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Total 899 record(s) from BioProject
- Accession: PRJEB41845
- Title: 3' UTR RNA-sequencing of human EGFR-mutant PC9 cells that were CRISPR engineered to additionally contain EGFR-mutations T790M and C797S
- Description: Lung adenocarcinoma PC9 cells were engineered to not only contain the driving EGFR-mutations, but also EGFR T790M and EGFR C797S that provide resistance to EGFR inhibitors.
- BasicInfo : PRJEB41845; Other;
- Accession: PRJEB49811
- Title: Selection of activating EGFR mutations from randomly mutated EGFR libraries
- Description: In this study, a randomly mutated human EGFR library (exons only) was selected for ligand-independent EGFR-activation in HEK293T cells using a high-throughput assay termed PhosphoFlowSeq. Briefly, HEK293T cells were transfected with plasmids containing randomly mutated EGFR genes. Next, the HEK293T cells expressing the mutated EGFR variants were screened for EGFR-phosphorylation in the absence of EGFR ligands using flow cytometry, followed by plasmid isolation from enriched cells, PCR-amplification of EGFR genes and deep sequencing analysis (Illumina sequencing).
- BasicInfo : PRJEB49811; Other;
- Accession: PRJNA232148
- Title: Suppression of MicroRNA-9 by Mutant EGFR Signaling Induces FOXP1 to Enhance Glioblastoma Tumorigenicity
- Description: The EGF-receptor (EGFR) is amplified and mutated in glioblastoma (GBM) where its common mutation, (∆EGFR, also called EGFRvIII) has a variety of activities that promote growth and inhibit death, thereby conferring a strong tumor-enhancing effect. This range of activities suggested to us that ∆EGFR might exert its influence through pleiotropic effectors and we hypothesized that microRNAs (miRs) might serve such a function. To test this, we determined the miR profiles of GBM cells with activated wild type EGFR (wtEGFR) and mutant EGFR (∆EGFR) to cells with non-activated EGFR or kinase dead ∆EGFR.
Overall design: To identify miRs regulated by EGFR, RNA from 2 different glioma cell lines (U87 and U373) were hybridized to miR expression arrays and analyzed. Each cell type was engineered to express wild type EGFR (wtEGFR), dead kinase ∆EGFR (DK) or ∆EGFR at elevated levels similar to those observed in primary glioblastomas displaying EGFR overexpression. Parental cells expressing endogenous EGFR and wtEGFR cells stimulated with EGF for 1hr were also included in the analyses.
- BasicInfo : PRJNA232148; Transcriptome or Gene expression; Medical
- Accession: PRJNA688205
- Title: Long non-coding RNA CRNDE Involved in Resistance to EGFR tyrosine kinase inhibitor in EGFR-mutant Lung Cancer via eIF4A3/MUC1/EGFR Signal.
- Description: Introduction: Overcoming of acquired resistance to EGFR-tyrosine kinase inhibitors (EGFR-TKIs) is an intractable obstacle for many clinical oncologists. The mechanisms of resistance to EGFR-TKIs are very complex. Long non-coding RNAs (lncRNAs) may play an important role in cancer development and metastasis. However, the biological process between lncRNAs and drug resistance to EGFR mutated lung cancer largely unknown.
Methods: Osimertinib and afatinib-resistant EGFR-mutated lung cancer cells were established using by a stepwise method. Microarray analysis of non-coding and coding RNAs was performed using parental and resistant EGFR-mutant NSCLC cells.
Results: Microarray analysis was evaluated by bioinformatics analysis through medical-industrial collaboration. CRNDE and DGCR5 lncRNAs were highly expressed in EGFR-TKIs-resistant cells. CRNDE binds to eIF4A3 protein, down-regulates eIF4A3 and MUC1 expression, and down-regulates p-EGFR expression. CRNDE inhibition activated the eIF4A3/MUC1/EGFR signaling pathway and apoptotic activity and restored sensitivity to EGFR-TKIs.
Conclusions: We identified lncRNA CRNDE associated with resistance to EGFR-TKIs in EGFR-mutant NSCLC cells. CRNDE may be a novel therapeutic target for EGFR mutant NSCLC patients.
Overall design: We performed the microarray analysis of non-coding and coding RNAs using parental and resistant EGFR-mutant cell lines.
- BasicInfo : PRJNA688205; Transcriptome or Gene expression; Medical
- Accession: PRJNA271792
- Title: Expression comparison of mutant EGFR-driven gliomas with relapse tumors upon mutant EGFR ablation
- Description: To determine the roles of oncogenic EGFR signaling in gliomagenesis and tumor maintenance, we generated a novel glioma mouse model driven by inducible expression of a mutant EGFR (EGFR*). Genetic suppression of EGFR* induction led to significant tumor regression and prolonged survival. But in spite of the initial response, the tumors relapsed invariably and propagated independent of EGFR*.
We used microarrys to directly compare geen expression of control and relapse tumors and identified gene sets specifically activated in relapse tumors.
Overall design: Control and relasped glioma samples upon mutant EGFR extinction were selected for RNA extraction and hybridization on Affymetrix microarrays.
- BasicInfo : PRJNA271792; Transcriptome or Gene expression; ModelOrganism
- Accession: PRJEB15863
- Title: Emergence of RAS or EGFR extracellular domain mutations and duration of response to EGFR blockade in colorectal cancer
- Description: Blockade of the Epidermal Growth Factor Receptor (EGFR) with the monoclonal antibodies cetuximab or panitumumab is effective in a subset of colorectal cancers (CRC), but the emergence of resistance limits the efficacy of these therapeutic agents. At relapse, the majority of patients develop RAS mutations, while a subset acquires EGFR extracellular domain (ECD) mutations. How clonal dynamics impact the emergence of resistance during EGFR blockade is poorly understood. We find that patients who experience greater and longer responses to EGFR blockade preferentially develop EGFR ECD mutations, while RAS mutations emerge more frequently in patients with smaller tumor shrinkage and shorter progression-free survival. In circulating cell-free tumor DNA (ctDNA) of patients treated with anti-EGFR antibodies, RAS mutations emerge earlier than EGFR ECD variants. Subclonal RAS but not EGFR ECD mutations are present in CRC samples obtained before exposure to EGFR blockade. When CRC cell populations are challenged with stressful conditions, RAS, but not EGFR-ECD, mutant subclones appear. These data indicate that clonal evolution of drug-resistant cells is associated with the clinical outcome of CRC patients treated with anti-EGFR antibodies.
- BasicInfo : PRJEB15863; Other;
- Accession: PRJNA284760
- Title: Expression data for EGFR TKI resistant EGFR-mutated Cells
- Description: Intratumoral heterogeneity in EGFR mutant NSCLC results in divergent resistance mechanisms in response to EGFR tyrosine kinase inhibition
We used microarrays to investigate the gene expression underlying EGFR TKI resistance with a mesenchymal phenotype.
Overall design: Total 4 samples in triplicates were analyzed.
- BasicInfo : PRJNA284760; Transcriptome or Gene expression; Medical
- Accession: PRJNA473846
- Title: microRNA data in human EGFR positive versus EGFR negative colorectal cancer tissues
- Description: This study was to identify microRNAs responsible for colorectal cancer
Overall design: Total RNAs were extracted from human EGFR positive versus EGFR nagative colorectal cancer tissues and paired adjacent normal tissue, and then subjected to microRNA array analysis (Agilent Human miRNA).
- BasicInfo : PRJNA473846; Transcriptome or Gene expression; Medical
- Accession: PRJNA721680
- Title: Differential mRNA expression analysis of EGFR-TKI-sensitive cells vs. EGFR-TKI-resistant cells
- Description: Epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) resistance remains unknown. We determined gene expression profiling in EGFR-TKI-resistant cells using RNA-seq analysis
Overall design: Transcription profiling of lung cancer cells
- BasicInfo : PRJNA721680; Transcriptome or Gene expression; Medical
- Accession: PRJNA106031
- Title: H1299 EGF and Iressa stimulation
- Description: Controlled activation of epidermal growth factor receptor (EGFR) is systematically guaranteed at the molecular level, however aberrant activation of EGFR is frequently found in cancer. Transcription induced by EGFR activation often involves coordinated expression of genes that positively and negatively regulate the original signaling pathway, therefore alterations in EGFR kinase activity may reflect changes in gene expression associated with the pathway. In this study, we investigated transcriptional changes following EGF stimulation with or without the EGFR kinase inhibitor Iressa in H1299 human non-small-cell lung cancer cells (parental H1299, H1299 cells which overexpress wild-type: EGFR-WT and mutant EGFR: L858R). Our results clearly showed differences in transcriptional activity in the absence or presence of EGFR kinase activity, and genes sharing the same molecular functions showed distinct expression dynamics. The results showed particular enrichment of EGFR/ErbB signaling-related genes in a differentially expressed gene set, and significant protein expression of MIG6/RALT(ERRFI1), an EGFR negative regulator, was confirmed in L858R. High MIG6 protein expression was correlated with basal EGFR phosphorylation and inversely correlated with EGF-induced ERK phosphorylation levels. Investigation of NCI-60 cell lines showed that ERRFI1 expression was correlated with EGFR expression regardless of tissue type. These results suggest that cells accumulate MIG6 as an inherent negative regulator to suppress excess EGFR activity when basal EGFR kinase activity is considerably high. Taken together, an EGFR mutation can cause transcriptional changes to accommodate the activation potency of the original signaling pathway at the cellular level.
Overall design: H1299 human non-small cell lung cancer cells were stimulated by the growth hormone (epidermal growth factor (EGF)) or EGFR kinase inhibitor (Iressa). Control was set as non-treated cells.
- BasicInfo : PRJNA106031; Transcriptome or Gene expression; Medical