Publications by authors named "Fengkai Xu"

Gram-negative (G-) microflora dysbiosis occurs in multiple digestive tumors and is found to be the dominant microflora in the esophageal squamous cell carcinoma (ESCC) microenvironment. The continuous stimulation of G- bacterium metabolites may cause tumorigenesis and reshape the microimmune environment in ESCC. However, the mechanism of G- bacilli causing immune evasion in ESCC remains underexplored.

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The complexity of the tumor microenvironment (TME) is a crucial factor in lung adenocarcinoma (LUAD) progression. To gain deeper insights into molecular mechanisms of LUAD, we perform an integrative single-cell RNA sequencing (scRNA-seq) data analysis of 377,574 cells from 117 LUAD patient samples. By linking scRNA-seq data with bulk gene expression data, we identify a cluster of prognostic-related UPP1 tumor cells.

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Background: Neoadjuvant chemoimmunotherapy has offered novel therapeutic options for patients with locally advanced oesophageal squamous cell carcinoma (ESCC). Depicting the landscape of genomic and immune profiles is critical in predicting therapeutic responses.

Methods: We integrated whole-exome sequencing, single-cell RNA sequencing, and immunofluorescence data of ESCC samples from 24 patients who received neoadjuvant treatment with PD-1 inhibitors plus paclitaxel and platinum-based chemotherapy to identify correlations with therapeutic responses.

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Article Synopsis
  • The study investigates the role of toll-like receptors (TLRs) in esophageal squamous cell cancer (ESCC) by analyzing differentially expressed genes (DEGs) from existing databases.
  • A TLR-prognostic model was developed using six key genes (CD36, LGR4, MAP2K3, NINJ1, PIK3R1, TRAF3) to differentiate patients into high- and low-risk groups based on their risk scores (RS).
  • The high-risk group exhibited worse survival rates, lower immune activity, and reduced sensitivity to various chemotherapy drugs, indicating the model's potential in predicting patient outcomes and guiding treatment options.
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Article Synopsis
  • KLF11 plays a crucial role in promoting ferroptosis, a type of cell death linked to tumor growth and chemotherapy resistance in lung adenocarcinoma (LUAD).
  • Through experiments, it was found that KLF11 expression increases in LUAD cells treated with ferroptosis inducers, leading to reduced cell proliferation and enhanced sensitivity to chemotherapy.
  • The study unveils that KLF11 inhibits the transcription of GPX4, a key regulator in the ferroptosis pathway, linking its low expression to poorer patient survival outcomes in LUAD.
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Article Synopsis
  • Pembrolizumab in combination with chemotherapy was evaluated for its effectiveness and safety in patients with potential resectable clinical stage III non-small-cell lung cancer (NSCLC).
  • A study involving 25 patients who received this neoadjuvant treatment revealed that 21 underwent successful pulmonary resections, with 13 showing major pathological response and 6 achieving complete pathological response.
  • While the treatment showed promising results without significant adverse effects, further evaluation and research are necessary to confirm its reliability for this specific patient group.
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The goal of this study was to create a risk model based on the ferroptosis gene set that affects lung adenocarcinoma (LUAD) patients' prognosis and to investigate the potential underlying mechanisms. A cohort of 482 LUAD patients from the TCGA database was used to develop the prognostic model. We picked the module genes from the ferroptosis gene set using weighted genes co-expression network analysis (WGCNA).

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Lung adenocarcinoma (LUAD) is the most prevalent thoracic cancer with the highest incidence and mortality worldwide. Baculoviral IAP Repeat Containing 5 (BIRC5) is well studied in many malignancies, its prognosis value and correlation with the tumor microenvironment (TME) in LAUD remains largely elusive. The Wilcoxon signed-rank test and logistic regression were used to evaluate the relationship between clinical features and BIRC5 expression in LUAD.

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Background: Tumor spread through air spaces (STAS) has been shown to adversely affect the prognosis of lung cancer. The correlation between clinicopathological and genetic features and STAS remains unclear.

Method: We retrospectively reviewed 3075 NSCLC patients between2017-2019.

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To figure out the molecular mechanism in the esophageal squamous carcinoma (ESCC) with the discrepancy in the tissue-resident microbiota, we selected clinical features, RNA sequences, and transcriptomes of ESCC patients from The Cancer Genome Atlas (TCGA) website and detailed tissue-resident microbiota information from The Cancer Microbiome Atlas ( = 60) and explored the infiltration condition of particular microbiota in each sample. We classified the tissue-resident micro-environment of ESCC into two clusters (A and B) and built a predictive classifier model. Cluster A has a higher proportion of certain tissue-resident microbiota with comparatively better survival, while Cluster B has a lower proportion of certain tissue-resident microbiota with comparatively worse survival.

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Background: Immune checkpoint blockade (ICB) has been improving patient outcomes of non-small cell lung cancer (NSCLC), but its effectiveness is highly subjective to individual tumor microenvironment. As dominant immune cells in NSCLC, tumor-associated macrophages (TAMs) display high diversity and plasticity. This study aims to find crucial TAM subtypes associated with ICB response in NSCLC.

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Background: Esophageal squamous cell carcinoma (ESCC) remains one of the deadly cancer types. Comprehensively dissecting the molecular characterization and the heterogeneity of ESCC paves the way for developing more promising therapeutics.

Methods: Expression profiles of multiple ESCC datasets were integrated.

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Background: Anastomotic leakage with empyema is one of the most severe complications of esophagectomy. We invented a new type of slow-flow irrigation drainage tube to improve the smooth pleural drainage, which contributed to the recovery of anastomotic leakage.

Methods: In this study, 42 patients, from 2012 to 2019, who underwent esophagectomy and postoperative anastomotic leakage with persistent empyema, were enrolled and distributed into irrigation drainage tube group (I+) or non-irrigation drainage tube group (I-).

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N6-methyladenosine (m6A) modification can regulate a variety of biological processes. However, the implications of m6A modification in lung adenocarcinoma (LUAD) remain largely unknown. Here, we systematically evaluated the m6A modification features in more than 2400 LUAD samples by analyzing the multi-omics features of 23 m6A regulators.

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Background: Esophageal squamous cell cancer (ESCC) is one kind of frequent digestive tumor. The inflammatory environment plays an important role in the tumorigenesis and development of ESCC. Cancer stem cells are a small group of tumor cells with stem cell characteristics, which can potentially hinder the tumor management and treatment.

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Primary adenosquamous carcinoma (ASC) is a rare malignant tumor in the lung and its biological behavior has not yet been thoroughly described. In this study, we aimed to explore the clinical and biological role of CXCR4 in patients with resected lung ASC. We retrospectively reviewed the clinical records of patients with histologically confirmed lung ASC who underwent surgical resection with systematic lymph node dissection.

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Background: Predicting lung adenocarcinoma (LUAD) risk is crucial in determining further treatment strategies. Molecular biomarkers may improve risk stratification for LUAD.

Methods: We analyzed the gene expression profiles of LUAD patients from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO).

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Background: Esophageal squamous cell carcinoma (ESCC) is one of the most frequent malignant digestive tumors around the world. We previously demonstrated that eIF3b could promote the progression of ESCC. The exact mechanisms underlying these effects remained unknown.

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Lung cancer remains the leading cause of cancer death. DNA methylation plays an essential role in carcinogenesis through regulating gene expression and gene alternative splicing. However, the role of methylation in the tumorigenesis of lung squamous cell carcinoma (SCC) and its association with prognosis remains unclear.

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Background: Large cell neuroendocrine carcinoma (LCNEC) was categorized into pulmonary neuroendocrine tumors (NETs) according to the World Health Organization classification guideline. However, LCNEC patients often received the chemotherapy regimens similar to non-small cell lung carcinoma (NSCLC) in advanced stage and the therapeutic effect was unsatisfactory. Therefore, this study aimed to investigate the hidden clinical features, prognosis and immunoprofile of the LCNEC, compared with carcinoid and SCLC, to explore whether LCNEC shares similarity with SCLC and potential treatment approaches could be revealed.

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Lung cancer is one of the most frequent malignant tumors, with the top morbidity and mortality, in China. Calpain family regulates cellular processes including migration and invasion. However, the role of Calpain-2 in non-small cell lung cancer (NSCLC) remains unclear.

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Cancer stem-like cells (CSCs) are regarded as sources of tumorigenesis, metastasis, and drug resistance, which limits current cancer therapies. Elucidating the molecular modes governing CSC properties is necessary to optimize therapeutic approaches. In this study, we discovered that ubiquitin-protein ligase E3C (UBE3C)-mediated ubiquitination is a key posttranslational mechanism involved in maintaining CSC properties of non-small-cell lung cancer (NSCLC).

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Lung squamous cell carcinoma (LUSC) is associated with poor clinical prognosis and lacks available targeted therapy. Novel molecules are urgently required for the diagnosis and prognosis of LUSC. Here, we conducted our data mining analysis for LUSC by integrating the differentially expressed genes acquired from Gene Expression Omnibus (GEO) database by comparing tumor tissues versus normal tissues (GSE8569, GSE21933, GSE33479, GSE33532, GSE40275, GSE62113, GSE74706) into The Cancer Genome Atlas (TCGA) database which includes 502 tumors and 49 adjacent non-tumor lung tissues.

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: Esophageal cancer is one of the most common malignant tumors in the world. Eukaryotic translation initiation factors 3e (eIF3e) makes a notable difference in the initiation of protein synthesis and tumor progression. However, the role of eIF3e in ESCC has not been revealed yet.

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Introduction: Esophageal squamous cell carcinoma (ESCC) is one of the most aggressive malignant tumors. Eukaryotic translation initiation factors 3B (EIF3B) is considered to influence tumor proliferation, invasion, apoptosis and cell cycle, which act together to promote the progression of tumors. However, the role of EIF3B in ESCC is unknown.

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