Alcohol Dehydrogenase 3 Genotype as a Risk Factor for Upper Aerodigestive Tract Cancers

Nishimoto, Inês Nobuko; Pinheiro, Nídia Alice; Rogatto, Sílvia Regina; Carvalho, André Lopes; Moura, Ricardo P.; Caballero, Otávia L.; Simpson, Andrew J.G.; Kowalski, Luiz Paulo

doi:10.1001/archotol.130.1.78

Cited by 21 publications

(14 citation statements)

References 21 publications

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“…A single study in Brazil demonstrated elevated odds (OR 3.7, 95% CI, 1.5-9.7) of all head and neck squamous cell carcinomas (HNSCC; inclusive of oral cavity, oropharynx, larynx, and hypopharynx) for the homozygous ADH1C*1-1 genotype at low levels of alcohol consumption compared with the ADH1C*1-2 and ADH1C*2-2 genotypes. 58 Elevated odds (OR 5.3, 95% CI, 1.0-28.8) of oral cancer in association with the ADH1C*1-1 genotype were observed only among heavy alcohol users (57 drinks per week) in Puerto Rico 59 and among alcoholics in Germany 60 and France. 55,61 However, contradictory conclusions were reported in studies conducted in the U.S. 62,63 and Greece, 64 in which the ''slow metabolizing'' ADH1C*2-2 genotype was associated with increased risk for HNSCC among heavy drinkers.…”

Section: Alcohol Consumption and Metabolismmentioning

confidence: 99%

Current topics in the epidemiology of oral cavity and oropharyngeal cancers

2007

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Oral cancer incidence rates rose dramatically during the twentieth century in the United States and Europe, especially among individuals under the age of 60 years. Although influenced by age, sex, and country of origin, incidence trends were most strongly affected by elevated risk among individuals born after approximately 1915. This cohort effect was indicative of strong behavioral influences on oral cancer risk. In this article, associations between oral cancer risk and established behavioral risk factors including alcohol and tobacco use are reviewed. Additionally, possible associations between oral cancer risk and oral hygiene, diet, nutritional status, and sexual behavior as well as the influence of genetic factors on oral cancer risk are considered. Special emphasis is placed on evaluating possible risk differences in individuals above and below the age of 45 and in users and nonusers of alcohol and tobacco. Oral squamous cell carcinomas arise from several anatomic sites within the oral cavity and oropharynx, but most commonly from the oral, mobile tongue.1 In the 1980s, 2 cancer centers in the United States (U.S.) reported an increase in the proportion of incident oral tongue cancers diagnosed in men younger 40 years.2,3 Although absolute numbers had increased, these reports provided no real evidence of rising incidence. Shortly thereafter, however, a significant 2-fold increase in oral tongue cancer mortality rates between 1950 and 1982 was reported in the U.S. for men younger than 30 years. 4 This finding was corroborated by a study in Scotland. 5 Further analysis of the Scottish data revealed that the increase in incidence was not restricted to those younger than 40 but extended to all age groups less than 65 years of age born after 1920-a strong ''cohort effect.'' The cohort effect was indicated by a strong effect of year of birth on oral cancer incidence rates. A flurry of research on global changes in oral cancer incidence was stimulated by these reports.

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Section: Alcohol Consumption and Metabolismmentioning

confidence: 99%

Current topics in the epidemiology of oral cavity and oropharyngeal cancers

2007

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“…In contrast to ADH2, ADH3 is highly polymorphic in Caucasians. Of the 2 allelic variants, the ADH3*1 allele is associated with higher enzyme activity than the ADH3*2 allele and occurs in Caucasians at frequencies of 55-63% (253).In 5 (43,58,111-113) of 8 (63%) studies (43,58,(111)(112)(113)(114)(115)(116), ADH3*2/*1 heterozygotes showed decreased risk for HNC compared with *2/*2 homozygotes. However, in 6 (43,58, INTERNATIONAL JOURNAL OF ONCOLOGY 32: 945-973, 2008 …”

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confidence: 99%

Genetic polymorphisms and head and neck cancer risk (Review)

Hiyama¹,

Yoshihara²,

Tanaka³

et al. 2008

Int J Oncol

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Abstract. The aim of this report is to review and evaluate, in a comprehensive manner, the published data regarding the contribution of genetic polymorphisms to risk of head and neck cancer (HNC). All relevant studies available in MEDLINE and published before July 2007 were identified. Studies carried out in humans that compared HNC patients with at least 1 standard control group were considered for analysis. Two hundred and eighteen publications and 3 published metaanalyses were identified. Seventy-five (34%) studies were conducted in Asian, 72 (33%) in American, and 68 (31%) in European countries. The most widely studied gene was GSTM1 (58 studies), followed by GSTT1 (42 studies), GSTP1 (codon 105, 22 studies) and p53 (codon 72, 20 studies). GSTM1, GSTT1, GSTP1, XRCC1 codons 194 and 399, and CYP1A1 codon 462 were examined by meta-analyses, and significant relations were found between the GSTM1-null genotype and an increased risk for HNC. In addition, increased risk for HNC was associated consistently with the ALDH2*1/*2, p53 codon 72 Pro/Pro and EPHX1 codon 113 Tyr/His and His/His genotypes. Cohort studies that simultaneously consider multiple genetic and environmental factors possibly involved in carcinogenesis of the head and neck are needed to ascertain not only the relative contribution of these factors to tumor development but also the contributions of their putative interactions. IntroductionHead and neck cancers (HNCs), including cancers of the oral cavity, pharynx and larynx, represent the 6 most frequent cancers and the seventh leading cause of cancer-related death worldwide. There are approximately 540,000 new cases and 271,000 deaths annually worldwide for a mortality of approximately 50% (1). HNCs represent approximately 3% of all cancers in the United States whereas these cancers are much more prevalent in other areas of the world, such as India, Thailand and Brazil (1,2). Standard therapeutic approaches, which focus on surgery, irradiation and chemotherapy (alone or in combination), have been modified over the last 30 years; however, the overall survival of HNC patients has not improved substantially. For patients affected by early-stage cancers with a high disease-specific survival rate, secondary tumors represent the most common cause of death (3). Furthermore, patients with advanced cancers have a high risk of primary treatment failure and death.Development of HNC is a multifactorial process associated with a variety of risk factors. Major risk factors in developed countries include smoking tobacco and drinking alcohol, and chewing betel quid (4,5). For tobacco smoking, a dose-response trend has been reported. Relative risks of developing laryngeal and oropharyngeal cancers are 1.8 and 1.3, respectively, for persons who smoke ≤30 cigarettes per day and 7.7 and 2.9, respectively, for persons who smoke >30 cigarettes per day compared with non-smokers (6). Alcohol consumption is also linked to increased risk of HNCs. For persons who consume >4 drinks (=47.5 g of pure ethanol) per day, the relati...

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“…[22][23][24][25] Çalışmamızda CCND1 G870A polimorfizmi incelendiğinde, baş-boyun kanserli hastalar ile kontrol grubu arasında risk alleli olarak kabul edilen A allelinin dağılımı açısından önemli bir fark gözlenmemiştir. Hasta ve kontrol grupları arasında genotip ve allel dağılımları açısından fark bulunmaması mide kanseri, 26 hepatosellüler kanser, 22 üst solunum ve sindirim sisteminin yassı epitel hücreli kanserleri, 27 hipofiz adenomu, 15 34 hastalarda kombine GA+AA genotipi artmış hastalık riskiyle ilişkili bulunurken, larinks 21 kanserinde hem GA genotipi, hem de kombine GA + AA genotipi artmış hastalık riskiyle ilişkilendirilmiştir.…”

Section: Discussionunclassified

“…Literatürde sigara kullananlarda nazofarinks 18 ve özofagus kanserinde, 34 sigara kullanmayanlar da ise mesane 19 ve baş-boyun kanserinde 12 A alleli ile hastalık riski arasında ilişki bildirilmektedir. Ayrıca üst aerodigestive sistemin alkol kullanmayan yassı epitel kanserli hastalarında 27 da A alleli risk faktörü olarak bildirilmiş ve 50 yaş altı veya kadın baş-boyun kanserli hastalarda aynı allele bağlı olarak üç kat artmış hastalık riski gözlenmiştir. 12 A allelinin mesane 33 ve serviks 30 kanserinde etnik köken (Asyalılarda daha sık) ve risk ile ilişkili olduğu bildirilmiştir.…”

Section: Ccnd1 (G870a)unclassified

“…22,[23][24][25] Bir kısım çalışmada ise hasta ve kontrol grupları arasında allel ve genotip dağılımları açısından bir fark bildirilmemiştir. 3,22,[26][27][28][29][30][31] Türk toplumunda CCND1 geninin varyantları ile baş boyun kanseri riski arasındaki ilişkiyi araştıran çalışma bulunmamaktadır. Bu gendeki değişikliklerin tanımlanması ve kanser riski ile ilişkilerinin anlaşılması HNC'nin tanı ve takibinde yararlı olabilecektir.…”

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Analysis of Cyclin D1 G87 A Polymorphism in Patients with Head and Neck Cancers

Demokan¹,

Süoğlu²,

Ulusan³

et al. 2011

Turkiye Klinikleri J Med Sci

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Ö ÖZ ZE ET T A Am ma aç ç: : Baş-bo yun kan ser le ri (HNC) dün ya da en yay gın kan ser ler ara sın da al tın cı sı ra da yer al makta dır. Ya pı lan ça lış ma lar ge ne tik yat kın lı ğın bu kan se re ya ka lan ma ris ki açı sın dan önem li bir rol oy nadı ğı nı gös ter mek te, hüc re sik lu su nun dü zen len me sin de gö rev alan Sik lin D1 (CCND1) ge nin de ki bir po li mor fiz min ge ne tik yat kın lı ğın al tın da ya tan ne den ol du ğu dü şü nül mek te dir. Li te ra tür de HNC'de CCND1 gen po li mor fiz miy le ya pıl mış az sa yı da ça lış ma bu lun mak ta dır. Türk HNC has ta la rın da bu poli mor fiz mi in ce le yen ça lış ma ise mev cut de ğil dir. Ça lış ma mız da, CCND1 ge nin de ki G870A po li mor fizmi in ce len miş ve al lel ve ge no tip da ğı lım la rı ile kli nik pa ra met re ler ara sın da ki iliş ki de ğer len di ril miş tir. G Ge e r re eç ç v ve e Y Yö ön n t te em m l le er r: : Ça lış ma kap sa mın da, baş-bo yun kan ser li 95 has ta nın pe ri fe rik kan ör nek le ri ile sağ lık lı 40 ki şi ye ait pe ri fe rik kan ör nek le ri in ce len miş tir. Top la nan ör nek ler den DNA el de edil dik ten son ra CCND1 ge ni ne öz gü po li mor fik böl ge polimeraz zincir reaksiyonu ile ço ğal tıl mış, son ra uy gun res trik si yon en zi mi kul la nı la rak ke sil miş ve so nuç lar vi de o-gel dö kü man tas yon sis te mi yar dı mıy la değer len di ril miş tir. Po li mor fik da ğı lım lar, Fi net ti va ka-kon trol is ta tis tik prog ra mı kul la nı la rak sağ lık lı kişi ler de ki al lel fre kans la rı ile kı yas lan mış ve χ 2 (Ki-ka re) test le ri ile has ta la rın kli nik ve pa to lo jik bul gu la rıy la iliş ki le ri araş tı rıl mış tır. B Bu ul l g gu u l la ar r: : Baş-bo yun kan ser li has ta lar la kon trol gru bu ara sın da allel ve ge no tip da ğı lım la rı açı sın dan an lam lı bir fark göz len mez ken, yas sı epi tel hüc re li (YEH)-dı şı hasta lar da GA he te ro zi got ge no ti pi ile kom bi ne GA + AA ge no tip le ri dü şük has ta lık ris kiy le iliş ki li bu lun muş tur. Ay rı ca YEH kan ser gru bun da YEH-dı şı has ta la ra oran la A al le li ne an lam lı de re ce de sık rast lan mış tır. S So o n nu uç ç: : Baş-bo yun kar si no ge ne zin de tü mö rün his to lo ji si ne gö re CCND1 ge ni nin de ği şik var yant la rı nın et ki li ola bi le ce ği dü şü nül mek te dir.A An na ah h t ta ar r K Ke e l li i m me e l le er r: : Çok biçimlilik, tek nükleotid; siklin D1, baş ve boyun tümörleri A AB BS S T TR RA AC CT T O Ob b j je ec c t ti i v ve e: : He ad and neck can cer (HNC) is the sixth le a ding can cer among the most frequent can cers worl dwi de. Stu di es in di ca te that ge ne tic pre dis po si ti on plays an im por tant ro le for HNC risk and a poly morp hism in cyclin D1 (CCND1) ge ne ta king part in re gu la ti on of cell cycle is con si dered to be the un derl ying ca u se of ge ne tic pre dis po si ti on. A few stu di es are ava i lab le in li te ra tu re on CCND1 ge ne poly morp hism in HNC. No stu di es are ava i lab le in li te ra tu re investigating this poly morphism in Tur k...

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Alcohol Dehydrogenase 3 Genotype as a Risk Factor for Upper Aerodigestive Tract Cancers

Cited by 21 publications

References 21 publications

Current topics in the epidemiology of oral cavity and oropharyngeal cancers

Current topics in the epidemiology of oral cavity and oropharyngeal cancers

Genetic polymorphisms and head and neck cancer risk (Review)

Analysis of Cyclin D1 G87 A Polymorphism in Patients with Head and Neck Cancers

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