Ontology highlight
ABSTRACT:
PROVIDER: PRJNA622602 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11482800_1.fastq.gz | Fastqsanger.gz | |||
| SRR11482800_2.fastq.gz | Fastqsanger.gz | |||
| SRR11482801_1.fastq.gz | Fastqsanger.gz | |||
| SRR11482801_2.fastq.gz | Fastqsanger.gz | |||
| SRR11482802_1.fastq.gz | Fastqsanger.gz |
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Project description:Comprehensive Profiling of Cancer Cells and Their Microenvironment in Advanced NSCLC
| PRJNA622993 | ENA
Project description:Background: MET inhibitors have demonstrated efficacy in treating patients with non-small cell lung cancer (NSCLC) harboring METex14 skipping alterations. Advancements in spatial profiling technologies have unveiled the complex dynamics of the tumor microenvironment, a crucial factor in cancer progression and therapeutic response. Using spatial profiling, this study investigates the effects of the MET inhibitor tepotinib on the TME in a case of locally advanced NSCLC with a METex14 skipping alteration. Methods: A patient with resectable stage IIIB NSCLC, unresponsive to neoadjuvant platinum-based doublet chemotherapy, received tepotinib following detection of a METex14 skipping alteration. Paired pre- and post-treatment biopsies were subjected to GeoMx Digital Spatial Profiling using the Cancer Transcriptome Atlas and immune-related protein panels to evaluate shifts in the tumor immune microenvironment (TIME). Results: Tepotinib administration resulted in pathological downstaging to stage IA1, which allowed for a successful lobectomy and evidenced a significant pathological response. The TIME was transformed from an immunosuppressive to a more permissive state, with upregulation of antigen-presenting and pro-inflammatory immune cells. Moreover, a marked decrease in immune checkpoint molecules, including PD-L1, was noted. Spatial profiling identified discrete immune-enriched clusters, indicating the role of tepotinib in modulating immune cell trafficking and function. Conclusions: Tepotinib appears to remodel the TIME in a patient with METex14 skipping NSCLC, possibly increasing responsiveness to immunotherapy. This case supports the integration of genetic profiling into the management of early and locally advanced NSCLC to guide personalized, targeted interventions. These findings highlight the need to further evaluate combinations of MET inhibitors and immunotherapies.
2024-09-27 | GSE250509 | GEO
Project description:Background: MET inhibitors have demonstrated efficacy in treating patients with non-small cell lung cancer (NSCLC) harboring METex14 skipping alterations. Advancements in spatial profiling technologies have unveiled the complex dynamics of the tumor microenvironment, a crucial factor in cancer progression and therapeutic response. Using spatial profiling, this study investigates the effects of the MET inhibitor tepotinib on the TME in a case of locally advanced NSCLC with a METex14 skipping alteration. Methods: A patient with resectable stage IIIB NSCLC, unresponsive to neoadjuvant platinum-based doublet chemotherapy, received tepotinib following detection of a METex14 skipping alteration. Paired pre- and post-treatment biopsies were subjected to GeoMx Digital Spatial Profiling using the Cancer Transcriptome Atlas and immune-related protein panels to evaluate shifts in the tumor immune microenvironment (TIME). Results: Tepotinib administration resulted in pathological downstaging to stage IA1, which allowed for a successful lobectomy and evidenced a significant pathological response. The TIME was transformed from an immunosuppressive to a more permissive state, with upregulation of antigen-presenting and pro-inflammatory immune cells. Moreover, a marked decrease in immune checkpoint molecules, including PD-L1, was noted. Spatial profiling identified discrete immune-enriched clusters, indicating the role of tepotinib in modulating immune cell trafficking and function. Conclusions: Tepotinib appears to remodel the TIME in a patient with METex14 skipping NSCLC, possibly increasing responsiveness to immunotherapy. This case supports the integration of genetic profiling into the management of early and locally advanced NSCLC to guide personalized, targeted interventions. These findings highlight the need to further evaluate combinations of MET inhibitors and immunotherapies.
2024-09-27 | GSE249568 | GEO
Project description:Purpose: Our previous clinical trials have been demonstrated that Anlotinib can inhibit tumor growth upon refractory advanced non-small cell lung cancer (NSCLC) patients with the possibility mechanism of anti-angiogenesis. The present study sought to reveal the underlying molecular mechanism of Anlotinib-induced anti-angiogenesis in advanced NSCLC. Experimental Design: Computed tomography (CT) was used to evaluate the treatment effect of Anlotinib upon refractory advanced NSCLC patients. Transcriptome profiling was performed to identify the key gene expression alteration in NCI-H1975 cells before and after Anlotinib treatment. NCI-H1975 derived xenograft model was applied to investigate treatment effect and verify anti-angiogenesis mechanism of Anlotinib. Results: Anlotinib induces tumor cytotoxicity on refractory advanced NSCLC patients, NCI-H1975 derived xenograft models and lung adenocarcinoma cell lines. Transcriptome profiling revealed CCL2 blockade could be responsible for Anlotinib-induced anti-angiogenesis. NCI-H1975 derived xenograft model demonstrated Anlotinib-induced CCL2 blockade play an important role in anti-angiogenesis. Conclusions: This study not only offered the first evidence that Anlotinib inhibits angiogenesis via blocking CCL2 expression, but also provided a novel theoretical basis for the application of Anlotinib in advanced NSCLC patients.
2018-11-30 | E-MTAB-5997 | biostudies-arrayexpress
Project description:The stromal microenvironment plays a vital role in cancer initiation and progression. We performed a comparative expression profiling of pulmonary MSC derived from NSCLC and corresponding normal lung tissue of 5 newly diagnosed patients. The analysis indicated variable expression of genes involved in DNA repair, apoptosis, proliferation or angiogenesis between NSCLC-MSC and NLT-MSC. MSC were derived from NSCLC and corresponding normal lung tissue of 5 patients. Paired SAM test was performed to screen for differentially expressed genes between NSCLC-MSC and NLT-MSC.
2013-02-07 | E-GEOD-23066 | biostudies-arrayexpress
Project description:Immunotherapy has improved the prognosis of patients with advanced non-small cell lung
cancer (NSCLC), but only a small subset of patients achieved clinical benefit. The purpose of our study was to integrate multidimensional data using a machine learning method to predict the therapeutic efficacy of immune checkpoint inhibitors (ICIs) monotherapy in patients with advanced NSCLC.The authors retrospectively enrolled 112 patients with stage IIIB-IV NSCLC receiving ICIs monotherapy. The random forest (RF) algorithm was used to establish efficacy prediction models based on five different input datasets, including precontrast computed tomography (CT) radiomic data, postcontrast CT radiomic data, combination of the two CT radiomic data, clinical data, and a combination of radiomic and clinical data. The 5-fold cross-validation was used to train and test the random forest classifier. The performance of the models was assessed according to the area under the curve (AUC) in the receiver operating characteristic (ROC) curve. Among these models(RF MLP LR XGBoost), our reproduced onnx models have better performance, especially for random forest. The response variable with a value (1/0) indicates the (efficacy/inefficacy) of PD-1/PD-L1 monotherapy in patients with advanced NSCLC
2023-07-11 | BIOMD0000001074 | BioModels
Project description:The immunosuppressive tumour microenvironment constitutes a significant hurdle to immune checkpoint inhibitors response. Both soluble factors and specialised immune cells such as regulatory T cells (TReg) are key components of active intratumoural immunosuppression. Previous studies have shown that Inducible Co-Stimulatory receptor (ICOS) can be highly expressed in the tumour microenvironment, especially on immunosuppressive TReg, suggesting that it represents a relevant target for preferential depletion of these cells. Here, we performed immune profiling of samples from paired tumour and peripheral blood of 5 patients with non-small cell lung cancer (NSCLC). We found Icos mRNA expression in NSCLC samples was higher in TRegs than in other T cell subsets and higher in the TME than in the periphery with the expression pattern in both compartments following the general trend of: TReg > CD4non-TReg > CD8 > Other.
2020-09-01 | E-MTAB-9451 | biostudies-arrayexpress
Project description:The stromal microenvironment plays a vital role in cancer initiation and progression. We performed a comparative expression profiling of pulmonary MSC derived from NSCLC and corresponding normal lung tissue of 5 newly diagnosed patients. The analysis indicated variable expression of genes involved in DNA repair, apoptosis, proliferation or angiogenesis between NSCLC-MSC and NLT-MSC.
2013-02-07 | GSE23066 | GEO
Project description:Neutrophils infiltrated in the tumor microenvironment (TME) are heterogeneous populations associated with the prognosis of cancer and cancer immunotherapy. However, the plasticity and function of heterogeneous neutrophils in the TME of non-small cell lung cancer (NSCLC) remain poorly understood. Here, we show that neutrophils produce high levels of IL-8 which induce the differentiation of CD74highSiglecFlow neutrophils and suppress the generation of CD74lowSiglecFhigh neutrophils in the TME of IL-8-humanized (IL8-hu) KrasLSL-G12DTp53fl/fl (KP) and EGFRT790M/Del-Exon19 (EGFRTD) NSCLC mouse models. The CD74highSiglecFlow neutrophils exhibit antigen cross-presentation activity to augment anti-tumor T cell responses. Consistently, deletion of CD74 in IL8-hu neutrophils attenuates the activation of T cells and exacerbates the progression of NSCLC, whereas treatment of a CD74 agonist promotes anti-tumor T cell activation and enhances the effects of anti-PD1 or Osimertinib therapy in the IL8-hu NSCLC mouse models. In addition, we have found that the CD74highCD63low neutrophils in the TME and peripheral blood of advanced NSCLC patients pheno-copy the CD74highSiglecFlow neutrophils in the TME of NSCLC mice and correlate well with the responsiveness to anti-PD-1 plus chemotherapies. Collectively, these data demonstrate an IL-8-CD74high neutrophil axis that promotes anti-tumor immunity in NSCLC.
2024-09-13 | GSE252460 | GEO
Project description:Neutrophils infiltrated in the tumor microenvironment (TME) are heterogeneous populations associated with the prognosis of cancer and cancer immunotherapy. However, the plasticity and function of heterogeneous neutrophils in the TME of non-small cell lung cancer (NSCLC) remain poorly understood. Here, we show that neutrophils produce high levels of IL-8 which induce the differentiation of CD74highSiglecFlow neutrophils and suppress the generation of CD74lowSiglecFhigh neutrophils in the TME of IL-8-humanized (IL8-hu) KrasLSL-G12DTp53fl/fl (KP) and EGFRT790M/Del-Exon19 (EGFRTD) NSCLC mouse models. The CD74highSiglecFlow neutrophils exhibit antigen cross-presentation activity to augment anti-tumor T cell responses. Consistently, deletion of CD74 in IL8-hu neutrophils attenuates the activation of T cells and exacerbates the progression of NSCLC, whereas treatment of a CD74 agonist promotes anti-tumor T cell activation and enhances the effects of anti-PD1 or Osimertinib therapy in the IL8-hu NSCLC mouse models. In addition, we have found that the CD74highCD63low neutrophils in the TME and peripheral blood of advanced NSCLC patients pheno-copy the CD74highSiglecFlow neutrophils in the TME of NSCLC mice and correlate well with the responsiveness to anti-PD-1 plus chemotherapies. Collectively, these data demonstrate an IL-8-CD74high neutrophil axis that promotes anti-tumor immunity in NSCLC.
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