Tumor microenvironment remodeling plus immunotherapy could be used in mesenchymal-like tumor with high tumor residual and drug resistant rate.

Epithelial-mesenchymal transition (EMT) is a common process during tumor progression and is always related to residual tumor, drug resistance and immune suppression. However, considering the heterogeneity in EMT process, there is still a need to establish robust EMT classification system with reasonable molecular, biological and clinical implications to investigate whether these unfavorable survival factors are common or unique in different individuals. In our work, we classify tumors with four EMT status, that is, EMT, EMT, EMT-NOS (Not Otherwise Specified), and EMT-AKT (AKT pathway overactivation) subtypes.

T cells, NK cells, and tumor-associated macrophages in cancer immunotherapy and the current state of the art of drug delivery systems.

The immune system provides full protection for the body by specifically identifying 'self' and removing 'others'; thus protecting the body from diseases. The immune system includes innate immunity and adaptive immunity, which jointly coordinate the antitumor immune response. T cells, natural killer (NK) cells and tumor-associated macrophages (TAMs) are the main tumor-killing immune cells active in three antitumor immune cycle.

Corrigendum: The m6A methyltransferase METTL16 inhibits the proliferation of pancreatic adenocarcinoma cancer cells via the p21 signaling pathway.

[This corrects the article DOI: 10.3389/fonc.2023.

The m6A methyltransferase METTL16 inhibits the proliferation of pancreatic adenocarcinoma cancer cells the p21 signaling pathway.

Background: Many studies have reported that N6-methyladenosine (m6A) modification plays a critical role in the epigenetic regulation of organisms and especially in the pathogenesis of malignant diseases. However, m6A research has mainly focused on methyltransferase activity mediated by METTL3, and few studies have focused on METTL16. The aim of this study was to investigate the mechanism of METTL16, which mediates m6A modification, and its role in pancreatic adenocarcinoma (PDAC) cell proliferation.

circMMD reduction following tumor treating fields inhibits glioblastoma progression through FUBP1/FIR/DVL1 and miR-15b-5p/FZD6 signaling.

Background: Tumor treating fields (TTF) is the latest treatment for GBM. Circular RNA (circRNA) has been demonstrated to play critical roles in tumorigenesis. However, the molecular mechanism of TTF remained largely unknown and the role of circRNA in TTF was not reported.

Preemptive interferon-α therapy could prevent relapse of acute myeloid leukemia following allogeneic hematopoietic stem cell transplantation: A real-world analysis.

Introduction: Measurable residual disease (MRD)-directed interferon-a treatment (i.e. preemptive IFN-α treatment) can eliminate the MRD in patients with acute myeloid leukemia (AML) after allogeneic hematopoietic stem cell transplantation (allo-HSCT).

Cancer cell intrinsic TIM-3 induces glioblastoma progression.

Glioblastoma (GBM) is identified to share common signal pathways between glioma and immune cells. Here, we find that T cell immunoglobulin domain and mucin domain protein 3 (TIM-3) is one of the most common co-inhibitory immune checkpoints in GBM shared by tumor and non-tumor cells. Glioma cell-intrinsic TIM-3 is involved in not only regulating malignant behaviors of glioma cells but also inducing macrophage migration and transition to anti-inflammatory/pro-tumorigenic phenotype by a TIM-3/interleukin 6 (IL6) signal.

Association between psychological symptoms and illegal driving behaviors in a sample of Chinese private car drivers.

Background: Findings on the associations between psychological symptoms and driving behaviors in private car drivers are inadequate.

Method: The study consisted of 3,115 private car drivers in Yulin, China. The measurements included socio-demographic data, traffic violations, accidents, and Symptom Checklist-90 (SCL-90).

Timing of glaucoma treatment in patients with MICOF: A retrospective clinical study.

Purpose: To summarize and discuss the treatment and timing of glaucoma in patients with MICOF keratoprosthesis implantation to guide follow-up clinical treatment.

Methods: The data of 39 eyes (39 patients) with the Moscow Eye Microsurgery Complex in Russia (MICOF) keratoprosthesis implantation in our hospital from 1 January 2002 to 31 December 2017 were collected, including patients with preexisting glaucoma and those who developed glaucoma after MICOF. The sex, age, preoperative diagnosis, glaucoma surgery, keratoplasty, times of keratoplasty, best corrected visual acuity (BCVA) and final follow-up corrected visual acuity, visual field (VF) defect, and cup-to-disk ratio (CDR) were statistically analyzed.

PIWI-interacting RNAs in cancer: Biogenesis, function, and clinical significance.

PIWI-interacting RNAs (piRNAs) are a less-studied class of small non-coding RNAs approximately 24-31 nucleotides in length. They express in germline and somatic cells and form complexes with PIWI proteins to exert regulatory effects. New studies show that piRNAs are aberrantly expressed in various cancers.

Whole transcriptome and proteome analyses identify potential targets and mechanisms underlying tumor treating fields against glioblastoma.

Glioblastoma (GBM) is one of the most malignant types of brain cancer. Tumor treating fields (TTFields) is the up-to-date treatment for GBM. However, its molecular mechanism requires additional investigation.

Noninvasively Assessed Portal Hypertension Grade Predicts Post-Hepatectomy Liver Failure in Patients With HepatocellCarcinoma: A Multicenter Study.

Purpose: To determine the predictive value of portal hypertension (PH) for the development of post-hepatectomy liver failure (PHLF) in patients with hepatocellular carcinoma (HCC).

Patients And Methods: This study enrolled a total of 659 patients with HCC that received hepatectomy as a first-line therapy. PH was classified as grade 0, 1, and 2 according to whether the indirect criteria for PH were met: 1) patients had obvious varicose veins and 2) splenomegaly was present and platelet count < 100 × 10/L.

Nosocomial Infections During Extracorporeal Membrane Oxygenation in Pediatric Patients: A Multicenter Retrospective Study.

Objective: Extracorporeal membrane oxygenation (ECMO) is increasingly used in critically ill patients with respiratory and/or cardiac failure. This study aimed to investigate the epidemiology and risk factors of nosocomial infection (NI) in pediatric patients who underwent ECMO for respiratory and/or circulatory failure.

Methods: Medical records for patients that were administered underwent ECMO support at Xiangya Second Hospital of Central South University, The Sixth Medical Center of PLA General Hospital, and Children's Hospital Affiliation of Zhengzhou University, from September 2012 to December 2019 were retrospectively reviewed.

The Potential Mechanism Behind Native and Therapeutic Collaterals in Moyamoya.

Background And Purpose: To explore the genetic basis and molecular mechanism of native arteriogenesis and therapeutic synangiosis in moyamoya disease (MMD).

Methods: An angiography-based study using patients from a prospective trial of encephaloduroarteriosynangiosis (EDAS) surgery was performed. The spontaneous collaterals grades were evaluated according to the system described by a new grading system.

CpG Site-Specific Methylation-Modulated Divergent Expression of Transcript Variants Facilitates Nongenetic Intratumor Heterogeneity in Human Hepatocellular Carcinoma.

Background: Hepatocellular carcinoma (HCC) is one of the most lethal human tumors with extensive intratumor heterogeneity (ITH). Serine protease 3 (PRSS3) is an indispensable member of the trypsin family and has been implicated in the pathogenesis of several malignancies, including HCC. However, the paradoxical effects of on carcinogenesis due to an unclear molecular basis impede the utilization of its biomarker potential.

Chemerin enhances mesenchymal features of glioblastoma by establishing autocrine and paracrine networks in a CMKLR1-dependent manner.

Glioblastoma multiforme (GBM) with mesenchymal features exhibits enhanced chemotherapeutic resistance and results in reduced overall survival. Recent studies have suggested that there is a positive correlation between the GBM mesenchymal status and immune cell infiltration. However, the mechanisms by which GBM acquires its mesenchymal features in a tumor immune microenvironment-dependent manner remains unknown.

Ferroptosis, as the most enriched programmed cell death process in glioma, induces immunosuppression and immunotherapy resistance.

Background: Immunosuppressive microenvironment is a major cause of immunotherapeutic resistance in glioma. In addition to secreting compounds, tumor cells under programmed cell death (PCD) processes release abundant mediators to modify the neighboring microenvironment. However, the complex relationship among PCD status, immunosuppressive microenvironment, and immunotherapy is still poorly understood.

Dual role of ARPC1B in regulating the network between tumor-associated macrophages and tumor cells in glioblastoma.

The tumor microenvironment (TME) plays a critical role in promoting the growth and metastasis of glioblastoma (GBM). Tumor-associated macrophages (TAMs), the most abundant myeloid cells infiltrating in TME, produce proinflammatory cytokines, regulate glioma cell pools, and lead to GBM progression. Understanding the mechanism of GBM-TAMs regulation can help to find new targeted therapeutic strategies against GBM.

Increased Platelet-CD4 T Cell Aggregates Are Correlated With HIV-1 Permissiveness and CD4 T Cell Loss.

Chronic HIV-1 infection is associated with persistent inflammation, which contributes to disease progression. Platelet-T cell aggregates play a critical role in maintaining inflammation. However, the phenotypic characteristics and clinical significance of platelet-CD4 T cell aggregates remain unclear in different HIV-infected populations.

Establishment of tumor inflammasome clusters with distinct immunogenomic landscape aids immunotherapy.

Inflammasome signaling is a reaction cascade that influences immune response and cell death. Although the inflammasomes participate in tumorigenesis, their role as an oncogenic booster or a tumor suppresser is still controversial. Therefore, it is important to comprehensively investigate the inflammasome signaling status across various cancers to clarify its clinical and therapeutic significance.