Association of angiotensin converting enzyme gene insertion/deletion polymorphism with lung cancer in Turkey

被引：28

作者：

Nacak, Muradiye ^{[1
,2
]}

Nacak, Ibrahim ^{[3
]}

Sanli, Maruf ^{[4
]}

Ozkur, Mehtap ^{[1
]}

Pektas, Mehtap ^{[2
]}

Aynacioglu, A. Suekrue ^{[1
]}

机构：

[1] Gaziantep Univ, Fac Med, Dept Pharmacol, TR-27310 Sahinbey, Gaziantep, Turkey

[2] Mersin Univ, Fac Med, Dept Pharmacol, TR-33169 Mersin, Turkey

[3] Sani Konukoglu Med Ctr, Dept Thorac Surg, TR-27090 Sehitkamil, Gaziantep, Turkey

[4] Gaziantep Univ, Fac Med, Dept Thorac Surg, TR-27310 Sahinbey, Gaziantep, Turkey

来源：

CANCER GENETICS AND CYTOGENETICS | 2010年 / 198卷 / 01期

关键词：

DELETION POLYMORPHISM; BRADYKININ ANTAGONISTS; LINKAGE ANALYSIS; KOREAN PATIENTS; GROWTH-FACTOR; RISK; DISEASES; ANGIOGENESIS; SEGREGATION; INHIBITORS;

D O I：

10.1016/j.cancergencyto.2009.11.019

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Angiotensin-converting enzyme (ACE) plays an important role in the physiological control of blood pressure and inflammation. We investigated an insertion/deletion (I/D) polymorphism of the gene for ACE in relation to cardiovascular, cerebrovascular, neurodegenerative, and inflammatory diseases. The purpose of the present study was to investigate a possible association between lung cancer and insertion/deletion polymorphism of the ACE gene. A total of 125 patients with lung cancer and 165 control subjects were enrolled in the present study. ACE I/D genotypes were determined by polymerase chain reaction. Allelic frequencies and genotype distribution of the ACE I/D polymorphism in the patient group were significantly different from control subjects (ACE II genotype 29.6 vs. 17.6%, P = 0.011; ACE I allele 49.6 vs. 39.4%, P = 0.009). Our data suggest that the ACE I/D polymorphism could be a risk factor for patients with lung cancer. (C) 2010 Elsevier Inc. All rights reserved.

引用

页码：22 / 26

页数：5

共 48 条

[1]

Akkoclu A, 2002, RESPIRATION, V69, P207

[2]

AMOS CI, 1992, CANCER EPIDEM BIOMAR, V1, P505

[3]

BAKAN N, 1988, Biofactors, V1, P177

[4]

BUNN PA, 1992, CANCER RES, V52, P24

[5]

Calabro S, 1990, Med Lav, V81, P283

[6] DELETION POLYMORPHISM IN THE GENE FOR ANGIOTENSIN-CONVERTING ENZYME IS A POTENT RISK FACTOR FOR MYOCARDIAL-INFARCTION [J].

CAMBIEN, F ;

POIRIER, O ;

LECERF, L ;

EVANS, A ;

CAMBOU, JP ;

ARVEILER, D ;

LUC, G ;

BARD, JM ;

BARA, L ;

RICARD, S ;

TIRET, L ;

AMOUYEL, P ;

ALHENCGELAS, F ;

SOUBRIER, F .

NATURE, 1992, 359 (6396) :641-644

[7] Bradykinin antagonist dimer, CU201, inhibits the growth of human lung cancer cell lines by a "biased agonist" mechanism [J].

Chan, D ;

Gera, L ;

Stewart, J ;

Helfrich, B ;

Verella-Garcia, M ;

Johnson, G ;

Baron, A ;

Yang, J ;

Puck, T ;

Bunn, P .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (07) :4608-4613

[8] Gene polymorphisms of endothelial nitric oxide synthase and angiotensin-converting enzyme in patients with lung cancer [J].

Cheon, KT ;

Choi, KH ;

Lee, HB ;

Park, SK ;

Rhee, YK ;

Lee, YC .

LUNG, 2000, 178 (06) :351-360

[9]

COSTEROUSSE O, 1992, CR SOC BIOL, V186, P586

[10] ANGIOTENSIN-CONVERTING ENZYME IN THE HUMAN HEART - EFFECT OF THE DELETION INSERTION POLYMORPHISM [J].

DANSER, AHJ ;

SCHALEKAMP, MADH ;

BAX, WA ;

VANDENBRINK, AM ;

SAXENA, PR ;

RIEGGER, GAJ ;

SCHUNKERT, H .

CIRCULATION, 1995, 92 (06) :1387-1388

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