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Impact of sunitinib resistance on clear cell renal cell carcinoma therapeutic sensitivity in vitro

ABSTRACT: Impact of sunitinib resistance on clear cell renal cell carcinoma therapeutic sensitivity in vitro

PROVIDER: PRJNA894090 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22032768_1.fastq.gz	Fastqsanger.gz
	SRR22032768_2.fastq.gz	Fastqsanger.gz
	SRR22032769_1.fastq.gz	Fastqsanger.gz
	SRR22032769_2.fastq.gz	Fastqsanger.gz
	SRR22032770_1.fastq.gz	Fastqsanger.gz

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Impact of sunitinib resistance on clear cell renal cell carcinoma therapeutic sensitivity in vitro

Project description:Sunitinib resistance creates a major clinical challenge for the treatment of advanced clear cell renal cell carcinoma (ccRCC) and functional and metabolic changes linked to sunitinib resistance are not fully understood. We sought to characterize the molecular and metabolic changes induced by the development of sunitinib resistance in ccRCC by developing and characterizing the transcriptome of two human ccRCC cell lines resistant to sunitinib.

2024-04-17 | GSE216494 | GEO

miRNA array of clear cell renal cell carcinoma from patients treated with sunitinib

Project description:A multiple receptor tyrosine kinase inhibitor, sunitinib, is a first-line therapy for clear cell renal cell carcinoma (CCRCC). Unfortunately, it has the major challenges of low initial response rate and resistance after about one year of treatment. Here we evaluated a microRNA (miRNA) and its target responsible for sunitinib resistance. Using miRNA profiling, we identified miR-96-5p upregulation in tumors from sunitinib-resistant CCRCC patients

2021-12-03 | GSE189331 | GEO

Sunitinib treatment exacerbates intratumoral heterogeneity in metastatic renal cancer

Project description:The aim of this study was to investigate the effect of VEGF targeted therapy (sunitinib) on intratumoral heterogeneity (ITH) in metastatic clear cell renal cancer (mRCC). 138 samples from patients with clear cell renal cell carcinoma, including biological replicates of nephrectomy samples. RNA extracted fresh frozen tissue samples.

2015-05-25 | E-GEOD-65615 | biostudies-arrayexpress

miRNA array of clear cell renal cell carcinoma from patients treated with sunitinib

Project description:miRNA array of clear cell renal cell carcinoma from patients treated with sunitinib

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Sunitinib treatment exacerbates intratumoral heterogeneity in metastatic renal cancer

Project description:The aim of this study was to investigate the effect of VEGF targeted therapy (sunitinib) on intratumoral heterogeneity (ITH) in metastatic clear cell renal cancer (mRCC).

2015-05-25 | GSE65615 | GEO

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

Sunitinib treatment exacerbates intratumoral heterogeneity in metastatic renal cancer (CGH)

Project description:The aim of this study was to investigate the effect of VEGF targeted therapy (sunitinib) on intratumoral heterogeneity (ITH) in metastatic clear cell renal cancer (mRCC). To explore ITH in detail, multiple tumor samples were taken from the primary renal tumors of mRCC patients who were sunitinib treated (n=23) or untreated (n=23). ITH of pathological grade, DNA (using array-based comparative genomic hybridisation), RNA (Illumina Beadarray) and protein (reverse phase protein array) were evaluated. Tumor grade heterogeneity was greater in treated compared to untreated tumors (P=0.002). Unsupervised and supervised analysis, for renal cancer driver, hypoxia and stromal gene signatures, was then performed. In untreated patient tumor samples, significant ITH occurred in chromosomal aberrations, RNA and protein expression, with clustering of DNA and RNA correlating for individual patients. In unsupervised analysis sunitinib therapy was not associated with increased ITH in DNA or RNA. However there was an increase in ITH for the driver mutation and hypoxia gene signatures (DNA and RNA) as well as increasing variability of protein expression with treatment (p<0.05). Despite this variability, significant chromosomal and RNA changes to targets of sunitinib, such as VHL, PBRM1 and CAIX, occurred in the treated samples. Together these findings suggest that sunitinib treatment has significant effects on the expression and ITH of key tumor and treatment specific genes. The results do not support the hypothesis that resistant clones are selected and predominate after initiation of targeted therapy; instead it appears that an initial clonal diversification occurs, supporting the hypothesis of polyclonal drug resistance. 128 samples from patients with clear cell renal cell carcinoma, including biological replicates of nephrectomy samples. Source of samples includes both biopsy and nephrectomy. DNA extracted from FFPE and fresh frozen tissue samples.

2015-05-25 | E-GEOD-67818 | 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

Enhanced YB1/EphA2 axis signaling promotes acquired resistance to sunitinib and metastatic potential of renal cell carcinoma

Project description:VHL mutations are the most common tumorigenic lesions in clear cell renal cell carcinoma (ccRCC) and result in continued activation of the HIF/VEGF pathway and uncontrolled cancer progression. Receptor tyrosine kinase (RTK) inhibitors such as sunitinib have been demonstrated to target tumorigenic signaling pathways, delay tumor progression and improve patient prognosis in metastatic renal cell carcinoma (mRCC). Although several mechanisms of sunitinib resistance have been reported, the solutions to overcome this resistance remain still unclear. In our study, we found that increased expression of YB1 (Y box binding protein 1, a multidrug resistance associated protein) and EphA2 (a member of erythropoietin-producing hepatocellular (Eph) receptors, belonging to the RTK family) mediated sunitinib resistance and mRCC exhibited a large phenotypic dependence on YB1 and EphA2. In addition, our findings confirm that YB1 promotes the invasion, metastasis and sunitinib resistance of ccRCC by regulating the EphA2 signaling pathway. Furthermore, pharmacological inhibition of EphA2 through the small molecule inhibitor ALW-II-41-27 reduced the proliferation of sunitinib-resistant tumor cells and suppressed tumor growth in vivo and restored the sensitivity of sunitinib-resistant tumor cells to sunitinib in vitro and in vivo. Mechanistically, YB1 increases the protein levels of EphA2 by maintaining the protein stabilization of EphA2 through inhibiting the proteasomal degradation pathway. Collectively, our findings provide the theoretical rationale that ccRCC metastasis and RTK-directed therapeutic resistance could be prospectively and purposefully targeted.

2020-05-28 | GSE151336 | GEO

Integrated miRNA-genomic analysis of sunitinib resistance in clear cell renal cell carcinoma (CCRCC) cell lines

Project description:Integrated miRNA-genomic analysis of sunitinib resistance in clear cell renal cell carcinoma (CCRCC) cell lines

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