Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We explored the association between single nucleotide polymorphisms (SNPs) in ACYP2 and liver cancer risk. Thirteen SNPs were genotyped in 473 cases and 564 controls. Genetic model, linkage disequilibrium, and haplotype analyses were performed to evaluate the association between ACPY2 SNPs and liver cancer risk. We found that rs6713088 (G allele: odds ratio [OR] = 1.27, 95% confidence interval [CI]: 1.07-1.52, P = 0.007; GG vs. CC: OR = 1.49, 95% CI: 1.02-2.1, P = 0.038), rs843711 (T allele: OR = 1.29, 95% CI: 1.09-1.54, P = 0.004; TT vs. CC: OR = 1.62, 95% CI: 1.13-2.31, P = 0.008), rs843706 (A allele: OR = 1.30, 95% CI: 1.09-1.55, P = 0.003; AA vs. CC: OR = 1.62, 95% CI: 1.13-2.31, P = 0.008), and rs843645 (GG vs. AG: OR = 1.40, 95% CI: 1.07-1.82, P = 0.014) were associated with an increased risk of liver cancer. In contrast, rs1682111 (A allele: OR = 0.77, 95% CI: 0.640-0.94, P = 0.007; AT vs. TT: OR = 0.69, 95% CI: 0.53-0.91, P = 0.007), rs843720 (additive model: OR = 0.82, 95% CI: 0.68-1.00, P = 0.049), ATATCGCC and CG haplotypes (OR = 0.76, 95% CI: 0.62-0.92, P = 0.006; OR = 0.78, 95% CI: 0.65-0.93, P = 0.006, respectively) were significantly decreased liver cancer risk. Our results confirmed that rs6713088, rs843645, rs843711 and rs843706 were significantly increased liver cancer risk, but rs1682111, rs843720 and haplotypes (ATATCGCC and CG) were significantly decreased liver cancer risk in a Han Chinese population.
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PMID:ACYP2 polymorphisms are associated with the risk of liver cancer in a Han Chinese population. 2897 66

Hepatocellular carcinoma (HCC) is the dominant histologic type of primary liver cancer, and hepatitis B virus (HBV) infection is one of the major causes of HCC in the chronic HBV. Our study was investigated the association between the polymorphisms of ACYP2 and MPHOSPH6 genes and the risk of HCC induced by HBV infection. A total of 490 subjects were divided into two groups: 248 HBV patients with HCC (Case group), and 242 HBV patients without HCC (Control group). Unconditional logistic regression analysis was used to evaluate the association. The genetic association analysis revealed variant of rs12621038 in ACYP2 gene had a significant association with increasing the risk of HBV-induced HCC based on the genotype, dominant and additive model (P<0.05). Moreover, our results also showed that minor allele "C" of rs3751862 was prevalent in cases than controls (P<0.05), and rs3751862 significantly increased the risk of HCC in chronic HBV carriers under genotype and dominant model (P<0.05). In addition, the haplotype "T-G-G" in MPHOSPH6 showed a harmful factor for the HBV-induced HCC (P<0.05). The results suggested that ACYP2 and MPHOSPH6 as the plausible candidate genes may predict the risk of HCC after chronic HBV infection in Chinese Han population, and further investigations in studies with a larger sample size and other races are needed to validate our findings. These data provide a theoretical foundation for future studies of this correlation between the polymorphisms of ACYP2 and MPHOSPH6 genes and the HCC in chronic HBV carriers.
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PMID:Association of ACYP2 and MPHOSPH6 genetic polymorphisms with the risk of hepatocellular carcinoma in chronic hepatitis B virus carriers. 2915 73

Exposure to herbicides can induce long-term chronic adverse effects such as respiratory diseases, malignancies and neurodegenerative diseases. Oxadiazon, a pre-emergence or early post-emergence herbicide, despite its low acute toxicity, may induce liver cancer and may exert adverse effects on reproductive and on endocrine functions. Unlike other herbicides, there are no indications on neurotoxicity associated with long-term exposure to oxadiazon. Therefore, we have analyzed in primary neuronal precursor cells isolated from human striatal primordium the effects of non-cytotoxic doses of oxadiazon on neuronal cell differentiation and migration, and on the expression and activity of the mitochondrial aldehyde dehydrogenase 2 (ALDH2) and of the acylphosphatase (ACYP). ALDH2 activity protects neurons against neurotoxicity induced by toxic aldehydes during oxidative stress and plays a role in neurodegenerative conditions such as Alzheimer's disease and Parkinson's disease. ACYP is involved in ion transport, cell differentiation, programmed cell death and cancer, and increased levels of ACYP have been revealed in fibroblasts from patients affected by Alzheimer's disease. In this study we demonstrated that non-cytotoxic doses of oxadiazon were able to inhibit neuronal striatal cell migration and FGF2- and BDNF-dependent differentiation towards neuronal phenotype, and to inhibit the expression and activity of ALDH2 and to increase the expression and activity of ACYP2. In addition, we have provided evidence that in human primary neuronal precursor striatal cells the inhibitory effects of oxadiazon on cell migration and differentiation towards neuronal phenotype were achieved through modulation of ACYP2. Taken together, our findings reveal for the first time that oxadiazon could exert neurotoxic effects by impairing differentiative capabilities of primary neuronal cells and indicate that ALDH2 and ACYP2 are relevant molecular targets for the neurotoxic effects of oxadiazon, suggesting a potential role of this herbicide in the onset of neurodegenerative diseases.
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PMID:Oxadiazon affects the expression and activity of aldehyde dehydrogenase and acylphosphatase in human striatal precursor cells: A possible role in neurotoxicity. 3039 Dec 65