Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA169351 | ENA |
REPOSITORIES: ENA
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Project description:Expression data from non-small cell lung carcinoma (NSCLC)
| PRJNA266553 | ENA
Project description:The functions of EGR1, a multifunctional transcription factor, in prostate cancer are well documented. However, little is known about the functions of EGR1 in lung cancer. we observed the function of EGR1 in non-small cell lung carcinoma (NSCLC) and identified the genes that influence cell fate and tumor development. We used microarrays to detail the global programme of gene expression and identified genes differentially expressed when EGR1-overexpressed.
2013-09-17 | GSE50913 | GEO
Project description:Through multidimensional genomic/protein multiomics analysis and clinical information integration of cancer tissue samples, a prognostic method for lung cancer, including non-small cell lung cancer (NSCLC), is developed and applied to precision medical care after discovering new drug targets.
2024-11-01 | PXD053903 | JPOST Repository
Project description:Through multidimensional genomic/protein multiomics analysis and clinical information integration of cancer tissue samples, a prognostic method for lung cancer, including non-small cell lung cancer (NSCLC), is developed and applied to precision medical care after discovering new drug targets.
2024-11-01 | PXD053921 | JPOST Repository
Project description:Through multidimensional genomic/protein multiomics analysis and clinical information integration of cancer tissue samples, a prognostic method for lung cancer, including non-small cell lung cancer (NSCLC), is developed and applied to precision medical care after discovering new drug targets.
2024-11-01 | PXD053969 | JPOST Repository
Project description:The tumor microenvironment strongly influences cancer development, progression and metastasis. The role of carcinoma-associated fibroblasts (CAFs) in these processes and their clinical impact has not been studied systematically in non-small cell lung carcinoma (NSCLC). We established primary cultures of CAFs and matched normal fibroblasts (NFs) from 15 resected NSCLC. We demonstrate that CAFs have greater ability than NFs to enhance the tumorigenicity of lung cancer cell lines. Microarray gene expression analysis of the 15 matched CAF and NF cell lines identified 46 differentially expressed genes, encoding for proteins that are significantly enriched for extracellular proteins regulated by the TGF-beta signaling pathway. We have identified a subset of 11 genes that formed a prognostic gene expression signature, which was validated in multiple independent NSCLC microarray datasets. Functional annotation using protein-protein interaction analyses of these and published cancer stroma-associated gene expression changes revealed prominent involvement of the focal adhesion and MAPK signalling pathways. Fourteen (30%) of the 46 genes also were differentially expressed in laser-capture micro-dissected corresponding primary tumor stroma compared to the matched normal lung. Six of these 14 genes could be induced by TGF-beta1 in NF. The results establish the prognostic impact of CAF-associated gene expression changes in NSCLC patients. This SuperSeries is composed of the following subset Series: GSE22862: Prognostic Gene Expression Signature of Carcinoma Associated Fibroblasts in Non-Small Cell Lung Cancer [expression profiling_CAFs] GSE22863: Prognostic Gene Expression Signature of Carcinoma Associated Fibroblasts in Non-Small Cell Lung Cancer [expression profiling_NSCLC stroma] GSE27284: Prognostic Gene Expression Signature of Carcinoma Associated Fibroblasts in Non-Small Cell Lung Cancer [methylation profiling] GSE27289: Prognostic Gene Expression Signature of Carcinoma Associated Fibroblasts in Non-Small Cell Lung Cancer [genome variation profiling]
2011-04-08 | E-GEOD-22874 | biostudies-arrayexpress
Project description:Affymetrix exon array data set (HuEx-1.0_st) derived from matched pairs of non-small cell lung cancer (NSCLC) and normal adjacent lung tissue (NAT). This data set includes both the adenocarcinoma (AdCa) as well as the squamous cell carcinoma (SCC) subtype of NSCLC.
2011-03-01 | E-MEXP-2644 | biostudies-arrayexpress
Project description:Non-small cell lung cancer (NSCLC, n=22) and normal adjacent control biopsies (n=18) from patients with lung cancer were obtained for Affymetrix GeneChip analysis. NSCLC samples were grouped into squamous cell carcinoma (SCC, n=11) and adenocarcinoma (AC, n=11) samples.
2017-07-01 | E-MTAB-5231 | biostudies-arrayexpress
Project description:Expression data of primary and metastasic tissues from ALK+ NSCLC patients (Anaplastic lymphoma kinase fusion positive non-small cell lung carcinoma)
2020-02-28 | GSE125864 | GEO
Project description:The identification of novel therapeutic strategies to overcome the intrinsic or acquired resistance to trametinib in mutant KRAS lung adenocarcinoma (LUAD) is a major challenge. This study analyzes the effects of trametinib in Id1, a key factor involved in the oncogenic KRAS pathway, and investigates the Id1 role in acquire resistance and synergy with immunotherapy in KRAS-driven LUAD. Restoring the antitumor immune response by blocking programmed-cell death protein 1 (PD-1) and programmed-cell death-ligand 1 (PD-L1) pathway represents a major breakthrough in non-small-cell lung cancer (NSCLC) treatment. Nevertheless, a high proportion of LUAD patients with KRAS alterations remain refractory to this therapy. Material and Methods: To explore whether MEK1/2 inhibition reduces Id1 expression, in vitro and in vivo experiments were conducted in KRAS-mutant NSCLC cells and murine models. RNAseq analysis was performed to elucidate the pathways involved in Id1 inhibition. Apoptosis and PD-L1 expression was measured by flow cytometry. Synergy of trametinib combined with anti-PD1 was investigated in KRAS-mutant LUAD mouse models. Results: Using preclinical syngeneic KRAS-mutant lung cancer mouse models, we demonstrate that trametinib synergizes with PD-1 blockade to reduce lung cancer progression and increase mice overall survival. This antitumor activity was linked to the degradation of Id1 via proteasome, and an enhanced INF-Y-mediated PD-L1 tumor cell expression in KRAS-mutant tumor cells. This effect required CD8+ T cells, boosted the intratumoral CD8+/Treg ratio, reducing the intratumoral Treg/CD4+ ratio. Conclusions: Our data may support the role of Id1 in the trametinib antitumoral effect, sustaining the mitogen-activated protein kinases (MAPK) signaling pathway involved in the trametinib acquired resistance cells and sensitizing KRAS-mutant lung tumors to PD-1 inhibitors, through PD-L1 overexpression.
2024-05-17 | GSE236258 | GEO