Publications by authors named "Zhilei Lv"

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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Human microorganisms, including bacteria, fungi, and viruses, play key roles in several physiological and pathological processes. Some studies discovered that tumour tissues once considered sterile actually host a variety of microorganisms, which have been confirmed to be closely related to oncogenesis. The concept of intratumoural microbiota was subsequently proposed.

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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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Lung adenocarcinoma (LUAD) is a highly heterogeneous tumor with substantial somatic mutations and genome instability, which are emerging hallmarks of cancer. Long non-coding RNAs (lncRNAs) are promising cancer biomarkers that are reportedly involved in genomic instability. However, the identification of genome instability-related lncRNAs (GInLncRNAs) and their clinical significance has not been investigated in LUAD.

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We aimed to compare the age-related clinical characteristics between younger and elderly deceased COVID-19 patients. This single-center retrospective study included 163 adult deceased COVID-19 patients who were admitted to Wuhan Union Hospital West Campus from January 12, 2020, to March 30, 2020. Demographic and clinical features were collected by reviewing the medical records.

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Background: Patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can shed virus, thereby causing human-to-human transmission, and the viral RNA shedding is commonly used as a proxy measure for infectivity.

Methods: We retrospectively reviewed confirmed cases of COVID-19 who attended the fever clinic of Wuhan Union Hospital from January 14 to February 24. In terms of the viral RNA shedding (median values) at first visit, patients were divided into a high-viral RNA shedding group and a low-viral RNA shedding group.

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Background: Coronavirus disease 2019 (COVID-19) has become a public health emergency of global concern. We aimed to explore the risk factors of 14-day and 28-day mortality and develop a model for predicting 14-day and 28-day survival probability among adult hospitalized patients with COVID-19.

Methods: In this multicenter, retrospective, cohort study, we examined 828 hospitalized patients with confirmed COVID-19 hospitalized in Wuhan Union Hospital and Central Hospital of Wuhan between January 12 and February 9, 2020.

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Purpose: The role of serum tumor markers (STMs) in the modern management of epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) mutations in lung cancer remains poorly described. In this study, we investigated whether STMs could be a valuable noninvasive tool to predict EGFR mutations and ALK positivity in non-small-cell lung cancer (NSCLC) patients.

Experimental Design: We retrospectively reviewed and included 1089 NSCLC patients who underwent EGFR or ALK mutation testing and STMs measurement prior to treatment.

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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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Objective: The aim of this study was to explore the predictive value of carcinoembryonic antigen (CEA), squamous cell carcinoma antigen (SCCAg), and neuron-specific enolase (NSE) in the prediction of anaplastic lymphoma kinase (ALK) mutations in advance stage non-small cell lung cancer (NSCLC).

Subjects And Methods: A total of 482 cases with untreated lung adenocarcinoma were retrospectively reviewed. Finally, 72 patients with stage IV were enrolled because of intact data of the detection of ALK rearrangement and serum tumor markers, as well they have not received any previous anticancer therapy.

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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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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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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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Purpose: Epidermal growth factor receptor (EGFR) mutations and the anaplastic lymphoma kinase (ALK) rearrangement are the two most common druggable targets in non-small cell lung cancer (NSCLC). However, genetic testing is sometimes unavailable. Previous studies regarding the predictive role of F-FDG PET/CT for EGFR mutations in NSCLC patients are conflicting.

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Cancer remains one of the most common causes of death and disability and represents a major economic burden in industrialized nations. The renin-angiotensin system (RAS) has been well-recognized as one of the most important regulators of both normal and pathological physiological processes in the brain, kidney, heart, and blood vessels. The activation of the angiotensin-converting enzyme 2/angiotensin-(1-7)/mitochondrial assembly receptor [ACE2/Ang-(1-7)/MasR] axis, which is one component of the RAS, has recently been identified as a critical component of pulmonary systems, gastric mucosa, and cancer.

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Tumour-associated inflammation is a hallmark of malignant carcinomas, and lung cancer is a typical inflammation-associated carcinoma. Interleukin-17 (IL-17) is an important inflammatory cytokine that plays an important role in chronic inflammatory and autoimmune diseases and in inflammation-associated tumours. Numerous studies have shown that IL-17 directly or indirectly promotes tumour angiogenesis and cell proliferation and that it inhibits apoptosis via the activation of inflammatory signalling pathways.

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Inflammation and angiogenesis are two hallmarks of carcinoma. The proinflammatory cytokine interleukin-17 (IL-17) facilitates angiogenesis in lung cancer; however, the underlying mechanism is not fully understood. In this study, tumour microvessel density (MVD) was positively associated with IL-17, interleukin-6 (IL-6), interleukin-8 (IL-8), and vascular endothelial cell growth factor (VEGF) expression in human lung adenocarcinoma tissues, and it was increased in tumour tissues of A549-IL-17 cell-bearing nude mice.

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Epithelial-mesenchymal transition (EMT) plays a vital role in lung inflammatory diseases, including lung cancer. However, the role and mechanism of action of the proinflammatory cytokine IL-17 in EMT in lung adenocarcinoma remain unresolved. In our study, we discovered that the expression of N-cadherin, Vimentin, Snail1, Snail2, and Twist1 was positively correlated with IL-17 expression, while E-cadherin expression was negatively correlated with IL-17 expression in human lung adenocarcinoma tissues.

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Background: Lactare dehydrogenase (LDH) has been proven to be a prognostic and a potential pro-tumor factor in patients with lung cancer. But the prognostic value of serum LDH in small cell lung cancer (SCLC) has not been quantified systematically.

Objective: Thus, this study was to evaluate the correlations between serum LDH and overall survival of SLCLC by systematic review with meta-analysis.

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Interleukin (IL)-36RN, previously known as IL1-F5 and IL-1δ, shares a 360-kb region of chromosome 2q13 with members of IL-1 systems. IL-36RN encodes an anti-inflammatory cytokine, IL-36 receptor antagonist (IL-36Ra). In spite of IL-36Ra showing the highest homology to IL-1 receptor (IL-1R) antagonist, it differs from the latter in aspects including its binding to IL-lRrp2 but not to IL-1R1.

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Background: Retinoic acid-related orphan receptor C isoform 2 (RORC2) is regarded as a pathogenic factor for autoimmune and inflammatory diseases and tumours. Previous studies have primarily focused on RORC2 expression in IL-17-producing immune cells but not in carcinoma cells; thus, little is known about the roles of RORC2 in the progression of human non-small cell lung cancer (NSCLC). In this study, we analysed the expression of RORC2 and its participation in tumour progression in NSCLC.

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Interleukin-17 receptor (IL-17RA) is essential for proinflammatory cytokine IL-17-mediated pathogenesis of various tumors. IL-17RA is upregulated by some proinflammatory cytokines such as IL-21 and IL-15 and downregulated by IL-2, while the effect of IL-1β, IL-6, IL-8, TNF-α on IL-17RA expression in non-small cell lung caner (NSCLC) remains unknown. Our findings revealed that IL-17RA mRNA was increased in NSCLC tissues compared with the corresponding peritumor tissues (P = 0.

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