Dack of evidence for lung cancer predisposing role of NAT2 gene polymorphism
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2023-06-13 09:53
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IMEANITOV, Evghenii, ŞUTKIN, Vladimir, BELOGUBOVA, Evghenia, CULIGHINA, Ecaterina, TOGO, Alexandr, CARPOVA, Maria, ULÎBINA, Iulia, BRENIŞTER, Sergiu, POPOWSKI, Katrin, MOSIAGHIN, Igor, CASCORBI, Ingolf, HIRVONEN, Ari. Dack of evidence for lung cancer predisposing role of NAT2 gene polymorphism . In: Buletinul Academiei de Ştiinţe a Moldovei. Ştiinţe Medicale, 2010, nr. 4(27), pp. 210-216. ISSN 1857-0011.
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Buletinul Academiei de Ştiinţe a Moldovei. Ştiinţe Medicale
Numărul 4(27) / 2010 / ISSN 1857-0011

Dack of evidence for lung cancer predisposing role of NAT2 gene polymorphism

Pag. 210-216

Imeanitov Evghenii, Şutkin Vladimir, Belogubova Evghenia, Culighina Ecaterina, Togo Alexandr, Carpova Maria, Ulîbina Iulia, Brenişter Sergiu, Popowski Katrin, Mosiaghin Igor, Cascorbi Ingolf, Hirvonen Ari
 
IMSP Institutul Oncologic
 
 
Disponibil în IBN: 13 decembrie 2013


Rezumat

Polimorfi smul NAT2 (arilaminice N-acetil 2), determinant-cheie al variaţiilor individuale în capacitatea de acetilare, este suspectat de modifi carea risculului de tumori maligne. Ca fumul de tutun şi alte substanţe inhalate, conţine o varietate de substraturi NAT2. Relaţia dintre fenotipul NAT2 şi cancerul pulmonar este obiectul de cercetare intensivă al diferitor studii de caz-control, ale căror rezultate au produs controverse.

NAT2 (arylamine N-acetyltransferase 2) polymorphism, being a key determinant of individual variations in acetylation capacity, is suspected to modify the risk of carcinogen-related malignancies. As tobacco smoke and other inhaled hazards contain a variety of NAT2 substrates, the relationship between NAT2 phenotype and lung cancer (LC) risk has been a subject of intensive research, however different case-control studies produced controversial data. In the present report, we employed a novel ,,comparison of extremes” approach, i.e., we compared the distribution of NAT2 genotypes in lung cancer patients (LC, n = 178) not only to the population controls (healthy donors (HD), n = 364), but also to the subjects with a putative cancer-resistant constitution (elderly tumor-free smokers and non-smokers (ED), n = 351). Frequencies of homozygous rapid, heterozygous rapid and slow acetylators were 6%, 39% and 56% in LC, 8%, 32% and 60% in HD, and 6%, 35% and 59% in ED, respectively). Comparison of the NAT2 genotype frequencies between affected and non-affected individuals did not reveal any statistical deviations, irrespectively of smoking history, gender, age, or histological type of LC. Adjusted odds ratio for rapid vs. slow acetylators was 1.12 (95% confi dence intervals (CI): 0.73 - 1.74) comparing LC vs. HD, and 1.10 (95% CI: 0.74 - 1.62) comparing LC vs. ED. Similar distribution of NAT2 acetylator genotypes both in tumor-prone and in tumor-resistant groups suggests that, despite the presence of NAT2 carcinogenic substrates in tobacco smoke. NAT2 polymorphism does not play a noticeable role in lung cancer susceptibility.