NFKBIA is often deleted but not mutated in glioblastomas; most deletions occur in nonclassical subtypes of the disease. Deletion of NFKBIA and amplification of EGFR show a pattern of mutual exclusivity. Restoration of the expression of NFKBIA attenuated the malignant phenotype and increased the vulnerability to chemotherapy of cells cultured from tumors with NFKBIA deletion; it also reduced the viability of cells with EGFR amplification but not of cells with normal gene dosages of both NFKBIA and EGFR. Deletion and low expression of NFKBIA were associated with unfavorable outcomes. Patients who had tumors with NFKBIA deletion had outcomes that were similar to those in patients with tumors harboring EGFR amplification. These outcomes were poor as compared with the outcomes in patients with tumors that had normal gene dosages of NFKBIA and EGFR. A two-gene model that was based on expression of NFKBIA and O 6 -methylguanine DNA methyltransferase was strongly associated with the clinical course of the disease. Conclusions Deletion of NFKBIA has an effect that is similar to the effect of EGFR amplification in the pathogenesis of glioblastoma and is associated with comparatively short survival.

/pdf/nfkbia-deletion-in-glioblastomas-3k71aopu93.pdf

NFKBIA Deletion in Glioblastomas

Single nucleotide polymorphisms and risk of hepatocellular carcinoma in cirrhosis

Human cytidine deaminases facilitate hepatitis B virus evolution and link inflammation and hepatocellular carcinoma

Liver cancer is the fifth and seventh most common cause of cancer in men and women, respectively. Wnt/β-catenin signalling has emerged as a critical player in both the development of normal liver as well as an oncogenic driver in hepatocellular carcinoma (HCC). Based on the current understanding, this article summarizes the possible mechanisms for the aberrant activation of this pathway with specific focus on HCC. Furthermore, we will discuss the role of dickkopfs (DKKs) in regulating Wnt/β-catenin signalling, which is poorly understood and understudied. DKKs are a family of secreted proteins that comprise at least four members, namely DKK1-DKK4, which act as inhibitors of Wnt/β-catenin signalling. Nevertheless, not all members antagonize Wnt/β-catenin signalling. Their functional significance in hepatocarcinogenesis remains to be further characterized for which these studies should provide new insights into the regulatory role of DKKs in Wnt/β-catenin signalling in hepatic carcinogenesis. Because of the important oncogenic roles, there are an increasing number of therapeutic molecules targeting β-catenin and the Wnt/β-catenin pathway for potential therapy of HCC.

/pdf/dickkopfs-and-wnt-b-catenin-signalling-in-liver-cancer-3y51gwgtfr.pdf

Dickkopfs and Wnt/β-catenin signalling in liver cancer

Hepatocellular carcinoma (HCC) is a deadly and emerging disease leading to death in Asian countries High hepatitis B virus (HBV) load and chronic hepatitis B (CHB) infection increase the risk of developing HCC HBV is a DNA virus that can integrate DNA into host genome thereby increase the yield of transactivator protein HBxAg that may deregulate many pathways involving in metabolism of cells Several monogenic and polygenic risk factors are also involved in HCC development This review summarizes the mechanism involved in HCC development and discusses some promising therapies to make HCC curative

/pdf/hbv-induced-hcc-major-risk-factors-from-genetic-to-molecular-1ufy4upz8v.pdf

HBV induced HCC: major risk factors from genetic to molecular level.

In order to solve the optimization problem of carbon nanotube (CNT) yarn sensor network embedded in three-dimensional (3D) braided composite materials and realize the structural health monitoring of internal damage of aerospace parts, the multi-objective optimization of the number and location of sensors was studied using non-dominated neighborhood immune algorithm (NNIA). Through the research of 3D six-direction braiding process, stress sensitivity of single CNT yarn sensor, and damage location of 3D braided composites, the number, position, and coverage constraint functions based on NNIA algorithm are constructed. In addition, the number and position of three-dimensional braided composite embedded CNT yarn sensors with different sizes are solved. Through the stress experiment and data analysis of damaged parts, it is proved that the optimized configuration result of CNT yarn sensor obtained by NNIA algorithm is suitable for the damage monitoring of 3D braided composites. The damage location error is less than 1 mm. This study lays a foundation for the establishment of damage source localization model of 3D braided composites.

https://www.mdpi.com/1996-1944/15/23/8534/pdf?version=1670481639

Network Optimization of CNT Yarn Sensor Based on NNIA Algorithm in Damage Monitoring of 3D Braided Composites

We study the conductivities and entanglement structures of two different holographic gapped systems at zero density in the presence of boundaries within AdS/BCFT. The first gapped system is described by the Einstein-scalar gravity and the second one is the dual of AdS soliton geometry. We show that in both these two systems the bulk and boundary conductivities along the spatial direction of the boundary of BCFT are trivial. For the first system, when we increase the size of the subsystem the renormalized entanglement entropy is always non-negative and monotonically decreasing with discontinuous, or continuous, or smooth behavior, depending on the effective tension of the brane. While for the AdS soliton with a boundary, the renormalized entanglement entropy only exhibits a discontinuous drop when we increase the size of the subsystem.

Properties of gapped systems in AdS/BCFT

Gastrin plays a vital role in the development and progression of gastric cancer (GC). Its expression is up-regulated in GC tissues and several GC cell lines. Yet, the underlying mechanism remains to be investigated. Here, we aim to investigate the role and mechanism of gastrin in GC proliferation. Gastrin-overexpressing GC cell model was constructed using SGC7901 cells. Then the differentially expressed proteins were identified by iTRAQ analysis. Next, we use flow cytometry and immunofluorescence to study the effect of gastrin on the mitochondrial potential and mitochondria-derived ROS production. Finally, we studied the underlying mechanism of gastrin regulating mitochondrial function using Co-IP, mass spectrometry and immunofluorescence. Overexpression of gastrin promoted GC cell proliferation in vitro and in vivo. A total of 173 proteins were expressed differently between the controls and gastrin- overexpression cells and most of these proteins were involved in tumorigenesis and cell proliferation. Among them, Cox17, Cox5B and ATP5J that were all localized to the mitochondrial respiratory chain were down-regulated in gastrin-overexpression cells. Furthermore, gastrin overexpression led to mitochondrial potential decrease and mitochondria-derived ROS increase. Additionally, gastrin-induced ROS generation resulted in the inhibition of cell apoptosis via activating NF-kB, inhibiting Bax expression and promoting Bcl-2 expression. Finally, we found gastrin interacted with mitochondrial membrane protein Annexin A2 using Co-IP and mass spectrometry. Overexpr ession of gastrin inhibits GC cell apoptosis by inducing mitochondrial dysfunction through interacting with mitochondrial protein Annexin A2, then up-regulating ROS production to activate NF-kB and further leading to Bax/Bcl-2 ratio decrease. 

Over-Expression of Gastrin Inhibits Apoptosis of Gastric Cancer Cells via Reactive Oxygen Species and Annexin A2-Mediated Mitochondrial Dysfunction

Genetic predisposition of human leucocyte antigen (HLA)-DR has been linked to nonresponse to hepatitis B virus (HBV) vaccination. We sought to reveal their effects on chronic infection and evolution of HBV and development of hepatocellular carcinoma (HCC). Genetic polymorphisms at HLA-DR enhancer regions were genotyped in 4588 participants using quantitative PCR. HBV mutations were determined by sequencing. A dual-luciferase assay was applied to detect the enhancer activity. Associations between HLA-DR polymorphisms and postoperative prognosis were investigated in another cohort of 397 HBV-infected HCC patients. Variant alleles (rs3135395-T, rs3135338-C and rs477515-T) were significantly associated with a decreased risk of HBV persistence in Chinese patients. rs3135395-T, rs3135338-C, rs477515-T and rs2395178-G also significantly decreased HCC risk. rs3135395-T, rs477515-T and rs2395178-G were inversely associated with the generation of A1762T/G1764A, T1753V and C1653T, the HCC-risk HBV mutations. Multiplicative interactions of the variant genotypes with the HCC-risk HBV mutations were significantly associated with a decreased risk of HCC. In multivariate Cox analysis, rs477515-T independently predicted a favourable prognosis, with a hazard ratio of 0.48 (P = .002). The activity of the HLA-DRB1 enhancer with rs477515-T was significantly higher than that with rs477515-C. The activity of the HLA-DRB1 enhancer with rs477515-T and that with rs477515-C was significantly up-regulated by interferon-γ and interleukin-4, respectively. Interleukin-6 significantly inhibited the HLA-DRB1 enhancer activity, and this effect was more evident in those carrying rs477515-T. Polymorphisms predisposing to down-regulation of HLA-DR facilitate the Th1-to-Th2 transition and promote HCC development, possibly via selecting the HCC-risk HBV mutations. This can be transformed into specific prophylaxis of HCC.

The genetic polymorphism down-regulating HLA-DRB1 enhancer activity facilitates HBV persistence, evolution and hepatocarcinogenesis in the Chinese Han population

Genetic predisposition of nuclear factor-kappa B (NF-κB)-signaling pathways linking inflammation to hepatitis B virus (HBV)-induced hepatocellular carcinoma (HCC) remains unresolved. We conducted a case–control study to determine the associations of the polymorphisms within the promoter regions of NFKB1 encoding NF-κB1 and NFKBIA encoding IkappaBalpha with the development of HCC. A total of 404 healthy controls, 482 non-HCC subjects with HBV infection and 202 patients with HCC were included. NFKB1 −94ATTG2 allele and GG allele in the 3′-untranslated region of NFKBIA were more prevalent in HCC patients than in the healthy controls. NFKBIA −826CT and NFKBIA −881AG allelic carriages were more prevalent in HCC patients than in the non-HCC subjects with HBV infection. The estimated haplotype frequency of NFKBIA promoter −881G−826T−519C was significantly higher in the patients with HCC than in the HBV-infected subjects without HCC (odds ratio = 3.142, P = 0.002). As compared with the HBV-infected subjects without HCC, NFKBIA −826 T and NFKBIA −881AG allelic carriages were only associated with HCC risk in the subjects with HBV genotype C. The association of NFKBIA −881AG allelic carriage with HCC risk was not affected by liver cirrhosis (LC) status, alanine aminotransferase level and hepatitis B e antigen status. By multivariate regression analysis, NFKB1 −94ATTG2, NFKBIA −826T, NFKBIA −881AG and HBV genotype C were independently associated with an increased risk of HCC. In conclusion, NFKB1 −94ATTG2 allele and haplotype −881G−826T−519C in NFKBIA promoter were associated with hepatocarcinogenesis. NFKBIA −826T and −881AG were associated with the risk of HCC in the subjects infected with HBV genotype C.

hepatocarcinogenesis in patients infected with hepatitis B virus genotype C

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