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MicroRNA sequencing of clear-cell renal cell carcinoma tissues (FFPE) treated with VEGFR-TKIs in first line.

ABSTRACT: MicroRNA sequencing of clear-cell renal cell carcinoma tissues (FFPE) treated with VEGFR-TKIs in first line.

PROVIDER: PRJEB45952 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR6133070.fastq.gz	Fastqsanger.gz
	ERR6133080.fastq.gz	Fastqsanger.gz
	ERR6133090.fastq.gz	Fastqsanger.gz
	ERR6133100.fastq.gz	Fastqsanger.gz
	ERR6133110.fastq.gz	Fastqsanger.gz

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MicroRNA sequencing of clear-cell renal cell carcinoma tissues (FFPE) treated with VEGFR-TKIs in first line.

Project description:We investigated tumoral miRNA expression of patients with clear-cell renal cell carcinoma treated with VEGFR-TKIs in first line. Sequencing was performed on 109 FFPE resection specimens. The samples were sequenced in 2 major batches (2014 and 2017).

2021-06-07 | E-MTAB-10586 | biostudies-arrayexpress

Transcriptomic analysis of fresh frozen clear-cell renal cell carcinoma tissues treated with VEGFR-TKIs in first line

Project description:Transcriptomic analysis using qRT-PCR was performed on fresh frozen clear-cell renal cell carcinoma tissues treated with VEGFR-TKIs in first line (n=109). The transcriptomic data from this experiment were analyzed together with miRNA sequencing data from FFPE samples from the same tumor (E-MTAB-10586), to identify miRNA which were correlated with lower expression of EPAS1, FLT1and KDR and were also predicted to target these genes by miRNA-mRNA interaction databases.

2021-06-07 | E-MTAB-10592 | biostudies-arrayexpress

Identification of HGF/c-MET as a biomarker of resistance to Vascular Endothelial Growth Factor Receptor (VEGFR) inhibitors

Project description:Therapeutic resistance to VEGFR signaling inhibitors is a major obstacle in the treatment of non-small cell lung cancer (NSCLC). We investigated the contribution of stromal and tumor cells to resistance of NSCLC to VEGFR tyrosine kinase inhibitors (TKIs). Gene expression analysis of stromal (mouse) and tumor (human) compartments enabled us to identify the HGF/c-MET pathway as a driver and a potential biomarker of VEGFR TKI resistance.

2017-07-06 | GSE64472 | GEO

Gene expression changes during resistance toward vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor (TKI) therapy in renal cell carcinoma (RCC)

2015-05-21 | GSE64052 | GEO

Gene expression changes during resistance toward vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor (TKI) therapy in renal cell carcinoma (RCC)

Project description:This study was performed to understand the gene expression changes that accompany treatment of renal cell carcinoma (RCC) with vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor (TKI) therapy. Human RCC cell lines were implanted into the flanks of nude beige mice, allowed to reach 12mm in long axis, and then treated with TKIs (sunitinib or sorafenib). Tumors were excised at 2 timepoints (prior to any therapy and at the 20mm endpoint of the study) and gene expression analysis was performed. Sunitinb or sorafenib were administered to mice bearing either 786-O or A498 xenografts. Mice were sacrificed and tumors excised for RNA extraction at pretreatment size of 12mm, or at 20mm, the mandated maximum tumor size allowed at our institution.

2015-05-21 | E-GEOD-64052 | biostudies-arrayexpress

Expression Profiling of Clear cell renal carcinoma

Project description:Selecting patients with metastatic clear-cell renal cell carcinoma (m-ccRCC) who might benefit from treatment with targeted tyrosine kinase inhibitors (TKIs) is a challenge. Our aim was to identify molecular markers associated with outcome in m-ccRCC patients treated with sunitinib. A Cartes d’Identite des Tumeurs (CIT) study from the 'Institut Curie' and the french 'Ligue Nationale Contre le Cancer' (http://cit.ligue-cancer.net).

2015-01-27 | E-MTAB-3267 | biostudies-arrayexpress

Genotyping by array of 108 clear cell renal cell carcinoma

Project description:A Cartes d'Identite des Tumeurs (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net); Selecting patients with metastatic clear-cell renal cell carcinoma (m-ccRCC) who might benefit from treatment with targeted tyrosine kinase inhibitors (TKIs) is a challenge. Our aim was to identify molecular markers associated with outcome in m-ccRCC patients treated with sunitinib.

2015-01-27 | E-MTAB-3269 | biostudies-arrayexpress

Methylation profiling by array of 108 clear cell renal cell carcinoma

Project description:A Cartes d'Identite des Tumeurs (CIT) project from the French Ligue Nationale Contre le Cancer (<a href=\\ttp://cit.ligue-cancer.net/\\ target=\\_blank\\>http://cit.ligue-cancer.net</a>). Selecting patients with metastatic clear-cell renal cell carcinoma (m-ccRCC) who might benefit from treatment with targeted tyrosine kinase inhibitors (TKIs) is a challenge. Our aim was to identify molecular markers associated with outcome in m-ccRCC patients treated with sunitinib.\

2016-02-26 | E-MTAB-3274 | biostudies-arrayexpress

Outcomes of patients with metastatic clear-cell renal cell carcinoma treated with second-line VEGFR-TKI after first-line immune checkpoint inhibitors.

Project description:BACKGROUND:Immune checkpoint inhibitors (ICIs) are being increasingly utilised in the front-line (1L) setting of metastatic clear-cell renal cell carcinoma (mccRCC). Limited data exist on responses and survival on second-line (2L) vascular endothelial growth factor-receptor tyrosine kinase inhibitor (VEGFR-TKI) therapy after 1L ICI therapy. PATIENTS AND METHODS:This is a retrospective study of mccRCC patients treated with 2L VEGFR-TKI after progressive disease (PD) with 1L ICI. Patients were treated at MD Anderson Cancer Center or Memorial Sloan Kettering Cancer Center between December 2015 and February 2018. Objective response was assessed by blinded radiologists' review using Response Evaluation Criteria in Solid Tumours v1.1. Descriptive statistics and Kaplan-Meier method were used. RESULTS:Seventy patients were included in the analysis. Median age at mccRCC diagnosis was 59 years; 8 patients (11%) had international metastatic database consortium favourable-risk disease, 48 (69%) had intermediate-risk disease and 14 (20%) had poor-risk disease. As 1L therapy, 12 patients (17%) received anti-programmed death ligand-1 (PD-(L)1) monotherapy with nivolumab or atezolizumab, 33 (47%) received nivolumab plus ipilimumab and 25 (36%) received combination anti-PD-(L)1 plus bevacizumab. 2L TKI therapies included pazopanib, sunitinib, axitinib and cabozantinib. On 2L TKI therapy, one patient (1.5%) achieved a complete response, 27 patients (39.7%) a partial response and 36 patients (52.9%) stable disease. Median progression-free survival (mPFS) was 13.2 months (95% confidence interval: 10.1, NA). Forty-five percent of subjects required a dose reduction, and twenty-seven percent of patients discontinued treatment because of toxicity. CONCLUSIONS:In this retrospective study of patients with mccRCC receiving 2L TKI monotherapy after 1L ICI, we observed 2L antitumour activity and tolerance comparable to historical data for 1L TKI.

| S-EPMC7537491 | biostudies-literature

Lysine Methylation Promotes VEGFR-2 Activation and Angiogenesis

Project description:We have used a chimeric VEGFR-2 in which the extracellular domain of mouse VEGFR-2 was replaced with the extracellular domain of human CSF-1 receptor. VEGFR-2 was immunoprecipitated with anti-VEGFR-2 antibody from PAE cells ectopically expressing VEGFR-2. The immunoprecipitated proteins were eluted and separated on SDS-PAGE, followed by in-gel chymotrypsin or trypsin digestion. The digested samples were analyzed by nano LC/MS/MS on a Thermo Fisher LTQ Orbitrap XL. The LC-MS/MS data were analyzed using Proteome Discoverer (Thermo Fisher Scientific; Version 1.3.0.339). MS/MS search was carried out using Sequest search algorithm against the sequence of target mouse protein from the UniProtKB database. Search parameters included chymotrypsin as the enzyme with four missed cleavage allowed; methylation at lysine and arginine, phosphorylation of serine, threonine, and tyrosine, alkylation at cysteine, and oxidation of methionine were set as dynamic modifications. Precursor and fragment mass tolerance were set to 5 ppm and 0.8 Da, respectively. The false discovery rate was calculated by enabling the peptide sequence analysis using a decoy database. High confidence peptide identifications were obtained by setting a target false discovery rate threshold of 1% at the peptide level.

2019-11-22 | PXD000520 | Pride

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