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MicroRNA expression in peripheral blood predicts poor and prolonged response to sunitinib.

ABSTRACT: Peripheral blood samples were taken before initiation of therapy and 2 weeks later from patients with advanced renal cell carcinoma treated with sunitinib in first line. MicroRNA expression in peripheral blood was assessed using microarrays and several models predicting poor response and prolonged response to sunitinib were constructed and evaluated. Peripheral blood samples obtained before initiation of therapy with sunitinib and 14 days later were used to assess expression values of miRNAs.

ORGANISM(S): Homo sapiens

SUBMITTER: Juan M-CM-^Angel Fresno Vara

PROVIDER: E-GEOD-32099 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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MicroRNA expression profiling of peripheral blood samples predicts resistance to first-line sunitinib in advanced renal cell carcinoma patients.

Gámez-Pozo Angelo A Antón-Aparicio Luis M LM Bayona Cristina C Borrega Pablo P Gallegos Sancho María I MI García-Domínguez Rocío R de Portugal Teresa T Ramos-Vázquez Manuel M Pérez-Carrión Ramón R Bolós María V MV Madero Rosario R Sánchez-Navarro Iker I Fresno Vara Juan A JA Espinosa Arranz Enrique E

Neoplasia (New York, N.Y.) 20121201 12

Anti-angiogenic therapy benefits many patients with advanced renal cell carcinoma (RCC), but there is still a need for predictive markers that help in selecting the best therapy for individual patients. MicroRNAs (miRNAs) regulate cancer cell behavior and may be attractive biomarkers for prognosis and prediction of response. Forty-four patients with RCC were recruited into this observational prospective study conducted in nine Spanish institutions. Peripheral blood samples were taken before init ...[more]

PMID: 23308047

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MicroRNA expression in peripheral blood predicts poor and prolonged response to sunitinib.

Project description:Peripheral blood samples were taken before initiation of therapy and 2 weeks later from patients with advanced renal cell carcinoma treated with sunitinib in first line. MicroRNA expression in peripheral blood was assessed using microarrays and several models predicting poor response and prolonged response to sunitinib were constructed and evaluated.

2013-02-11 | GSE32099 | GEO

Differentially expressed genes analysis between dihydroberberine, sunitinib and dihydroberberine plus sunitinib.

2015-06-26 | GSE70282 | GEO

Differentially expressed genes analysis between dihydroberberine, sunitinib and dihydroberberine plus sunitinib.

Project description:To gain insights into the mechanisms of dihydroberberine, sunitinib and dihydroberberine plus sunitinib on inhibition to A549 cells, we have employed whole genome microarray expression profiling as a discovery platform to identify different genes between dihydroberberine, sunitinib and dihydroberberine plus sunitinib-treated sample and control. A549 cells were cultivated in the absence or presence of 25?mol/L dihydroberberine, 2?mol/L sunitinib, 25?mol/L dihydroberberine plus 2?mol/L sunitinib for 48 h, followed by the Agilent Whole Human Genome Oligo Microarray

2015-06-26 | E-GEOD-70282 | biostudies-arrayexpress

Transgelin contributes to a poor response of metastatic renal cell carcinoma to sunitinib treatment

Project description:Renal cell carcinoma (RCC) represents about 2-3% of all cancers with over 400,000 new cases per year. Sunitinib, a vascular endothelial growth factor tyrosine kinase receptor inhibitor, has been used mainly for first-line treatment of metastatic clear-cell RCC with good or intermediate prognosis. However, about one third of metastatic RCC patients do not respond to sunitinib, leading to disease progression. Here we aim to find and characterize proteins associated with poor sunitinib response in a pilot proteomics study. 16 RCC tumors from patients responding (8) vs. non-responding (8) to sunitinib in 3 months after treatment initiation, together with their adjacent non-cancerous tissues, were analyzed using data independent acquisition mass spectrometry. Proteomics analysis quantified 1996 protein groups (q<0.01) and revealed 27 proteins deregulated between tumors non-responding vs. responding to sunitinib, representing a pattern of deregulated proteins potentially contributing to sunitinib resistance. Gene set enrichment analysis showed up-regulation of epithelial-to-mesenchymal transition with transgelin as one of the most significantly abundant protein. Transgelin expression was silenced by CRISPR/Cas9 and RNA interference, and the cells with reduced transgelin level exhibited significantly slower proliferation. Our data indicate that transgelin is an essential protein supporting RCC cell proliferation which could contribute to intrinsic sunitinib resistance.

2021-11-03 | PXD027065 | Pride

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

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

2015-05-25 | GSE67818 | GEO

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

Effect of depletion of FUS on gene expression during in sunitinib-resistance cell lines

Project description:To investigate the function FUS in the regulation of sunitinib-resistance， we used lentiviral transduction to knock down FUS expression in the sunitinib-resistant RCC cells.

2023-03-31 | GSE226245 | GEO

Gene expression profiling of generated sunitinib-resistant RCC cell lines

Project description:The clinical response to sunitinib in advanced renal-cell carcinoma (RCC) is frequently limited in magnitude and duration due to drug resistance, but the underlying mechanisms remain elusive. To discover mechanisms of resistance, we developed drug-resistant cell lines and have their gene expressions profiled and compared. Results provide insight into the molecular mechanisms underlying sunitinib-resistance.

2016-09-30 | GSE69535 | GEO

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