Publications by authors named "Changjian Shao"

This open-label, single-arm, phase 2 trial evaluated the efficacy and safety of neoadjuvant sintilimab combined with anlotinib and chemotherapy, followed by adjuvant sintilimab, for resectable NSCLC. Forty-five patients received anlotinib (10 mg, QD, PO, days 1-14), sintilimab (200 mg, day 1), and platinum-based chemotherapy of each three-week cycle for 3 cycles, followed by surgery within 4-6 weeks. Adjuvant sintilimab (200 mg) was administered every 3 weeks.

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Histone deacetylases (HDACs) are proteases that play a key role in chromosome structural modification and gene expression regulation, and the involvement of HDACs in cancer, the nervous system, and the metabolic and immune system has been well reviewed. Our understanding of the function of HDACs in the vascular system has recently progressed, and a significant variety of HDAC inhibitors have been shown to be effective in the treatment of vascular diseases. However, few reviews have focused on the role of HDACs in the vascular system.

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Background: The significance of long non-coding RNAs (lncRNAs) as pivotal mediators of histone acetylation and their influential role in predicting the prognosis of lung adenocarcinoma (LUAD) has been increasingly recognized. However, there remains uncertainty regarding the potential utility of acetylation-related lncRNAs (ARLs) in prognosticating the overall survival (OS) of LUAD specimens.

Methods: The RNA-Seq and clinical information were downloaded from The Cancer Genome Atlas (TCGA).

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Background: This study aimed to investigate the prospects of using chemotherapy in combination with atezolizumab in the neoadjuvant or conversion treatment of small cell lung cancer (SCLC).

Methods: Prior to surgery, untreated patients with limited-stage SCLC received three cycles of neoadjuvant or conversion atezolizumab combined with chemotherapy of etoposide and platinum. The primary endpoint of the trial was pathological complete response (pCR) in the per-protocol (PP) cohort.

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Mucin 16 (MUC16) mutation ranks third among all common mutations in lung adenocarcinoma (LUAD), and it has a certain effect on LUAD development and prognostic outcome. This research aimed to analyze the effects of MUC16 mutation on LUAD immunophenotype regulation and determine the prognostic outcome using an immune prognostic model (IPM) built with immune-related genes. The MUC16 mutation status and mRNA expression profiles were analyzed using diverse platforms and among several LUAD patients (n = 691).

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Advanced esophageal squamous cell carcinoma (ESCC) still has a dismal prognostic outcome. However, the current approaches are unable to evaluate patient survival. Pyroptosis represents a novel programmed cell death type which widely investigated in various disorders and can influence tumor growth, migration, and invasion.

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Background: is found at the centromere and plays an important role in recruiting centromere protein-A (CENP-A) through interacting with Holliday junction recognition protein during cell mitosis. is considered to be a cancer-testis specific gene, but its function in tumor development remains unclear. Increased expression of has been reported in testis as well as in different cancers; however, the underlying mechanisms remain obscure.

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Choroidal melanoma (CM) is the most common type of diagnosed uveal melanoma (UM), which is prone to metastasis and exhibits a poor prognosis. The molecular mechanisms underlying CM progression need further elucidation to research effective therapeutic strategies. Histone deacetylase 7 (HDAC7) is very important in regulating cancer progression, but the significance and effect of HDAC7 on CM progression are unclear.

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Background: Melatonin, a natural hormone secreted by the pineal gland, has been reported to exhibit antitumor properties through diverse mechanisms of action. However, the oncostatic function of melatonin on esophageal squamous cell carcinoma (ESCC) remains elusive. This study was conducted to investigate the potential effect and underlying molecular mechanism of melatonin as single anticancer agent against ESCC cells.

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Article Synopsis
  • Ferroptosis is a newly recognized form of programmed cell death linked to tumor growth, particularly in lung adenocarcinoma (LUAD), prompting research into its associated long non-coding RNAs (lncRNAs).
  • This study utilized data from The Cancer Genome Atlas and a database called FerrDb to establish a prognostic model by analyzing a specific group of ferroptosis-related lncRNAs, ultimately identifying 10 key lncRNAs that can predict LUAD outcomes.
  • Findings suggest that these lncRNAs play a role in immune responses related to LUAD, offering potential insights for new therapeutic and diagnostic approaches.
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Background: Neoadjuvant immunotherapy for patients with locally advanced esophageal cancer (EC) has developed rapidly in recent years. The efficacy and safety outcomes may change the recommended neoadjuvant therapeutic regimens for patients with EC.

Methods: Systematic screening for articles focusing on the efficacy and safety of neoadjuvant immunotherapy in locally advanced and surgically resectable EC was performed using PubMed, Embase, Web of Science and international tumor congresses.

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Background: In this single-arm study, the efficacy and safety of neoadjuvant pembrolizumab plus chemotherapy were evaluated in patients with resectable esophageal squamous cell carcinoma (ESCC).

Methods: This study included patients with ESCC of clinical stages II-IVA who underwent surgery within 4 to 6 weeks after completing treatment with pembrolizumab (200 mg) combined with a conventional chemotherapy regimen (3 cycles). The safety and efficacy of this combination treatment were evaluated as primary endpoints of the study.

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Melatonin is a hormone synthesized in the pineal gland and has widespread physiological and pharmacological functions. Moreover, it can activate protective receptor-dependent processes. These processes can prevent tissue carcinogenesis and inhibit malignant tumor progression and metastasis.

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Esophageal squamous cell carcinoma (ESCC) is one of the most common cancers worldwide, with high incidence and mortality rates and low survival rates. However, the detailed molecular mechanism of ESCC progression remains unclear. Here, we first showed significantly higher WNT5A and SNAIL expression in ESCC samples than in corresponding paracancerous samples.

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As major post-translational modifications (PTMs), acetylation and deacetylation are significant factors in signal transmission and cellular metabolism, and are modulated by a dynamic process two pivotal categories of enzymes, histone acetyltransferases (HATs) and histone deacetylases (HDACs). In previous studies, dysregulation of lysine acetylation and deacetylation has been reported to be associated with the genesis and development of malignancy. Scientists have recently explored acetylation/deacetylation patterns and prospective cancer therapy techniques, and the FDA has approved four HDAC inhibitors (HDACi) to be used in clinical treatment.

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Background: Finding new immune-related biomarkers is one of the promising research directions for tumor immunotherapy. The gene could stimulate the WNT pathway and regulate the progression of various tumors. Recent studies have partially revealed the relationship between and tumor immunity, but the correlation and underlying mechanisms in pan-cancer remain obscure.

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Background: Histone deacetylases (HDACs) play crucial roles in cancers, but the role and mechanism of HDAC7 in NSCLC have not been fully understood.

Methods: A total of 319 patients with non-small cell lung cancer (NSCLC) who underwent surgery were enrolled in this study. Immunohistochemistry and Kaplan-Meier survival analysis were performed to investigate the relationship between HDAC7, fibroblast growth factor 18 (FGF18) expression, and clinicopathologic characteristics.

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As members of the immune checkpoint family, PD-1 and its ligand PD-L1 play critical roles in maintaining the balance between autoimmunity and tolerance. The interaction of PD-1/PD-L1 is also involved in tumor evasion inside the tumor microenvironment, caused by reduced T cell activation, proliferation, cytotoxic secretion, and survival. Previous research has shown that the expression level of PD-1/PD-L1 may be regulated by ubiquitin-mediated proteasome degradation, which is an important mode of post-translational modification (PTM).

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Background: Centromere protein U () is a component of the kinetochore and can regulate the cell cycle as a receptor of polo-like kinase 1 (). Recent studies have partially identified the role of in tumor progression, but the underlying mechanisms of in tumor immunity remain obscure.

Methods: We performed pan-cancer analysis to evaluate the role of in immunity and proliferation with data from The Cancer Genome Atlas (TCGA), Cancer Cell Line Encyclopedia (CCLE) datasets, and Genotype-Tissue Expression (GTEx) project.

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Background: Protein kinase membrane associated tyrosine/threonine 1 () regulates cell cycle and is a part of DNA damage repair (DDR)-related signaling. Recent studies have identified a role for in tumor immunity and DDR. Thus, we initiated this study aiming to characterize the molecular and immunological portrait of in cancer.

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Background: Senescence marker protein 30 (), which plays a pivotal role as a suppressor protein in cell proliferation, among other regulatory actions, is a marker of aging that shows decreased expression during senescence. Decreased has been identified in several human cancers, but its expression and role in human non-small cell lung cancer (NSCLC) remain unclear.

Methods: Using tumor tissue and matched adjacent normal tissue from 341 patients with resected NSCLC, we assessed expression using immunohistochemical methods.

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Article Synopsis
  • Plasma ctDNA mutation testing serves as a non-invasive alternative to tissue biopsy for detecting EGFR mutations in non-small cell lung cancer (NSCLC) patients, but its impact on long-term survival outcomes is still underexplored.
  • In a study of 174 NSCLC patients, ctDNA mutations in preoperative plasma samples were correlated with tissue mutation results, and their presence was linked to worse overall survival and disease-free survival.
  • The study showed that patients with detectable ctDNA mutations had significantly lower 5-year survival rates (18.5% vs. 76.9%) compared to those without mutations, establishing ctDNA as an important independent risk factor for prognosis.
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