Effect of Helicobacter pylori infection on survival outcomes of patients undergoing radical gastrectomy after neoadjuvant chemotherapy: a multicenter study in China.

Background: Neoadjuvant chemotherapy (NAC) has been confirmed to improve the prognosis of patients with advanced gastric cancer (AGC). However, no study has investigated whether Helicobacter pylori (HP) infection affects the postoperative survival of patients who receive NAC.

Methods: This retrospective cohort study included 307 patients with AGC who underwent laparoscopic radical gastrectomy after NAC at three hospitals in China between January 1, 2016, and April 31, 2020.

Individualized patient tumor organoids faithfully preserve human brain tumor ecosystems and predict patient response to therapy.

Tumor organoids are important tools for cancer research, but current models have drawbacks that limit their applications for predicting response to therapy. Here, we developed a fast, efficient, and complex culture system (IPTO, individualized patient tumor organoid) that accurately recapitulates the cellular and molecular pathology of human brain tumors. Patient-derived tumor explants were cultured in induced pluripotent stem cell (iPSC)-derived cerebral organoids, thus enabling culture of a wide range of human tumors in the central nervous system (CNS), including adult, pediatric, and metastatic brain cancers.

Transketolase attenuates the chemotherapy sensitivity of glioma cells by modulating R-loop formation.

Glioblastoma (GBM) is a highly lethal malignant brain tumor with poor survival rates, and chemoresistance poses a significant challenge to the treatment of patients with GBM. Here, we show that transketolase (TKT), a metabolic enzyme in the pentose phosphate pathway (PPP), attenuates the chemotherapy sensitivity of glioma cells in a manner independent of catalytic activity. Mechanistically, chemotherapeutic drugs can facilitate the translocation of TKT protein from the cytosol into the nucleus, where TKT physically interacts with XRN2 to regulate the resolution and removal of R-loops.

The USP35-CXCR3 Axis plays an oncogenic role in JeKo-1 mantle cell lymphoma cells.

In B cells, the chemokine receptor CXCR3 is expressed only by a subset of B cells. However, CXCR3 is highly expressed in a rare type of B-cell lymphoma known as Mantle Cell Lymphoma (MCL) and CXCR3 inhibitor impairs proliferation and induces apoptosis in the MCL cell line JeKo-1. Despite this, the mechanism responsible for maintaining high levels of CXCR3 in MCL cells remains unclear.

SOX10 mediates glioblastoma cell-state plasticity.

Phenotypic plasticity is a cause of glioblastoma therapy failure. We previously showed that suppressing the oligodendrocyte-lineage regulator SOX10 promotes glioblastoma progression. Here, we analyze SOX10-mediated phenotypic plasticity and exploit it for glioblastoma therapy design.

A multidimensional atlas of human glioblastoma-like organoids reveals highly coordinated molecular networks and effective drugs.

Recent advances in the genomics of glioblastoma (GBM) led to the introduction of molecular neuropathology but failed to translate into treatment improvement. This is largely attributed to the genetic and phenotypic heterogeneity of GBM, which are considered the major obstacle to GBM therapy. Here, we use advanced human GBM-like organoid (LEGO: Laboratory Engineered Glioblastoma-like Organoid) models and provide an unprecedented comprehensive characterization of LEGO models using single-cell transcriptome, DNA methylome, metabolome, lipidome, proteome, and phospho-proteome analysis.

Distinct aneuploid evolution of astrocytoma and glioblastoma during recurrence.

Astrocytoma and glioblastoma (GB) are reclassified subtypes of adult diffuse gliomas based on distinct isocitrate dehydrogenase (IDH) mutation in the fifth edition of the WHO Classification of Tumors of the Central Nervous System. The recurrence of gliomas is a common and inevitable challenge, and analyzing the distinct genomic alterations in astrocytoma and GB could provide insights into their progression. This study conducted a longitudinal investigation, utilizing whole-exome sequencing, on 65 paired primary/recurrent gliomas.

Study on the Antioxidant Effect of Tanshinone IIA on Diabetic Retinopathy and Its Mechanism Based on Integrated Pharmacology.

Aim: To explore the effect of tanshinone IIA on diabetic retinopathy (DR) and its mechanism.

Methods: GeneCards and OMM databases were used to mine DR-related genes. The chemical structure of tanshinone IIA was searched by PubChem, and the potential target was predicted by PharmMapper.

High-Speed Shift Register with Dual-Gated Thin-Film Transistors for a 31-Inch 4K AMOLED Display.

In this work, a promising dual-gated thin film transistor (TFT) structure has been proposed and introduced in the shift register (SR)-integrated circuits to reduce the rising time. The threshold voltage can be simultaneously changed by the top gate and the bottom gate in the proposed dual-gated TFTs. When the SR circuits start to export the scan signals in the displays, the driving currents in the SR circuits are increased by switching the working station of driving TFTs from the enhancement characterization to the depletion characterization.

Research on the Mechanism of Liuwei Dihuang Decoction for Osteoporosis Based on Systematic Biological Strategies.

Background: Osteoporosis is an important health problem worldwide. Liuwei Dihuang Decoction (LDD) and its main ingredients may have a good clinical effect on osteoporosis. Meanwhile, its mechanism for treating osteoporosis needs to be further revealed in order to provide a basis for future drug development.

The Anti-Glioma Effect of Juglone Derivatives through ROS Generation.

Juglone has been extensively reported as a natural antitumor pigment. However, it is easy to be oxidized due to active hydroxy in the quinone. Here, we designed some new juglone derivatives, as the hydroxy was replaced by methyl (D1), allyl (D2), butyl (D3), and benzyl (D4) groups.

Corrigendum to "Exploring the Pharmacological Mechanism of Liuwei Dihuang Decoction for Diabetic Retinopathy: A Systematic Biological Strategy-Based Research".

[This corrects the article DOI: 10.1155/2021/5544518.].

Exploring the Effect of Jiawei Buguzhi Pills on TGF--Smad Pathway in Postmenopausal Osteoporosis Based on Integrated Pharmacological Strategy.

Objective: To explore the effect of Jiawei Buguzhi Pills (JWBGZP) on the TGF--Smad pathway in postmenopausal osteoporosis (PMO) based on integrated pharmacological strategy.

Method: The ETCM database was used to collect JWBGZP. GeneCards and OMIM databases were utilized to obtain PMO-related genes.

Exploring the Pharmacological Mechanism of Liuwei Dihuang Decoction for Diabetic Retinopathy: A Systematic Biological Strategy-Based Research.

Objective: To explore the pharmacological mechanism of Liuwei Dihuang decoction (LDD) for diabetic retinopathy (DR).

Methods: The potential targets of LDD were predicted by PharmMapper. GeneCards and other databases were used to collect DR genes.

Exploring the Regulatory Mechanism of Modified Huanglian Maidong Decoction on Type 2 Diabetes Mellitus Biological Network Based on Systematic Pharmacology.

Objective: To explore the mechanism of modified Huanglian Maidong decoction (Maidong-Sanqi-Huanglian Compounds, MSHCs) intervention in type 2 diabetes mellitus (T2DM).

Method: This study used PubChem and SciFinder to collect the molecular structure of MSHCs, used PharmMapper to predict the potential targets of MSHC, and combined them with the T2DM gene to construct MSHC-T2DM protein-protein interaction (PPI) network. The plugin MCODE in Cytoscape 3.

Integrative Ranking of Enhancer Networks Facilitates the Discovery of Epigenetic Markers in Cancer.

Regulation of gene expression through multiple epigenetic components is a highly combinatorial process. Alterations in any of these layers, as is commonly found in cancer diseases, can lead to a cascade of downstream effects on tumor suppressor or oncogenes. Hence, deciphering the effects of epigenetic alterations on regulatory elements requires innovative computational approaches that can benefit from the huge amounts of epigenomic datasets that are available from multiple consortia, such as Roadmap or BluePrint.

Glioblastoma epigenome profiling identifies SOX10 as a master regulator of molecular tumour subtype.

Glioblastoma frequently exhibits therapy-associated subtype transitions to mesenchymal phenotypes with adverse prognosis. Here, we perform multi-omic profiling of 60 glioblastoma primary tumours and use orthogonal analysis of chromatin and RNA-derived gene regulatory networks to identify 38 subtype master regulators, whose cell population-specific activities we further map in published single-cell RNA sequencing data. These analyses identify the oligodendrocyte precursor marker and chromatin modifier SOX10 as a master regulator in RTK I-subtype tumours.

Hypoxia and the hypoxia inducible factor 1α activate protein kinase A by repressing RII beta subunit transcription.

Overactivation of the cAMP signal transduction pathway plays a central role in the pathogenesis of endocrine tumors. Genetic aberrations leading to increased intracellular cAMP or directly affecting PKA subunit expression have been identified in inherited and sporadic endocrine tumors, but are rare indicating the presence of nongenomic pathological PKA activation. In the present study, we examined the impact of hypoxia on PKA activation using human growth hormone (GH)-secreting pituitary tumors as a model of an endocrine disease displaying PKA-CREB overactivation.

GPD1 Specifically Marks Dormant Glioma Stem Cells with a Distinct Metabolic Profile.

Brain tumor stem cells (BTSCs) are a chemoresistant population that can drive tumor growth and relapse, but the lack of BTSC-specific markers prevents selective targeting that spares resident stem cells. Through a ribosome-profiling analysis of mouse neural stem cells (NSCs) and BTSCs, we find glycerol-3-phosphate dehydrogenase 1 (GPD1) expression specifically in BTSCs and not in NSCs. GPD1 expression is present in the dormant BTSC population, which is enriched at tumor borders and drives tumor relapse after chemotherapy.

Evolutionary Trajectories of IDH Glioblastomas Reveal a Common Path of Early Tumorigenesis Instigated Years ahead of Initial Diagnosis.

We studied how intratumoral genetic heterogeneity shapes tumor growth and therapy response for isocitrate dehydrogenase (IDH)-wild-type glioblastoma, a rapidly regrowing tumor. We inferred the evolutionary trajectories of matched pairs of primary and relapsed tumors based on deep whole-genome-sequencing data. This analysis suggests both a distant origin of de novo glioblastoma, up to 7 years before diagnosis, and a common path of early tumorigenesis, with one or more of chromosome 7 gain, 9p loss, or 10 loss, at tumor initiation.

Branched-chain ketoacids secreted by glioblastoma cells via MCT1 modulate macrophage phenotype.

Elevated amino acid catabolism is common to many cancers. Here, we show that glioblastoma are excreting large amounts of branched-chain ketoacids (BCKAs), metabolites of branched-chain amino acid (BCAA) catabolism. We show that efflux of BCKAs, as well as pyruvate, is mediated by the monocarboxylate transporter 1 (MCT1) in glioblastoma.