Publications by authors named "KuiKui Zhu"

Article Synopsis
  • The era of precision therapy has made treating patients with positive driver genes, especially EGFR mutations in non-small cell lung cancer (NSCLC), a critical area of global research, with EGFR mutations found in about 17% of cases.
  • Targeted therapies for EGFR mutations are effective initially, but patients often develop resistance over time.
  • A case study illustrates that a patient with advanced lung adenocarcinoma experienced a transformation to small cell lung cancer and developed hypertropic pulmonary osteoarthropathy (HPOA) after 6 months of treatment, suggesting that early detection of HPOA may indicate potential resistance and disease progression.
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Cancer cells inevitably develop radioresistance during lung adenocarcinoma radiotherapy. However, the mechanisms are incompletely clarified. In this study, we show that FIBP protein expression in lung adenocarcinoma tissues is upregulated and associated with worse overall survival.

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Thymomas and thymic carcinomas are rare and primary tumors of the mediastinum which is derived from the thymic epithelium. Thymomas are the most common primary anterior mediastinal tumor, while ectopic thymomas are rarer. Mutational profiles of ectopic thymomas may help expand our understanding of the occurrence and treatment options of these tumors.

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Objective: The combination of stereotactic body radiation therapy (SBRT) and immune checkpoint inhibitors (ICIs) is actively being explored in advanced non-small-cell lung cancer (NSCLC) patients. However, little is known about the optimal fractionation and radiotherapy target lesions in this scenario. This study investigated the effect of SBRT on diverse organ lesions and radiotherapy dose fractionation regimens on the prognosis of advanced NSCLC patients receiving ICIs.

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Radioresistance is the major factor of glioblastoma multiforme (GBM) treatment failure and relapse. Hypoxia and autophagy are linked to radioresistance and poor prognosis in solid tumors, but mechanisms remain unknown. Thus, we hypothesize that hypoxia may activate autophagy through two critical factors, HIF1A and Beclin-1, resulting in radioresistance of GBM and .

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Metastasis remains the primary cause of small cell lung cancer (SCLC)-related deaths. Growing evidence links tumor metastasis with a pre-metastatic microenvironment characterized by an anti-inflammatory response, immunosuppression, and the presence of tumor-derived exosomes. To clarify the relationships among these factors in SCLC, we analyzed SCLC patient samples as well as a mouse model.

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Background: Few studies have focused on the subclinical cardiotoxicity of immune checkpoint inhibitors (ICIs) in cancer patients. This study aimed to evaluate the manifestations of subclinical cardiotoxicity of ICI therapy using cardiovascular magnetic resonance (CMR) and to explore whether CMR parameters can help predict cardiotoxicity at the early stage of ICI therapy.

Methods: A prospective, longitudinal study was conducted among patients with lung cancer.

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The regulation of fibrotic activities is key to improving pathological remodelling post-myocardial infarction (MI). Currently, in the clinic, safe and curative therapies for cardiac fibrosis and improvement of the pathological fibrotic environment, scar formation and pathological remodelling post-MI are lacking. Previous studies have shown that miR-486 is involved in the regulation of fibrosis.

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Background: Programmed cell death protein 1 (PD-1) antibody has been approved for a variety of tumors, but its effective rate is unsatisfactory. New evidence suggests that mast cells are an important component of the tumor microenvironment and are associated with resistance to immunotherapy, but the underlying mechanism is not clear.

Methods: Bioinformatics analysis of patients with melanoma in TCGA-SKCM and GSE91061 was used to determine the prognostic value of mast cells and their association with anti-PD-1 immunotherapy.

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The efficacy of apatinib has been confirmed in the treatment of solid tumors, including non-small-cell lung cancer (NSCLC). However, the direct functional mechanisms of tumor lethality mediated by apatinib and the precise mechanisms of drug resistance are largely unknown. In this study, we demonstrated that apatinib could reprogram glutamine metabolism in human NSCLC via a mechanism involved in amino acid metabolic imbalances.

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Vesicles, also known as "microparticles", are vesicle-like structures that are released outside the cell in a "sprouting" manner when the cytoskeleton is changed during cell activation or apoptosis, with a diameter of about 100-1000 nm, and are carriers of material information exchange between cells. Tumor-derived extracellular vesicles can effectively deliver drugs to the nucleus of tumor stem cells, thus effectively killing them without toxic side effects. The underlying mechanism involves the soft nature of tumor stem cells that allows better uptake of vesicles, and the entry of drug-carrying vesicles into lysosomes and facilitation of lysosomal movement toward the nucleus to deliver drugs to the nucleus.

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Pulmonary large-cell neuroendocrine carcinoma (LCNEC) is a rare and highly aggressive cancer with a very poor prognosis. The proper treatment decision and possible prognosis outcome for advanced LCNEC is always an enormous challenge due to its scarcity. Here, we presented a 59-year-old male patient with advanced LCNEC with a non-neuroendocrine immunophenotype who received endostar plus pembrolizumab combined with a platinum-based dual chemotherapy regime as a first-line treatment.

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Background: Lung cancer is the most prevalent malignancy worldwide. Most cases are sporadic and carry somatic mutations in hotspot genes. However, accumulating studies have identified several germline mutations that predispose patients to lung cancer at present.

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Background: Chemoradiotherapy-induced PD-L1 upregulation leads to therapeutic resistance and treatment failure. The PD-1/PD-L1 blocking antibodies sensitize cancers to chemoradiotherapy by blocking extracellular PD-1 and PD-L1 binding without affecting the oncogenic function of intracellular PD-L1. Reversing the chemoradiation-induced PD-L1 expression could provide a new strategy to achieve a greater anti-tumour effect of chemoradiotherapy.

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The incidence of head and neck squamous cell carcinoma (HNSC) is increasing year by year. The nerve is an important component of the tumor microenvironment, which has a wide range of cross-talk with tumor cells and immune cells, especially in highly innervated organs, such as head and neck cancer and pancreatic cancer. However, the role of cancer-nerve cross-talk-related genes (NCCGs) in HNSC is unclear.

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This study analyzed the effect of Arbidol, a broad-spectrum antiviral compound, on the outcomes of COVID-19 patients. Records of 252 COVID-19 patients were retrospectively analyzed from February 13 to February 29, 2020 in 4 inpatient wards in the Cancer Center, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China. The rate of clinical improvement was significantly greater among patients treated with Arbidol than among those who did not receive Arbidol (86.

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Promotion of cardiac angiogenesis in ischemic myocardium is a critical strategy for repairing and regenerating the myocardium after myocardial infarction (MI). Currently, effective methods to aid in the survival of endothelial cells, to avoid apoptosis in ischemic myocardium and to achieve long-term cardiac angiogenesis are still being pursued. Here, we investigated whether cardiac telocyte (CT)-endothelial cell communication suppresses apoptosis and promotes the survival of endothelial cells to facilitate cardiac angiogenesis during MI.

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Thus far, the cellular and molecular mechanisms related to early (especially within 24 hours after acute myocardial infarct (MI)) exercise-mediated beneficial effects on MI have not yet been thoroughly established. In the present study, we demonstrated that acute MI rats that underwent early moderate exercise training beginning one day after MI showed no increase in mortality and displayed significant improvements in MI healing and ventricular remodelling, including an improvement in cardiac function, a decrease in infarct size, cardiomyocyte apoptosis, cardiac fibrosis and cardiomyocyte hypertrophy, and an increase in myocardial angiogenesis, left ventricular wall thickness and the number of cardiac telocytes in the border zone. Integrated miRNA-mRNA profiling analysis performed by the ingenuity pathway analysis system revealed that the inhibition of the TGFB1 regulatory network, activation of leucocytes and migration of leucocytes into the infarct zone comprise the molecular mechanism underlying early moderate exercise-mediated improvements in cardiac fibrosis and the pathological inflammatory response.

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Purpose: Our purpose was to explore which immobilization is more suitable for clinical practice in postmastectomy intensity modulation radiotherapy, the single-pole position or the double-pole position?

Methods: Patients treated with postmastectomy intensity modulation radiotherapy were eligible. They were selected randomly for single-pole position or double-pole position. Dose-volume histogram (DVH) was used to evaluate plans.

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