AIM:To evaluate the contribution of alcohol dehydrogenase-1B(ADH1B)and aldehyde dehydrogenase-2 (ALDH2)polymorphisms to the risk of esophageal cancer.METHODS:Nineteen articles were included by searching MEDLINE,EMBASE...AIM:To evaluate the contribution of alcohol dehydrogenase-1B(ADH1B)and aldehyde dehydrogenase-2 (ALDH2)polymorphisms to the risk of esophageal cancer.METHODS:Nineteen articles were included by searching MEDLINE,EMBASE and the Chinese Biomedical Database,13 on ADH1B and 18 on ALDH2.We performed a meta-analysis of case-control studies including 13 studies on ADH1B(cases/controls:2390/7100)and 18 studies on ALDH2(2631/6030).RESULTS:The crude odds ratio[OR(95%confidence interval)]was 2.91(2.04-4.14)for ADH1B*1/*1(vs ADH1B*2/*2)and 1.32(1.17-1.49)for ADH1B*1/*2.The crude OR for ALDH2*1/*2(vs ALDH2*1/*1)was 2.52(1.76-3.61).ADH1B*1/*1 increased the risk of esophageal cancer among never/rare[1.56(0.93-2.61)],moderate[2.71(1.37-5.35)],and heavy drinkers[3.22 (2.27-4.57)].ADH1B*1/*2 was associated with a modest risk among moderate drinkers[1.43(1.09-1.87)].ALDH2*1/*2 increased the risk among never/rare[1.28 (0.91-1.80)],moderate[3.12(1.95-5.01)],and heavy [7.12(4.67-10.86)]drinkers,and among ex-drinkers [5.64(1.57-20.25)].ALDH2*2/*2 increased the risk among drinkers[4.42(1.72-11.36)].ADH1B*1/*1 plus ALDH2*1/*2 was associated with the highest risk for heavy drinkers[12.45(2.9-53.46)].The results of the meta-regression analysis showed that the effects of ADH1B*1/*1 and ALDH2*1/*2 increased with the level of alcohol consumption.ALDH2*1/*2 was associated with a high risk among Taiwan Chinese and Japanese drinkers,as opposed to a moderate risk among drinkers in high-incidence regions of China's Mainland.ADH1B*1/*1 in heavy drinkers and ALDH2*1/*2 in moderate-toheavy drinkers was associated with similarly high risk among both men and women.CONCLUSION:ADH1B/ALDH2 genotypes affect the risk of esophageal cancer,and the risk is modified by alcohol consumption,ethnicity,and gender.展开更多
Objective Triple negative breast cancer(TNBC) contains a high proportion of breast cancer stem cells(BCSCs) and exhibits resistance to chemotherapy treatments. Therefore, the identification of BCSCs that are novel mol...Objective Triple negative breast cancer(TNBC) contains a high proportion of breast cancer stem cells(BCSCs) and exhibits resistance to chemotherapy treatments. Therefore, the identification of BCSCs that are novel molecular targets may improve patient survival. Aldehyde dehydrogenase-1(ALDH 1 A1) has been considered a cancer stem cell marker in different tumors. Caveolin-1(Cav-1), a membrane transporter protein, regulates cancer chemo-resistance and stem cell signaling. Thus, the aim of this study was to evaluate the expression of ALDH 1 A1 and Cav-1 in patients with TNBC by immunohistochemistry(IHC) and to correlate their expression with clinical and pathological parameters.Methods Paraffin blocks of 30 breast cancer patients who underwent modified radical mastectomy between January 2013 and December 2016 in Zagazig University Hospitals(Egypt) were evaluated. Antibodies to ALDH 1 A1 and Cav-1 were used. Results ALDH 1 A1 and Cav-1 significantly correlated with tumor size. A significant association between ALDH 1 A1/Cav-1 IHC staining and relapse was found. Cav-1 and ALDH 1 A1-positive expression correlated with a short 3-year disease-free survival rate and a 3-year overall survival rate(P < 0.001). Conclusion ALDH 1 A1 and Cav-1 expression in TNBC was significantly positively correlated with poor clinicopathological parameters and shortened survival. Expression of both markers was significantly positively correlated with each other(P < 0.001). ALDH 1 A1 and Cav-1 could be potential therapeutic targets in breast cancer.展开更多
Background: Unlike with esophageal cancer, acetaldehyde levels and genetic polymorphisms in alcohol dehydrogenase have not yet been shown to be contributing factors for colorectal cancer (CRC). This study aimed to cla...Background: Unlike with esophageal cancer, acetaldehyde levels and genetic polymorphisms in alcohol dehydrogenase have not yet been shown to be contributing factors for colorectal cancer (CRC). This study aimed to clarify the mechanism of CRC development related to alcohol consumption and to the presence of genetic polymorphisms in the alcohol dehydrogenase, ADH1B and aldehyde dehydrogenase, ALDH2. Methods: This was a case-control study (221 cases and 179 controls) in patients with adenomas and intramucosal tumors who underwent endoscopic removal of all tumors. The amount of alcohol consumption was determined using a self-recorded questionnaire, and the tumor information was obtained from colonoscopy results. Blood samples were taken to analyze the following polymorphisms: ALDH2 Glu504Lys and ADH1B His48Arg. Results: The polymorphisms in ADH1B and ALDH2 had little influence on the development of colorectal adenoma or intramucosal cancer. Patients with ALDH2 (Glu/Glu) were more tolerant of alcohol than those with ALDH2 (Glu/Lys and Lys/Lys). Next, we examined certain combinations of the ADH1B genotypes. In the ALDH2 (Glu/Glu) group, an increased risk (OR = 3.4;95% CI 1.4 - 8.4;P = 0.009) was observed among moderate/heavy drinkers with ADH1B (His/His). In the ALDH2 (Glu/Lys and Lys/Lys) group, an increased risk (OR = 4.2;95% CI 1.1 - 16.7;P = 0.041) was found among moderate/heavy drinkers with ADH1B (Arg/His and Arg/Arg). Conclusions: ADH1B and ALDH2 activity may be involved in the development of CRC.展开更多
文摘AIM:To evaluate the contribution of alcohol dehydrogenase-1B(ADH1B)and aldehyde dehydrogenase-2 (ALDH2)polymorphisms to the risk of esophageal cancer.METHODS:Nineteen articles were included by searching MEDLINE,EMBASE and the Chinese Biomedical Database,13 on ADH1B and 18 on ALDH2.We performed a meta-analysis of case-control studies including 13 studies on ADH1B(cases/controls:2390/7100)and 18 studies on ALDH2(2631/6030).RESULTS:The crude odds ratio[OR(95%confidence interval)]was 2.91(2.04-4.14)for ADH1B*1/*1(vs ADH1B*2/*2)and 1.32(1.17-1.49)for ADH1B*1/*2.The crude OR for ALDH2*1/*2(vs ALDH2*1/*1)was 2.52(1.76-3.61).ADH1B*1/*1 increased the risk of esophageal cancer among never/rare[1.56(0.93-2.61)],moderate[2.71(1.37-5.35)],and heavy drinkers[3.22 (2.27-4.57)].ADH1B*1/*2 was associated with a modest risk among moderate drinkers[1.43(1.09-1.87)].ALDH2*1/*2 increased the risk among never/rare[1.28 (0.91-1.80)],moderate[3.12(1.95-5.01)],and heavy [7.12(4.67-10.86)]drinkers,and among ex-drinkers [5.64(1.57-20.25)].ALDH2*2/*2 increased the risk among drinkers[4.42(1.72-11.36)].ADH1B*1/*1 plus ALDH2*1/*2 was associated with the highest risk for heavy drinkers[12.45(2.9-53.46)].The results of the meta-regression analysis showed that the effects of ADH1B*1/*1 and ALDH2*1/*2 increased with the level of alcohol consumption.ALDH2*1/*2 was associated with a high risk among Taiwan Chinese and Japanese drinkers,as opposed to a moderate risk among drinkers in high-incidence regions of China's Mainland.ADH1B*1/*1 in heavy drinkers and ALDH2*1/*2 in moderate-toheavy drinkers was associated with similarly high risk among both men and women.CONCLUSION:ADH1B/ALDH2 genotypes affect the risk of esophageal cancer,and the risk is modified by alcohol consumption,ethnicity,and gender.
文摘Objective Triple negative breast cancer(TNBC) contains a high proportion of breast cancer stem cells(BCSCs) and exhibits resistance to chemotherapy treatments. Therefore, the identification of BCSCs that are novel molecular targets may improve patient survival. Aldehyde dehydrogenase-1(ALDH 1 A1) has been considered a cancer stem cell marker in different tumors. Caveolin-1(Cav-1), a membrane transporter protein, regulates cancer chemo-resistance and stem cell signaling. Thus, the aim of this study was to evaluate the expression of ALDH 1 A1 and Cav-1 in patients with TNBC by immunohistochemistry(IHC) and to correlate their expression with clinical and pathological parameters.Methods Paraffin blocks of 30 breast cancer patients who underwent modified radical mastectomy between January 2013 and December 2016 in Zagazig University Hospitals(Egypt) were evaluated. Antibodies to ALDH 1 A1 and Cav-1 were used. Results ALDH 1 A1 and Cav-1 significantly correlated with tumor size. A significant association between ALDH 1 A1/Cav-1 IHC staining and relapse was found. Cav-1 and ALDH 1 A1-positive expression correlated with a short 3-year disease-free survival rate and a 3-year overall survival rate(P < 0.001). Conclusion ALDH 1 A1 and Cav-1 expression in TNBC was significantly positively correlated with poor clinicopathological parameters and shortened survival. Expression of both markers was significantly positively correlated with each other(P < 0.001). ALDH 1 A1 and Cav-1 could be potential therapeutic targets in breast cancer.
文摘Background: Unlike with esophageal cancer, acetaldehyde levels and genetic polymorphisms in alcohol dehydrogenase have not yet been shown to be contributing factors for colorectal cancer (CRC). This study aimed to clarify the mechanism of CRC development related to alcohol consumption and to the presence of genetic polymorphisms in the alcohol dehydrogenase, ADH1B and aldehyde dehydrogenase, ALDH2. Methods: This was a case-control study (221 cases and 179 controls) in patients with adenomas and intramucosal tumors who underwent endoscopic removal of all tumors. The amount of alcohol consumption was determined using a self-recorded questionnaire, and the tumor information was obtained from colonoscopy results. Blood samples were taken to analyze the following polymorphisms: ALDH2 Glu504Lys and ADH1B His48Arg. Results: The polymorphisms in ADH1B and ALDH2 had little influence on the development of colorectal adenoma or intramucosal cancer. Patients with ALDH2 (Glu/Glu) were more tolerant of alcohol than those with ALDH2 (Glu/Lys and Lys/Lys). Next, we examined certain combinations of the ADH1B genotypes. In the ALDH2 (Glu/Glu) group, an increased risk (OR = 3.4;95% CI 1.4 - 8.4;P = 0.009) was observed among moderate/heavy drinkers with ADH1B (His/His). In the ALDH2 (Glu/Lys and Lys/Lys) group, an increased risk (OR = 4.2;95% CI 1.1 - 16.7;P = 0.041) was found among moderate/heavy drinkers with ADH1B (Arg/His and Arg/Arg). Conclusions: ADH1B and ALDH2 activity may be involved in the development of CRC.
