BACKGROUND: Despite the moderate incidence of papillary renal cell carcinoma
A molecular classification of papillary renal cell carcinoma.
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View SamplesAnalysis of adult and childhood tumors reveals activation of an E2F3 signature unique to Wilms tumors.
The E2F3-Oncomir-1 axis is activated in Wilms' tumor.
Sex, Age
View SamplesMyc oncogenic signature in Papillary type 2b
Detection of DNA copy number changes and oncogenic signaling abnormalities from gene expression data reveals MYC activation in high-grade papillary renal cell carcinoma.
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ACSL1 Is Associated With Fetal Programming of Insulin Sensitivity and Cellular Lipid Content.
Sex
View SamplesWe hypothesised that SGA as a proxy for intrauterine growth restriction promotes specific epigenetic marks and pathways, whose physiological implications may become apparent only in the fully differentiated state.
ACSL1 Is Associated With Fetal Programming of Insulin Sensitivity and Cellular Lipid Content.
Sex
View SamplesWe hypothesised that SGA as a proxy for intrauterine growth restriction promotes specific epigenetic marks and pathways, whose physiological implications may become apparent only in the fully differentiated state.
ACSL1 Is Associated With Fetal Programming of Insulin Sensitivity and Cellular Lipid Content.
Sex
View SamplesPURPOSE: Despite over 70,000 new cases of bladder cancer in the United States annually, patients with advanced disease have a poor prognosis due to limited treatment modalities. We evaluate the role of Aurora A, identified as an upregulated candidate molecule in bladder cancer, in regulating bladder tumor growth.
The investigational Aurora kinase A inhibitor MLN8237 induces defects in cell viability and cell-cycle progression in malignant bladder cancer cells in vitro and in vivo.
Specimen part
View SamplesThe pituitary tumor-transforming gene (PTTG1) is a recently discovered oncogene implicated in the malignant progression of a number of neoplasms. It has been shown to drive both endocrine and non-endocrine malignancies, but has not yet been studied in the context of renal cell carcinoma (RCC). Clear cell RCC (ccRCC) is cytogenetically characterized by deletion of chromosome 3p, harboring the von-Hippel Lindau tumor suppressor gene, and amplification of chromosome 5q. The significance of copy number gain of chromosome 5 is not clear, but is presumed to be the location of oncogenes that influence ccRCC development or progression. The PTTG1 oncogene maps to chromosome 5q, and here we show that PTTG1 is amplified in clear cell RCC, is overexpressed in tumor tissue relative to adjacent normal kidney, and expression is associated with high grade, high stage, and poor prognosis. Furthermore, we establish a functional role for PTTG1 in ccRCC tumorigenesis and progression. PTTG1 ablation reduces both the tumorigenic ability of ccRCC cells in vitro and in vivo and the invasive ability of these cells in vitro. An analysis of genes whose transcription is regulated by PTTG1 was supportive of an association with invasive and metastatic disease. PTTG1-dependent expression of the Rho-GEF ECT2, another proto-oncogene, is observed in a number of ccRCC cell lines, and ECT2 expression correlates with PTTG1 expression, high stage, high grade, and poor prognosis ccRCC. As GEF's have been promoted as potential drug targets for targeted cancer therapeutics, the relationship between the PTTG1 and ECT2 oncogenes may be able to be exploited for the treatment of this disease.
Expression of the PTTG1 oncogene is associated with aggressive clear cell renal cell carcinoma.
Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Molecular pathways reflecting poor intrauterine growth are found in Wharton's jelly-derived mesenchymal stem cells.
Specimen part
View SamplesIn order to identify gene-expression patterns in mesenchymal stem cells associated with different birth weights and intrauterine growth parameters,
Molecular pathways reflecting poor intrauterine growth are found in Wharton's jelly-derived mesenchymal stem cells.
Specimen part
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