A5011774539- Muscle Physiology and Disorders
- Lung Cancer Treatments and Mutations
- Myasthenia Gravis and Thymoma
- Cancer Immunotherapy and Biomarkers
- Nutrition and Health in Aging
- Neuroendocrine Tumor Research Advances
- Mesenchymal stem cell research
- Peptidase Inhibition and Analysis
- Histone Deacetylase Inhibitors Research
- Lung Cancer Diagnosis and Treatment
- Vascular Tumors and Angiosarcomas
- Neurogenetic and Muscular Disorders Research
- Cytokine Signaling Pathways and Interactions
- RNA Research and Splicing
- Lung Cancer Research Studies
- Chromatin Remodeling and Cancer
- Cancer Genomics and Diagnostics
- Adipokines, Inflammation, and Metabolic Diseases
- Galectins and Cancer Biology
- Infectious Diseases and Mycology
- NF-κB Signaling Pathways
- RNA modifications and cancer
Sun Yat-sen University
2024-2025
Sun Yat-sen University Cancer Center
2024-2025
Beijing Academy of Artificial Intelligence
2025
Shanghai Artificial Intelligence Laboratory
2025
Genecast (China)
2024
State Key Laboratory of Oncology in South China
2024
Harbin Medical University
2024
Second Affiliated Hospital of Harbin Medical University
2024
Baylor College of Medicine
2016-2020
Immunotherapy (IO) exhibits poor therapeutic effect in epidermal growth factor receptor (EGFR) mutant advanced non-small-cell lung cancer (NSCLC). However, previous studies reveal different IO efficacy between exon 19 deletion (19 Del) and 21 L858R mutation (21 L858R). In this study, we aimed to evaluate the difference patients with EGFR Del L858R. data of response rate, disease control rate (DCR), progression-free survival (PFS), overall (OS) stratified by subtypes were extracted synthesized...
Cellular mechanisms causing insulin resistance (IR) in chronic kidney disease (CKD) are poorly understood. One potential mechanism is that CKD-induced inflammation activates the signal transducer and activator of transcription 3 (Stat3) muscle. We uncovered increased p-Stat3 muscles mice with CKD or fed high-fat diet (HFD). Activated Stat3 stimulates expression Fbxo40, a muscle-specific E3 ubiquitin ligase conjugation leading to degradation receptor substrate 1 (IRS1). Evidence Fbxo40...
CKD induces loss of muscle proteins partly by suppressing protein synthesis. Muscles mice with have increased expression nucleolar 66 (NO66), as do biopsy specimens from patients or those undergoing hemodialysis. Inflammation stimulates NO66 and changes in NF-κB mediate the response.Subtotal nephrectomy created a mouse model BUN >80 mg/dl. Crossing NO66flox/flox MCK-Cre bred muscle-specific (MCK-NO66) knockout mice. Experiments assessed effect removing NO66.Muscle-specific blocks CKD-induced...
Abstract Background Combination of chidamide and anti‐PD‐L1 inhibitor produce synergistic anti‐tumor effect in advanced NSCLC patients resistant to anti‐PD‐1 treatment. However, the plus envafolimab has not been reported. Aims This study aimed evaluate efficacy toanti‐PD‐1 Materials Methods Eligible after therapy received envafolimab. The primary endpoint was objective response rate (ORR). secondary end points included disease control (DCR), progression‐free survival (PFS), safety....
Loss of muscle proteins increases the morbidity and mortality patients with chronic kidney disease (CKD), there are no reliable preventive treatments. We uncovered a STAT3/CCAAT-enhancer-binding protein-δ to myostatin signaling pathway that activates protein degradation in mice CKD or cancer; we also identified small-molecule inhibitor STAT3 (TTI-101) blocks this pathway. To evaluate TTI-101 as treatment for CKD-induced cachexia, measured pharmacokinetics pharmacodynamics control rats were...
Myasthenia gravis (MG) is an autoimmune disease characterized by pathogenic antibodies that target structures of the neuromuscular junction. The evidence suggests regulation long noncoding RNAs (lncRNAs) mediated transcription factors (TFs) plays a key role in pathophysiology MG. Nevertheless, detailed molecular mechanisms lncRNAs MG remain largely undetermined.