This study demonstrates that HLA alleles may influence cirrhosis development and disease activity in Turkish chronic hepatitis B patients.

Background The β3‐adrenergic receptor (ADRB3) is very important in the regulation of the human detrusor muscle function. The well‐known tryptophan64arginine polymorphism of the ADRB3 gene alters the response of the receptor to various stimuli, including adrenalin and noradrenalin, and may increase the susceptibility to develop overactive bladder (OAB). Therefore, this study was performed to determine whether ADRB3 Trp64Arg polymorphism is associated with the pathophysiology of OAB syndrome. Methods The study group (n = 150) consists of 72 patients with OAB and 78 controls without OAB. Venous blood samples were taken from all participants to analyze the ADRB3 gene Trp64Arg polymorphism using polymerase chain reaction (PCR)–restriction fragment length polymorphism (RFLP) assay. We compared the distribution of Trp64Arg polymorphism and symptom severity in both OAB and non‐OAB subjects using χ2 test and Mann–Whitney's U test, respectively. Results The frequency of the 64Arg variant (heterozygous plus homozygous) in OAB and non‐OAB subjects was 15.3% and 14.1%, respectively. There was no statistically significant difference between the OAB and non‐OAB groups in regard to the distribution frequency of ADRB3 Trp64Arg polymorphism. The total frequency (OAB + non‐OAB, 76 women and 74 men) of the Arg64 variant allele was 5.9% and 10.8% in women and in men, respectively. Although the frequency of the Arg64 variant was nearly twofold higher in men compared to women, the difference was not statistically significant. Conclusions These results demonstrated that the ADRB3 Trp64Arg polymorphism is not significantly associated with OAB syndrome in a sample of Turkish OAB patients.

Human ether-a-go-go related gene (herg) encoding HERG K(+) channel has been demonstrated in many previous studies with its association to cell cycle progression and growth in tumor cells. The upregulated expression of HERG K+ channels was determined in different tumor types. Furthermore, not only full-length transcript herg1 but also a truncated isoform herg1b was shown to be expressed in cancer cells. In this study, the expression levels of herg1 and herg1b and the impact of K897T mutation on their expressions were investigated in pediatric acute myeloid leukemia (pAML). Expression levels of herg1 and herg1b isoforms were analyzed by quantitative real time polymerase chain reaction (PCR) in pAML patients together with healthy donors, and their expressions were confirmed by western blotting. The 2690 A>C nucleotide variation in KCNH2 gene corresponding to K897T amino acid change was analyzed by PCR followed by restriction enzyme digestion. herg1b overexpression was observed in tumor cells compared to healthy controls (P = .0024). However, herg1 expression was higher in healthy control cells than tumor cells (P = .001). The prevalence of polymorphic allele 897T was 26% in our patient group and 897T carriers showed increased herg1b expression compared to wild-type allele carriers. Our results demonstrate the presence of the increased levels of herg1b expression in pAML. In addition, we report for the first time that, pAML subgroup with HERG 897K/K genotype compared to 897K/T and T/T genotypes express increased levels of herg1b. In conclusion, HERG 897K/K genotype with increased level of herg1b expression might well be a prognostic marker for pAML.

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Background/aim: BCL-3, upregulated in several cancers, functions as a crucial player not only in cell cycle and apoptosis, but also in metastasis. The study aimed to analyse the expression profile of BCL-3 and its interacting partners in metastatic breast cancer. Materials and methods: mRNA expression levels were evaluated in blood samples of metastatic breast cancer patients (n=55) and in healthy control donors (n=50) by RT qPCR. SPSS 26 program was used for statistical analysis. Results: Expression levels of BCL-3 mRNA was downregulated in metastatic breast cancers patients compared to healthy control group (p= 0.0004). Subsequently, expression levels of the NFKB1 (p= 0.0005), NFKB2 (p=0.0001), CYLD (p= 0.00042) and TP53 (p= 0.0287) were significantly lower in metastatic breast patients compared to healthy controls. CCND1 and CDH2 gene expressions were significantly upregulated in metastatic group (p=0.0009; and p= 0.0030, respectively). GSK3B, SMAD3 and TGFB1 expressions were not significantly different between groups. Conclusion: This study indicates significant expression difference between patients and controls. The NF-κB regulators might induce the metastatic potential through interaction with the other molecules in the microenvironment, nevertheless, it is needed further research whether the importance of BCL-3 as a biomarker for metastatic breast cancer.