Publications by authors named "Guanghai Yang"

Evaluating the invasiveness of lung adenocarcinoma is crucial for determining the appropriate surgical strategy, impacting postoperative outcomes. This study developed a multimodality model combining radiomics, intraoperative frozen section (FS) pathology, and clinical indicators to predict invasion status. The study enrolled 1,424 patients from two hospitals, divided into multimodal training, radiology testing, and pathology testing cohorts.

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Background: Malignant tumours seriously threaten human life and health, and effective treatments for cancer are still being explored. The ability of SHC SH2 domain-binding protein 1 (SHCBP1) to induce cell cycle disturbance and inhibit tumour growth has been increasingly studied, but its dynamic role in the tumour cell cycle and corresponding effects leading to mitotic catastrophe and DNA damage have rarely been studied.

Results: In this paper, we found that the nucleoprotein SHCBP1 exhibits dynamic spatiotemporal expression during the tumour cell cycle, and SHCBP1 knockdown slowed cell cycle progression by inducing spindle disorder, as reflected by premature mitotic entry and multipolar spindle formation.

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Despite advancements in therapeutic options, the overall prognosis for non-small cell lung cancer (NSCLC) remains poor. Therefore, it is crucial to further explore the etiology and targets for novel treatments to effectively manage NSCLC. In this study, immunohistochemistry was used to analyze the expression of aldolase, fructose-bisphosphate C (ALDOC) protein in tumor tissues and adjacent non-malignant tissues from 79 NSCLC patients.

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Introduction: Tyrosine kinase inhibitors (TKIs) that target epidermal growth factor receptor (EGFR) mutations are commonly administered to EGFR-positive lung cancer patients. However, resistance to EGFR-TKIs (mostly gefitinib and erlotinib) is presently a significant problem. Limited studies have focused on an EGFR-TKI resistance-related gene signature (ERS) in lung adenocarcinoma (LUAD).

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Lung adenocarcinoma (LUAD) is the primary histological subtype of lung cancer with a markedly heterogeneous prognosis. Therefore, there is an urgent need to identify optimal prognostic biomarkers. We aimed to explore the value of the circadian miRNA (cmiRNA) pair in predicting prognosis and guiding the treatment of LUAD.

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Tyrosine kinase inhibitors (TKIs) resistance is a challenge in patients with epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC). Here, we examined the effect of Fasudil in reversing TKIs resistance. The results of CCK8 assay, clone formation assay, cell cycle arrest analysis, and apoptosis analysis show that Fasudil treatment effectively suppressed the growth and induced apoptosis of the EGFR-mutant NSCLC cells.

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Background: The N6-methyladenosine (m A) can modify long non-coding RNAs (lncRNAs), thereby influencing a wide array of biological functions. However, the prognosis of m A-related lncRNAs (m ARLncRNAs) in non-small cell lung cancer (NSCLC) remains largely unknown.

Methods: Pearson correlation analysis was used to identify m ARLncRNAs in 1835 NSCLC patients and with the condition (|Pearson R| > 0.

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Background: Timely identification of epidermal growth factor receptor (EGFR) mutation and anaplastic lymphoma kinase (ALK) rearrangement status in patients with non-small cell lung cancer (NSCLC) is essential for tyrosine kinase inhibitors (TKIs) administration. We aimed to use artificial intelligence (AI) models to predict EGFR mutations and ALK rearrangement status using common demographic features, pathology and serum tumor markers (STMs).

Methods: In this single-center study, demographic features, pathology, EGFR mutation status, ALK rearrangement, and levels of STMs were collected from Wuhan Union Hospital.

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Lung adenocarcinoma (LUAD) represents the most frequently diagnosed histological subtype of non-small cell lung cancer with the highest mortality worldwide. Transcriptional dysregulation is a hallmark of nearly all kinds of cancers. In the study, we identified that the POU domain, class 6, transcription factor 1 (POU6F1), a member of the POU family of transcription factors, was closely associated with tumor stage and death in LUAD.

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Purpose: There is a major limitation in the immunotherapy for solid cancer is that it only benefited a minority of cancer patients. This study aims to investigate whether the differential composition of the lung microbiome could affect the sustained clinical responses in lung cancers treated with immunotherapy.

Methods: Twenty-seven non-responders and 19 responders treated with anti-PD-1 therapy were included in the discovery set.

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Background: Postdischarge immunity and its correlation with clinical features among patients recovered from coronavirus disease 2019(COVID-19) are poorly described. This prospective cross-sectional study explored the inflammatory profiles and clinical recovery of patients with COVID-19 at 3 months after hospital discharge.

Methods: Patients with COVID-19 discharged from 4 hospitals in Wuhan, recovered asymptomatic patients (APs) from an isolation hotel, and uninfected healthy controls (HCs) were recruited.

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Article Synopsis
  • Pleural effusion, a prevalent respiratory condition, poses challenges for rapid diagnosis, especially in differentiating between tuberculosis pleural effusion (TPE) and malignancy pleural effusion (MPE).
  • This study utilized advanced metabolomics and lipidomics to analyze the metabolite profiles of large and small extracellular vesicles (EVs) derived from pleural effusion, identifying a total of 579 metabolites.
  • A notable outcome was the identification of four potential biomarkers that effectively distinguish TPE from MPE, showing high diagnostic performance, particularly valuable for patients with prior misdiagnoses.
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Esophageal adenocarcinoma (EAC) is the cancer arising from the esophagus, which frequently develop from Barrett's esophagus (BE). Extracellular vesicles (EVs), particularly exosomes, are nanosized vesicles of endosomal origin released from various types of cells that have been implicated in cancers. However, the significance of circulating exosomes during the progression of BE to EAC remains unknown.

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Finding reliable markers for predicting the efficacy of immunotherapy is urgently needed. We sought to investigate the association between serum microRNAs (miRNAs) and checkpoint inhibitor response in non-small cell lung cancer (NSCLC). Discovery assay with sera miRNA profiling was performed, demonstrating 27 sera miRNAs (relative fold >2, p < .

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With the development of nanotechnology, significant progress has been made in the design, and manufacture of nanoparticles (NPs) for use in clinical treatments. Recent increases in our understanding of the central role of macrophages in the context of inflammation and cancer have reinvigorated interest in macrophages as drug targets. Macrophages play an integral role in maintaining the steady state of the immune system and are involved in cancer and inflammation processes.

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: Smoking is a strong relative risk factor for lung cancer. Extracellular vesicles (EVs), particularly exosomes, have been implicated in cancers. In this study, we characterized smoking induced extracellular vesicles in smokers with non-small cell lung cancer (NSCLC).

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Cysteine oxidation occurs at the active site of deubiquitinases (DUBs) during many biologic signaling cascades. Here we report that hepatocellular carcinoma cells (HCCs) generated higher levels of endogenous reactive oxygen species (ROS). This elevated ROS production was inhibited by NADPH oxidase inhibitor diphenylene iodonium (DPI) and mitochondria electron chain inhibitor rotenone in HCC cells.

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The six members of the interleukin (IL)‑17 gene family (IL‑17A‑F) have been identified in various types of cancer. Although lung cancer is the leading cause of cancer‑related death worldwide and IL‑17A was found to play a critical role in lung cancer, there is little knowledge concerning the association between the other five members of the IL‑17 family and lung cancer. The genetic mutations and expression of IL‑17 family members were investigated using the Catalogue of Somatic Mutations in Cancer (COSMIC), Oncomine, and cBio Cancer Genomics Portal (cBioPortal) databases.

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Cell membrane-derived microparticles (MPs), the critical mediators of intercellular communication, have gained much interest for use as natural drug delivery systems. Here, we examined the therapeutic potential of tumor cell-derived MPs (TMPs) in the context of malignant pleural effusion (MPE). TMPs packaging the chemotherapeutic drug methotrexate (TMPs-MTX) markedly restricted MPE growth and provided a survival benefit in MPE models induced by murine Lewis lung carcinoma and colon adenocarcinoma cells.

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The purpose of this study was to set up a beagle dog model, for radiation-induced lung injury, that would be able to supply fresh lung tissues in the different injury phases for research into oxidative stress levels and mitochondrial gene expression. Blood serum and tissues were collected via CT-guided core needle biopsies from dogs in the various phases of the radiation response over a 40-week period. Levels of reactive oxygen species (ROS) and manganese superoxide dismutase 2 (MnSOD) protein expression in radiation-induced lung injury were determined by in situ immunocytochemistry; malondialdehyde (MDA) content and reductase activity in the peripheral blood were also tested; in addition, the copy number of the mitochondrial DNA and the level of function of the respiratory chain in the lung tissues were assessed.

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Adrenergic receptors (ARs), especially β-ARs, are constitutively expressed in most mammalian cells and are associated with various malignancies including lung cancer. Epidemiologic studies have reported that activation of β-AR signalling promotes the development and progression of lung cancer and that pharmacological interference by β-AR blockers could partially reverse lung cancer progression. In this review, we mainly focus on the role of β-ARs in lung cancer and then reveal the possible application of AR blockers in anti-tumour therapy for lung cancer.

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The interleukin-(IL)-1 subfamily consists of IL-1α, IL-1β, IL-1 receptor antagonist IL-1Ra and IL-33. These cytokines are the main members of the IL-1 family and have been widely recognized as having significant roles in pro-inflammatory and immunomodulatory actions. Mounting evidence has revealed that these cytokines also play key roles in the regulation of glycolysis, which is an important metabolic pathway in most organisms that provides energy.

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Retinoic acid receptor-related orphan receptors (RORs) include RORα (NR1F1), RORβ (NR1F2), and RORγ (NR1F3). These receptors are reported to activate transcription through ligand-dependent interactions with co-regulators and are involved in the development of secondary lymphoid tissues, autoimmune diseases, inflammatory diseases, the circadian rhythm, and metabolism homeostasis. Researches on RORs contributing to cancer-related processes have been growing, and they provide evidence that RORs are likely to be considered as potential therapeutic targets in many cancers.

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The present study investigated the effect of tetrandrine on lung cancer cell growth and apoptosis, and its possible underlying molecular mechanism. A549 human lung cancer cells were incubated with between 2.5 and 10 µM tetrandrine for 12, 24 and 48 h, following which the effect of tetrandrine on cell viability and apoptosis were assessed using an MTT assay and flow cytometry.

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The importance of understanding how interleukin-33 (IL-33) is regulated (particularly by miRs) is critical in IL-33 biology, and evidence of this in asthma pathology is limited. MicroRNA profiling of cells isolated from bronchoalveolar lavage of 14 asthmatic patients and 11 healthy controls revealed miR-200b and miR-200c were significantly reduced in asthmatic patients compared with healthy controls. The reduction was validated in two independent models of allergen-induced allergic airway inflammation and further demonstrated to be inversely correlated with asthma severity, as well as increased IL-33 production in asthmatic patients.

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