Ontology highlight
ABSTRACT:
PROVIDER: PRJNA592439 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10556646.fastq.gz | Fastqsanger.gz | |||
| SRR10556647.fastq.gz | Fastqsanger.gz | |||
| SRR10556648.fastq.gz | Fastqsanger.gz | |||
| SRR10556649.fastq.gz | Fastqsanger.gz | |||
| SRR10556650.fastq.gz | Fastqsanger.gz |
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Project description:Proliferative verrucous leukoplakia (PVL) is a potentially malignant disorder characterized by contiguous spread, a spectrum of clinicopathological features and high malignant transformation risk. Despite many efforts to describe the clinicopathological features of PVL progression, so far, there is still a lack of knowledge on the dynamic changes in molecular signature during this process. Hence, we applied single-cell RNA sequencing to 3 biopsy samples from a large PVL lesion. These samples exhibited the histopathological continuum of PVL lesions progression. By analysis for transcriptome profiling of 27,611 cells from these samples, we identified 10 major cell lineages and revealed the cellular remodeling occurring in the progression of PVL lesions, including epithelial, stromal and immune cells. The epithelial cells are shifted to pro-tumorigenic transcriptional cell states and secretory patterns at premalignant stage. Immune cells showed growing immunosuppressive phenotypes during PVL progression. Remarkably, two novel cell subtypes INSR+ endothelial cells and ASPN+ fibroblasts were discovered and may play a vital role in microenvironment remodeling, such as angiogenesis and stromal fibrosis, closely involved in the malignant transformation. Our work preliminarily describes the dynamic molecular properties of PVL lesions, enhances the systematic understanding of the premalignant evolution of PVL and attempts to provide the framework for future research.
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Project description:Oral leukoplakia is common and may in some cases progress to carcinoma. Proliferative leukoplakia (PL) is a progressive, often multifocal subtype with a high rate of malignant transformation (MT) compared to the more common localized leukoplakia (LL). We hypothesized that the immune microenvironment and gene expression patterns would be distinct for PL compared to LL. We summarize key clinicopathologic features among PL and LL and compare cancer-free survival (CFS) between subgroups. We analyze immunologic gene expression profiling (GEP) in PL and LL tissue samples (NanoString PanCancer Immune Oncology Profiling). We integrate immune cell activation and spatial distribution patterns in tissue samples using multiplexed immunofluorescence and digital image capture to further define PL and LL. Among N=58 patients (PL: 29, LL: 29), only the clinical diagnosis of PL was associated with significantly decreased CFS (HR 11.25, p<0.01); 5-year CFS 46.8% and 83.6% among PL and LL patients, respectively. CD8+ T cells and Tregs were more abundant among PL samples (p<0.01) regardless of degree of epithelial dysplasia, and often colocalized to the dysplasia-stromal interface. Gene set analysis identified granzyme-M (GZMM) as the most differentially expressed gene favoring the PL subgroup (log2 fold change 1.93, adjusted p<0.001). PD-L1 was comparatively over-expressed among PL samples, with higher (>5) PD-L1 scores predicting worse CFS (p<0.01). PL predicts a high rate of MT within 5-years of diagnosis. Robust CD8+ T cell and Treg signature along with relative PD-L1 over-expression compared with LL provides strong rationale for PD-1/L1 axis blockade using preventative immunotherapy.
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Project description:Esophageal involvement in patients with systemic sclerosis (SSc) is common, but tissue-specific pathological mechanisms are poorly understood. Fibrosis in the esophagus is thought to disrupt smooth muscle function and lead to esophageal dilatation, but autopsy studies demonstrate esophageal smooth muscle atrophy and the absence of fibrosis in the majority of SSc cases. Molecular characterization of SSc esophageal pathology is lacking. Herein, we perform a detailed characterization of SSc esophageal histopathology and molecular signatures at the level of gene expression. Esophageal biopsies were prospectively obtained during esophagogastroduodenoscopy in 16 consecutive SSc patients and 7 subjects without SSc. Upper and lower esophageal biopsies were evaluated for histopathology and gene expression. Individual patient’s upper and lower esophageal biopsies showed nearly identical patterns of gene expression. Similar to skin, inflammatory and proliferative gene expression signatures were identified suggesting that molecular subsets are a universal feature of SSc end-target organ pathology. The inflammatory signature was present in biopsies without high numbers of infiltrating lymphocytes. Molecular classification of esophageal biopsies was independent of SSc skin subtype, serum autoantibodies and esophagitis. Proliferative and inflammatory molecular gene expression subsets in tissues from patients with SSc may be a conserved, reproducible component of SSc pathogenesis. The inflammatory signature is observed in biopsies that lack large inflammatory infiltrates suggesting that immune activation is a major driver of SSc esophageal pathogenesis.
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Project description:Head and neck squamous cell carcinoma (HNSCC) undergoes stepwise progression from normal tissue to metastasized tumors. To comprehensively delineate the heterogeneity of tumor cells and their interactions during the progression of HNSCC, we employed single-cell RNA-seq (scRNA-seq) profiling for the tissues of normal, leukoplakia, HNSCC, and metastasized HNSCC. We identified novel clones of malignant cells expressing LGALS7B and fibroblasts expressing CXCL8, and the abundance of these cells in the tumor tissue was associated with poorer prognostic outcomes. In addition, we demonstrated that fibroblasts in leukoplakia and tumor tissue express COL1A1, which interacts with CD44+ malignant cells, facilitating HNSCC progression. CD4+FOXP3+ regulatory T cells expand in leukoplakia and express LAIR2 with collagen stimulation, which may provide a favorable microenvironment for tumor progression. In conclusion, stromal and immune cell interactions play critical roles in the stepwise progression of HNSCC, and we have identified steps during HNSCC progression for possible therapeutic interventions
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Project description:RNAseq analysis of oral cancer and oral leukoplakia patients. Oral biopsies from 37 patients were obtained for sequencing using RNAseq including control, oral leukoplakia patients and oral cancer patients.
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