scholarly journals Deletion polymorphism of the angiotensin I converting enzyme gene is a potent risk factor for coronary artery ectasia

Heart ◽  
2003 ◽  
Vol 89 (2) ◽  
pp. 213-214 ◽  
Author(s):  
S Gulec
Keyword(s):  
Risk Factor ◽  
Coronary Artery ◽  
Converting Enzyme ◽  
Coronary Artery Ectasia ◽  
Angiotensin I ◽  
Deletion Polymorphism ◽  
Enzyme Gene ◽  
Angiotensin I Converting Enzyme

Angiotensin I–converting enzyme gene insertion/deletion polymorphism and endometrial human cancer in normotensive and hypertensive women

2004 ◽  
Vol 155 (1) ◽  
pp. 42-46 ◽  
Author(s):  
Margarida Freitas-Silva ◽  
Deolinda Pereira ◽  
Constança Coelho ◽  
Manuel Bicho ◽  
Carlos Lopes ◽  
...  
Keyword(s):  
Human Cancer ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Deletion Polymorphism ◽  
Enzyme Gene ◽  
Gene Insertion ◽  
Angiotensin I Converting Enzyme

Mistyping of the human angiotensin-converting enzyme gene polymorphism: frequency, causes and possible methods to avoid errors in typing

1996 ◽  
Vol 17 (1) ◽  
pp. 27-30 ◽  
Author(s):  
S Ueda ◽  
R P Heeley ◽  
K. R Lees ◽  
H L Elliott ◽  
J M C Connell
Keyword(s):  
Genetic Locus ◽  
Pcr Amplification ◽  
Angiotensin Converting Enzyme Gene ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Deletion Polymorphism ◽  
Gene Encoding ◽  
Enzyme Gene ◽  
Angiotensin I Converting Enzyme ◽  
Hot Start

ABSTRACT A polymorphism of the gene encoding the human angiotensin I-converting enzyme (ACE), which is defined by an insertion/deletion polymorphism in intron 16, has been identified as a candidate genetic locus in the development of cardiovascular and renal disease. We have demonstrated that the accuracy of ACE genotyping is critically dependent on the strategy of the PCR used in typing. Of 1238 individuals genotyped by a standard method, 335 were typed as DD, 645 as DI and 258 as II. However, when DD individuals were retyped using modified methods (including either 5% dimethyl sulphoxide, or a 'hot start') 35 of the original 335 samples (10·5%) were retyped as DI. In approximately half of these mistyped samples, PCR amplification was assessed as inefficient by the absence of a third faint heteroduplex band in a control ID sample: when the assay was repeated without any modifications, the mistyped samples were correctly genotyped. In the remainder, mistyping persisted. In these cases, the use of a third 'nested' PCR primer specific for the I allele was required for successful genotyping, providing a more reliable strategy without the need for further modification to the PCR technique. Our results suggest that the triple primer approach is the method of choice for accurate ACE genotyping.

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