR-365-1, miR-93, miR-153, miR-27a, miR-142, miR-29-b1, miR-340, and miR-34a, either through direct repression of Nrf2 messenger RNA (mRNA) in a Kelch-like ECH-associated protein 1 (Keap1)-independent manner or by enhancing the Keap1 cellular level, inhibit the Nrf2 activity. Keap1–Nrf2 interaction leads to the repression of miR-181c, which is involved in the Nuclear factor kappa light chain enhancer of activated B cells (NF-κB) signaling pathway. Nrf2’s role in cancer prevention, diagnosis, prognosis, and therapy is still in its infancy, and the future strategic planning of Nrf2-based oncological approaches should also consider the complex interaction between Nrf2 and its various activators and inhibitors.

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Biernacka, Joanna M., Jennifer R. Geske, Terry D. Schneekloth, et al. "Replication of Genome Wide Association Studies of Alcohol Dependence: Support for Association with Variation in ADH1C." PLoS ONE 8, no. 3 (2013): e58798. http://dx.doi.org/10.1371/journal.pone.0058798.

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33

Montane-Jaime, Karelia, Shelley Moore, Samuel Shafe, et al. "ADH1C*2 allele is associated with alcohol dependence and elevated liver enzymes in Trinidad and Tobago." Alcohol 39, no. 2 (2006): 81–86. http://dx.doi.org/10.1016/j.alcohol.2006.08.002.

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34

Hines, Lisa M., David J. Hunter, Meir J. Stampfer, et al. "Alcohol consumption and high-density lipoprotein levels: the effect of ADH1C genotype, gender and menopausal status." Atherosclerosis 182, no. 2 (2005): 293–300. http://dx.doi.org/10.1016/j.atherosclerosis.2005.02.005.

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35

Birley, A. J., J. B. Whitfield, M. C. Neale, et al. "Genetic Time-series Analysis Identifies a Major QTL for in vivo Alcohol Metabolism not Predicted by in vitro Studies of Structural Protein Polymorphism at the ADH1B or ADH1C Loci." Behavior Genetics 35, no. 5 (2005): 509–24. http://dx.doi.org/10.1007/s10519-005-3851-6.

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36

Peng, Dong Qiao, U. Suk Jung, Jae Sung Lee, et al. "Effect of alcohol dehydrogenase 1C (ADH1C) genotype on vitamin A restriction and marbling in Korean native steers." Asian-Australasian Journal of Animal Sciences 30, no. 8 (2017): 1099–104. http://dx.doi.org/10.5713/ajas.16.0708.

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37

Aktas, Ekin Ozgur, Aytaç Kocak, Ender Senol, et al. "Determination of the effects of Alcohol Dehydrogenase (ADH) 1B and ADH1C polymorphisms on alcohol dependence in Turkey." Science & Justice 52, no. 1 (2012): 58–61. http://dx.doi.org/10.1016/j.scijus.2011.05.002.

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Alsafi, Z., W. A. McCabe, A. R. Coker, and M. Y. Morgan. "OR1-1A STRUCTURAL AND FUNCTIONAL STUDY OF THE EFFECTS OF RS698 (IIE350VAL) AND RS1693482 (ARG272GLN) IN ADH1C." Alcohol and Alcoholism 52, suppl_1 (2017): i31—i49. http://dx.doi.org/10.1093/alcalc/agx074.01.

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39

Li, Dawei, Hongyu Zhao, and Joel Gelernter. "Further clarification of the contribution of the ADH1C gene to vulnerability of alcoholism and selected liver diseases." Human Genetics 131, no. 8 (2012): 1361–74. http://dx.doi.org/10.1007/s00439-012-1163-5.

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Kollock, Ronny, and Hansruedi Glatt. "Opposing – Activating or Inhibitory – Effects of Cimetidine and Daidzein on Human ADH1C Activity Depending on Substrates and Solvents." Drug Metabolism Letters 6, no. 4 (2013): 258–64. http://dx.doi.org/10.2174/1872312811206040005.

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Buervenich, Silvia, Andrea Carmine, Dagmar Galter, et al. "A Rare Truncating Mutation in ADH1C (G78Stop) Shows Significant Association With Parkinson Disease in a Large International Sample." Archives of Neurology 62, no. 1 (2005): 74. http://dx.doi.org/10.1001/archneur.62.1.74.

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Shimizu, Makiko, Yuki Ishii, Maho Okubo, Hideo Kunitoh, Tetsuya Kamataki, and Hiroshi Yamazaki. "Effects of ADH1C, ALDH2, and CYP2A6 Polymorphisms on Individual Risk of Tobacco-Related Lung Cancer in Male Japanese Smokers." Journal of Cancer Therapy 04, no. 08 (2013): 29–35. http://dx.doi.org/10.4236/jct.2013.48a005.

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Katsarou, Martha-Spyridoula, Konstantinos Karakonstantis, Nikolaos Demertzis, et al. "Effect of single-nucleotide polymorphisms inADH1B,ADH4,ADH1C,OPRM1,DRD2,BDNF, andALDH2genes on alcohol dependence in a Caucasian population." Pharmacology Research & Perspectives 5, no. 4 (2017): e00326. http://dx.doi.org/10.1002/prp2.326.

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Risch, Angela, Heribert Ramroth, Vivianne Raedts, et al. "Laryngeal cancer risk in Caucasians is associated with alcohol and tobacco consumption but not modified by genetic polymorphisms in class I alcohol dehydrogenases ADH1B and ADH1C, and glutathione-S-transferases GSTM1 and GSTT1." Pharmacogenetics 13, no. 4 (2003): 225–30. http://dx.doi.org/10.1097/00008571-200304000-00007.

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Kortunay, Selim, Aylin Köseler, Fatma Özdemir, and Erol Ömer Atalay. "Association of a Genetic Polymorphism of the Alcohol-Metabolizing Enzyme ADH1C with Alcohol Dependence: Results of a Case-Control Study." European Addiction Research 18, no. 4 (2012): 161–66. http://dx.doi.org/10.1159/000336314.

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Latella, Maria Carmela, Augusto Di Castelnuovo, Michel de Lorgeril, et al. "Genetic variation of alcohol dehydrogenase type 1C (ADH1C), alcohol consumption, and metabolic cardiovascular risk factors: Results from the IMMIDIET study." Atherosclerosis 207, no. 1 (2009): 284–90. http://dx.doi.org/10.1016/j.atherosclerosis.2009.04.022.

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Wang, Liping, Ying Zhang, Dapeng Ding, Xiaofeng He, and Zhenglan Zhu. "Lack of association of ADH1C genotype with breast cancer susceptibility in Caucasian population: A pooled analysis of case–control studies." Breast 21, no. 4 (2012): 435–39. http://dx.doi.org/10.1016/j.breast.2012.01.007.

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Huang, Wenqi, Mi Yang, Xixi Wu, et al. "Expression profile and co-expression analysis of ADH1A in human solid tumors." Journal of Clinical Oncology 38, no. 15_suppl (2020): e13533-e13533. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e13533.

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Abstract:

e13533 Background: The human alcohol dehydrogenase (ADH) gene family is associated with various solid cancers. It seems that the ADH1 gene cluster plays an important role in various solid tumors, so it aroused our interest in studying these genes to find out their functions and biological process within different solid tumors. Methods: Paired tumor and normal tissues gathered from 38 tumor patients, and 5 male BALB/c mice tissues were collected and Immunohistochemistry (IHC) assay was performed. The expression of ADH1A at RNA level in normal tissues and pan-solid tumors and the main functions of ADH1A in different solid tumors were analyzed by Bioinformatics mining. Results: At the RNA level, ADH1A was highly expressed in normal hepatocytes and was expressed lower in the tumor tissues than in the adjacent normal tissues or the corresponding normal tissues, suggesting the At the protein level, ADH1A was expressed to varying degrees in human alveoli, kidney, stomach, colon, and rectum. We predicted three major conserved functions of ADH1A, including angiogenesis, cell adhesion, and leukocyte migration function which might influence the prognosis of the immunotherapy and the immune response, and constructed an upstream regulation network of ADH1A and a downstream protein network. Besides, we also explored the functional differences of ADH1A in lung adenocarcinoma and lung squamous cell carcinoma and its effect on overall survival. And for investigating ADH1A, the BALB/c mice might be an option to consider in constructing an animal model of gastric cancer (GC), esophageal carcinoma (ESCA), liver hepatocellular carcinoma (LIHC), and pancreatic adenocarcinoma (PAAD). Conclusions: ADH1A has potential diagnostic and prognostic value in various solid tumors. Our findings highlight new avenues for further investigation of ADH1A biology process and provide a novel potential prognostic biomarker of immunotherapy.

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Peters, E. S. "The ADH1C Polymorphism Modifies the Risk of Squamous Cell Carcinoma of the Head and Neck Associated with Alcohol and Tobacco Use." Cancer Epidemiology Biomarkers & Prevention 14, no. 2 (2005): 476–82. http://dx.doi.org/10.1158/1055-9965.epi-04-0431.

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Bongaerts, Brenda W. C., Anton F. P. M. de Goeij, Kim A. D. Wouters, et al. "Alcohol consumption, alcohol dehydrogenase 1C (ADH1C) genotype, and risk of colorectal cancer in the Netherlands Cohort Study on diet and cancer." Alcohol 45, no. 3 (2011): 217–25. http://dx.doi.org/10.1016/j.alcohol.2010.10.003.

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