Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA147553 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
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. Peripheral blood samples obtained before initiation of therapy with sunitinib and 14 days later were used to assess expression values of miRNAs.
2013-02-11 | E-GEOD-32099 | biostudies-arrayexpress
Project description:The aim of the experiment was to discover differentially expressed miRNAs correlating with prolonged response to targeted therapy in patients with metastatic renal cell carcinoma treated with sunitinib or pazopanib
2018-02-08 | E-MTAB-6296 | biostudies-arrayexpress
Project description:Chronic Hypoxia predicts Poor Prognosis in Hepatocellular Carcinoma
| PRJNA117097 | ENA
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
Project description:Peripheral blood stem cell microRNA profiling
| PRJNA109191 | ENA
Project description:GSTP1 expression predicts poor pathological complete response to neoadjuvant chemotherapy in ER-negative breast cancer
| PRJNA146953 | ENA
Project description:Peripheral Blood Mononuclear Cell Gene Expression Profiles May Predict Poor Outcome in Idiopathic Pulmonary Fibrosis [Agilent]
| PRJNA141911 | ENA
Project description:Peripheral Blood Mononuclear Cell Gene Expression Profiles May Predict Poor Outcome in Idiopathic Pulmonary Fibrosis [Affymetrix]
| PRJNA141927 | ENA
Project description:Transcriptome analysis was used to identify gene expression changes during development of sunitinib resistance in a renal cell carcinoma patient-derived xenograft (PDX) model. During the response phase, tumors exhibited a 91% reduction in volume, characterized by induction of TNFRSF1A, TNFAIP3, NFKB2, CCL2, CCL20, BIRC3, and MOAP1. Ingenuity Pathway Analysis indicated decreased expression of cell survival genes during tumor response to sunitinib. In this model, after 4 weeks of treatment, tumors developed resistance despite continued administration of the tyrosine kinase inhibitor (TKI) sunitinib (40 mg/kg/d p.o.). Resistance was associated with increased expression of VEGFA, EPO, IL-8, ANGPT2, TNFRSF12, MAPK3/7, MAPKBP1, and increased cell survival genes, suggesting activation of angiogenesis and MAPK/ERK pathways. Tumor lysate mRNA evaluated for murine gene expression to examine the contribution of host effects, indicated that tumor response was associated with downregulation of immune cell trafficking, cellular movement, and inflammatory response genes. During tumor escape, genes associated with cellular movement, inflammatory response, and immune cell trafficking were strongly induced, along with intratumoral accumulation of myeloid derived suppressor cells (MDSC), indicating a role for host factors during emergence of sunitinib resistance. The same PDX model was used to assess anti-tumor efficacy of sunitinib combined with MEK inhibitor (MEKi) PD-0325901 (4 mg/kg/d p.o.) using different schedules. The most effective treatment regimen was either continuous treatment with both drugs or switching from sunitinib to PD-0325901 monotherapy at d30, which reduced tumor volume by 78.6% (p=0.0241) and 88.5% (p=0.0068), respectively. The combination of MEKi with TKI (sunitinib, axitinib, or pazopanib) suppressed levels of phospho-MEK1/2 and phospho-ERK1/2, and decreased intratumoral MDSC. Thus, continuous treatment with sunitinib alone did not maintain tumor response, and addition of a MEKi abrogated resistance leading to prolonged survival. Study was comprised of three experimental groups (pre-treatment, response, escape). All tumors came from the same PDX model. There were four biological replicates in each group. Four mice were used, with each of the 3 groups per mouse. There were no control or reference samples.
2015-12-17 | E-GEOD-76068 | biostudies-arrayexpress