Ontology highlight
ABSTRACT:
PROVIDER: PRJNA304376 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Establishment of Afatinib-Resistant Non-Small Cell Lung Cancer Cells Derived from Tumor Xenograft Model [Afatinib treatment]
| PRJNA304378 | ENA
Project description:Establishment of Afatinib-Resistant Non-Small Cell Lung Cancer Cells Derived from Tumor Xenograft Model [No treatment]
| PRJNA304379 | ENA
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:Acquired resistance to endocrine therapy occurs with high frequency in patients with luminal breast cancer (LBC). We report here the establishment of four patient-derived xenograft models of LBC with acquired resistance in vivo to tamoxifen and estrogen deprivation. CEL files represent expresison data generated from 5 replicates (independent mice) of the following tumor models: HBCx22 (parental), HBCx22 TamR (tamoxifen-resistant), HBCx22 OvaR (ovariectomy-resistant), HBCx34 (parental), HBCx34 TamR (tamoxifen-resistant), HBCx34 OvaR (ovariectomy-resistant)
2014-07-09 | E-GEOD-55561 | biostudies-arrayexpress
Project description:Despite the initial benefit of the tyrosine kinase inhibitors targeting ALK gene fusions in non-small cell lung cancer, resistance to ALK inhibitors is almost inevitable. To determine the acquired resistance mechanism to ALK inhibition, we generated crizotinib-resistant ALK lines by chronically treating H3122 cells (driven by EML4-ALK) with an ALK inhibitor, crizotinib for approximately 3 months. RNA-seq and differential expression analyses were performed to determine the transcriptional changes of H3122-CR cells in comparison to parental H3122 cells. Because we demonstrated EGFR could mediate the early adaptive resistance to crizotinib, we further explored the mechanism that contributes to the resistance to the combination of crizotinib and afatinib. H3122-CAR (crizotinib and afatinib-resistant) cells were generated by treating them with a combination of crizotinib and afatinib for approximately 6 months and then profiled by RNA-seq to determine the associated transcriptional reprogramming.
2023-07-31 | GSE239666 | GEO
Project description:Whole genome sequencing of non-metastatic non-small cell lung cancer primary tumor, patient-derived xenografts and Circulating tumor cells derived xenograft
| PRJNA752223 | ENA
Project description:Purpose: MET is a receptor tyrosine kinase (RTK) that has been considered a druggable target in non-small cell lung cancer (NSCLC). To understand the mechanisms of resistance to MET-TKIs and establish therapeutic strategies, we developed an in vitro model using capmatinib-resistant cell lines (EBC-CR1, CR2, and CR3) derived from the MET-amplified NSCLC cell line EBC-1. Methods: We established capmatinib-resistant NSCLC cell lines from the MET-amplified NSCLC cell line EBC-1 and identified alternative signaling pathways using 3’mRNA sequencing and human phospho-RTK arrays. Copy number alterations were evaluated by quantitative PCR and cell proliferation assay; activation of RTKs and downstream effectors were compared between the parental cell line EBC-1 and the EBC-CR1, -CR2, and -CR3 resistant cell lines. Results: We found that epidermal growth factor (EGFR) mRNA expression and protein activation were increased in EBC-CR1–3 cells compared to EBC-1 cells. EBC-CR1 cells showed EGFR-dependent growth and sensitivity to afatinib, an irreversible EGFR TKI. EBC-CR2 cells, which overexpressed the EGFR-MET heterodimer, responded dramatically to the combination of capmatinib and the phosphoinositide-3 kinase catalytic subunit α (PIK3CA) inhibitor afatinib. In addition, EBC-CR3 cells, which had activated EGFR along with amplified PIK3CA, were sensitive to the combination of afatinib and the PI3Kα inhibitor. Conclusions: Our in vitro studies suggested that activation of EGFR signaling and/or genetic alteration of downstream effectors like PIK3CA were alternative resistance mechanisms used by capmatinib-resistant NSCLC cell lines. In addition, combined treatments with MET, EGFR, and PI3Kα inhibitors may be an effective therapeutic strategy in MET-TKI-resistant NSCLC patients.
2017-05-01 | GSE94405 | GEO
Project description:To characterize sotorasib resistance in lung adenocarcinomas (LUAD), we implanted pieces derived from a patient-derived KRAS-G12C positive xenograft (PDX) lung tumor model in immunocompromised mice
2023-03-05 | GSE204753 | GEO
Project description:Transcriptomic analysis of sotorasib-resistant patient-derived xenograft (PDX) lung tumor cells
| PRJNA842089 | ENA
Project description:Single-nuncleus RNA sequencing for circulating tumor cell-derived xenograft models of non-metastatic non-small cell lung cancer
| PRJNA755249 | ENA