Relationship between polymorphism of angiotensin-converting enzyme gene insertion/deletion and risk of hepatocellular carcinoma in a Chinese Dai population

Abstract

The DD genotypes of ACE I/D polymorphism might contribute to the prediction of HCC risk in a Chinese Dai population.

Angiotensin-converting enzyme gene polymorphism (insertion/deletion) and liver fibrosis in Turkish patients from the western Black Sea region, Turkey

“…In a Chinese population, Yuan et al (2013) demonstrated the ACE gene D allele frequency in patients with HCC to be lower than in healthy controls. Zha et al (2014) also conducted a study on HCC patients, and contrary to the findings reported by Yuan et al (2013), found D allele frequencies to be higher in HCC patients than in the control subjects.…”

“…Fabris et al (2009), on the other hand, suggested a relationship between gender and ACE gene I/D polymorphism: ACE I/I homozygote women had liver fibrosis scores five times higher than ACE D/D homozygote and ACE I/D heterozygote women. The DD genotype has furthermore been found to be significantly associated with hepatocellular carcinoma (HCC) risk; however, results in this area have been somewhat conflicting: Yuan (2013) found D allele frequencies to be lower in HCC patients than in controls, whereas Zha (2014) found D allele frequencies of HCC patients to be higher than those of controls. The studies carried out to investigate the relationship between ACE gene I/D polymorphism and/or serum ACE levels with liver fibrosis between the years of 2000 and 2015 have yielded conflicting conclusions, which could be attrinuted to the small sample sizes used (Table 1).…”

“…Necroinflammatory activity (P < 0.001) and age (P < 0.001) were associated significantly with fibrosis (2012) 90 HCV patients 30 healthy controls Serum ACE levels in patients with ACE gene DD polymorphism is more than the patients with DI and II polymorphisms (P < 0.05) Purnak et al (2012) 50 HBV patients 20 healthy controls Serum ACE levels in patients with advanced fibrosis was found to be higher than patients with mild fibrosis (P < 0.001) Shahid et al (2013) Cirrhotic rats, control rats ACE gene expression in liver tissue of cirrhotic rats were higher than the controls (P < 0.05) Yuan et al (2013) 293 HCC patients, 384 healthy controls D allele frequencies in the ACE gene of HCC patients were lower than controls (P = 0.003). Significantly decreased HCC risk was associated with the DD genotype (P < 0.001) Zha et al (2014) 210 HCC patients 206 healthy controls D allele frequencies in the ACE gene of HCC patients were higher than controls (P = 0.036) Goh et al (2015) 290 hypertensive patients with NAFLD Patients treated with RAS blockers had less advanced hepatic fibrosis than the patients treated without RAS blockers (P = 0.002) HCV = hepatitis C virus; PBC = primary biliary cirrhosis; NAFLD = non-alcoholic fatty liver disease; HBV = hepatitis B virus; HCC = hepatocellular carcinoma; RAS = renin angiotensin system. Table 1.…”

The relationship between angiotensin-converting enzyme gene insertion/deletion polymorphism and digestive cancer risk: Insights from a meta-analysis

“…[9][10][11][12][16][17][18][19][20][21][22][23][24][25][26][27] The publication year was from 2001 16 to 2014. 27 …”

RETRACTED: Association of the ACE I/D gene polymorphism with sepsis susceptibility and sepsis progression

“…3 The angiotensin-converting enzyme (ACE) insertion/ deletion (I/D) gene polymorphism is a 287-bp sequence of DNA in the intron 16 of the ACE gene, and the ACE gene includes either an insertion (I) allele or a deletion (D) allele that form three possible genotypes: II, ID or DD. 4,5 ACE, directly involved in the process of cell proliferation, differentiation, apoptosis and angiogenesis, 6 can convert angiotensin I into angiotensin II, and angiotensin II is the main effector molecule of the renin-angiotensin system, is pleiotropic, and is a mediator of the development and progression of diseases. 7 The ACE I/D gene polymorphism, correlating with circulating ACE concentration, might be implicated in the etiology of sepsis and has been investigated in some epidemiologic studies.…”