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Dataset results
1,472 results for “EGFR”
Basket Study of Neratinib in Participants With Solid Tumors Harboring Somatic HER2 or EGFR Exon 18 Mutations
ClinicalTrials.gov study NCT01953926. IPD Sharing: YES. Countries: 13. Publications: 10.
Study of Safety and Efficacy of EGFR-TKI EGF816 in Combination With cMET Inhibitor INC280 in Adult Patients With EGFR Mutated Non Small Cell Lung Cancer.
ClinicalTrials.gov study NCT02335944. IPD Sharing: YES. Countries: 11. Publications: 2.
Study of Oral cMET Inhibitor INC280 in Patients With EGFR Wild-type (wt), Advanced Non-small Cell Lung Cancer (NSCLC) (Geometry Mono-1)
ClinicalTrials.gov study NCT02414139. IPD Sharing: YES. Countries: 20. Publications: 3.
Computational models from: Allele-specific activation, enzyme kinetics, and inhibitor sensitivities of EGFR exon 19 deletion mutations in lung cancer
<p>Computational models, compressed molecular dynamics (MD) simulation trajectories, and sample input files for "Allele-specific activation, enzyme kinetics, and inhibitor sensitivities of EGFR exon 19 deletion mutations in lung cancer". An early version of this manuscript is available as a preprint here: https://www.biorxiv.org/content/10.1101/2022.03.16.484661v1</p>
Uncovering the molecular basis for the better Gefitinib sensitivity of EGFR with complex mutations over single rare mutation: insights from molecular simulations
<p>Molecular Dynamics trajectories and topology files of APO and Gefitinib(IRE)-bound Epidermal growth factor receptor (EGFR) mutants: rare (G719S), rare + rare (G719S/L861Q) and rare + classical (G719S/L858R). The trajectories presented in this work were analyzed and presented in "Uncovering the molecular basis for the better Gefitinib sensitivity of EGFR with complex mutations over single rare mutation: insights from molecular simulations".</p>
Screening EGFR and GAK Inhibitors in Chordoma
<p>Screening of inhibitors of the kinases EGFR and GAK in chordoma cell models to investigate the roles of each kinase in the biology of this rare cancer.</p>
The EGFR signaling modulates in mesenchymal stem cells the expression of miRNAs involved in the interaction with breast cancer cells
<p>We previously demonstrated that the epidermal growth factor receptor (EGFR) modulates in mesenchymal stem cells (MSCs) the expression of a number of genes coding for secreted proteins that promote breast cancer progression. However, the role of the EGFR in modulating in MSCs the expression of miRNAs potentially involved in the progression of breast cancer remains largely unexplored. Following small RNA-sequencing, we identified 36 miRNAs differentially expressed between MSCs untreated or treated with the EGFR ligand transforming growth factor α (TGFα), with a fold change (FC) <0.56 or FC ≥1.90 (CI, 95%). KEGG analysis revealed a significant enrichment in signaling pathways involved in cancer development and progression. EGFR activation in MSCs downregulated the expression of different miRNAs, including miR-23c. EGFR signaling also reduced the secretion of miR-23c in conditioned medium from MSCs. Functional assays demonstrated that miR-23c acts as tumor suppressor in basal/claudin-low MDA-MB-231 and MDA-MB-468 cells, through the repression of IL-6R. MiR-23c downregulation promoted cell proliferation, migration and invasion of these breast cancer cell lines. Collectively, our data suggested that the EGFR signaling regulates in MSCs the expression of miRNAs that might be involved in breast cancer progression, providing novel information on the mechanisms that regulate the MSC-tumor cell cross-talk.We previously demonstrated that the epidermal growth factor receptor (EGFR) modulates in mesenchymal stem cells (MSCs) the expression of a number of genes coding for secreted proteins that promote breast cancer progression. However, the role of the EGFR in modulating in MSCs the expression of miRNAs potentially involved in the progression of breast cancer remains largely unexplored. Following small RNA-sequencing, we identified 36 miRNAs differentially expressed between MSCs untreated or treated with the EGFR ligand transforming growth factor α (TGFα), with a fold change (FC) <0.56 or FC ≥1.90 (CI, 95%). KEGG analysis revealed a significant enrichment in signaling pathways involved in cancer development and progression. EGFR activation in MSCs downregulated the expression of different miRNAs, including miR-23c. EGFR signaling also reduced the secretion of miR-23c in conditioned medium from MSCs. Functional assays demonstrated that miR-23c acts as tumor suppressor in basal/claudin-low MDA-MB-231 and MDA-MB-468 cells, through the repression of IL-6R. MiR-23c downregulation promoted cell proliferation, migration and invasion of these breast cancer cell lines. Collectively, our data suggested that the EGFR signaling regulates in MSCs the expression of miRNAs that might be involved in breast cancer progression, providing novel information on the mechanisms that regulate the MSC-tumor cell cross-talk.</p>
Cellular uptake of silica particles influences EGFR signaling pathway and is affected in response to EGF
<p><strong>Background:</strong> The human epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase that is involved in several key cellular processes such as cell proliferation and differentiation, and it has been linked to the development and progression of various cancers (e.g. breast and lung). Researchers have attempted to improve current cancer-targeted therapies by conjugating molecules on the surface of (nano)particles to efficiently target and inhibit EGFR. However, very few in vitro studies have investigated the effect of particles per se on EGFR signaling and dynamics. Furthermore, the impact of concomitant exposure of particles and EGFR ligands, such as epidermal growth factor (EGF) on cellular uptake efficiency has received little attention. </p> <p><strong>Purpose: </strong>The purpose of this research was to determine the effects of silica (SiO2) particles on EGFR expression and intracellular signaling pathways in A549 lung epithelial cells, in the presence or absence of epidermal growth factor (EGF).</p> <p><strong>Results: </strong>We showed that A549 cells are able to internalize SiO<sub>2</sub> particles with core diameters of 130 nm and 1 µm without affecting cell proliferation or migration. However, both SiO<sub>2</sub> particles interfere with the EGFR signaling pathway by raising the endogenous levels of extracellular signal-regulated kinase (ERK) 1/2. Furthermore, both in the presence and absence of SiO<sub>2</sub> particles, the addition of EGF increased cell migration. EGF also stimulated cellular uptake of 130 nm SiO<sub>2</sub> particles but not 1 µm particles. The increased uptake is primarily associated with EGF-stimulated macropinocytosis.</p> <p><strong>Conclusion: </strong>This study shows that SiO<sub>2</sub> particle uptake interferes with cellular signaling pathways and can be boosted by concurrent exposure to the bioactive molecule EGF. SiO<sub>2</sub> particles, both alone and in combination with the ligand EGF, interfere with EGFR signaling pathway in a size-dependent manner.</p>
Millions of lung tumors harboring KRAS, BRAF, EGFR, and tumor suppressor alterations from genetically engineered mouse models
<p><span>Tumors acquire alterations in oncogenes and tumor suppressor genes in an adaptive walk through the fitness landscape of tumorigenesis. However, the <a>interactions </a></span><span>between oncogenes and tumor suppressor genes that shape this landscape remain poorly resolved and cannot be revealed by human cancer genomics alone. Here, we use a multiplexed, autochthonous mouse platform to model and quantify the initiation and growth of more than one hundred genotypes of lung tumors across four oncogenic contexts: KRAS G12D, KRAS G12C, BRAF V600E, and EGFR L858R. We show that the fitness landscape is rugged—the effect of tumor suppressor inactivation often switches between beneficial and deleterious depending on the oncogenic context—and shows no evidence of diminishing-returns epistasis within variants of the same oncogene. These findings argue against a simple linear signaling relationship amongst these three oncogenes and imply a critical role for off-axis signaling in determining the fitness effects of inactivating tumor suppressors.</span></p>
LUX-Lung 7: A Phase IIb Trial of Afatinib(BIBW2992) Versus Gefitinib for the Treatment of 1st Line EGFR Mutation Positive Adenocarcinoma of the Lung
ClinicalTrials.gov study NCT01466660. IPD Sharing: Not stated. Countries: 14. Publications: 3.
A Study of Lazertinib in Participants With Epidermal Growth Factor Receptor (EGFR) Mutation Positive Advanced Non-Small Cell Lung Cancer (NSCLC)
ClinicalTrials.gov study NCT04075396. IPD Sharing: YES. Countries: 3. Publications: 1.
Phase III Study (Tarceva®) vs Chemotherapy to Treat Advanced Non-Small Cell Lung Cancer in Patients With Mutations in the TK Domain of EGFR
ClinicalTrials.gov study NCT00446225. IPD Sharing: NO. Countries: 3. Publications: 4.
BIBW 2992 (Afatinib) Versus Chemotherapy as First Line Treatment in NSCLC With EGFR Mutation
ClinicalTrials.gov study NCT00949650. IPD Sharing: Not stated. Countries: 25. Publications: 9.
Phase 2 Study of Poziotinib in Participants With NSCLC Having EGFR or HER2 Exon 20 Insertion Mutation
ClinicalTrials.gov study NCT03318939. IPD Sharing: NO. Countries: 8. Publications: 1.
A Study of Erlotinib (Tarceva) After Surgery With or Without Adjuvant Chemotherapy in Non-Small Cell Lung Carcinoma (NSCLC) Patients Who Have Epidermal Growth Factor Receptor (EGFR) Positive Tumors
ClinicalTrials.gov study NCT00373425. IPD Sharing: Not stated. Countries: 19. Publications: 1.
Study of Dacomitinib and Osimertinib for Patients With Advanced EGFR Mutant Lung Cancer
ClinicalTrials.gov study NCT03810807. IPD Sharing: YES. Countries: 1. Publications: 1.
Study to Assess the Effect of Itraconazole (a CYP3A4 Inhibitor) on the Pharmacokinetics of AZD9291, in Patients With EGFR Positive Non-small Cell Lung Cancer. Patients Will be Chosen From Those Who Ha
ClinicalTrials.gov study NCT02157883. IPD Sharing: YES. Countries: 6. Publications: 1.
Study of Pemetrexed + Platinum Chemotherapy With or Without Pembrolizumab (MK-3475) in Adults With Tyrosine Kinase Inhibitor- (TKI)-Resistant Epidermal Growth Factor Receptor- (EGFR)-Mutated Metastati
ClinicalTrials.gov study NCT03515837. IPD Sharing: YES. Countries: 17. Publications: 1.
Efficacy and Safety of Add-on Timolol for EGFR-TKI and ALK-TKI Induced Paronychia
ClinicalTrials.gov study NCT06643416. IPD Sharing: NO. Countries: 1. Publications: 17.
Phase II AZD9291 Open Label Study in NSCLC After Previous EGFR TKI Therapy in EGFR and T790M Mutation Positive Tumours
ClinicalTrials.gov study NCT02094261. IPD Sharing: YES. Countries: 8. Publications: 5.
ScienceDex guides
Understand access before you commit
These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.