This SuperSeries is composed of the SubSeries listed below.
Systematic sequencing of renal carcinoma reveals inactivation of histone modifying genes.
No sample metadata fields
View SamplesSystematic somatic mutation screening of 4000 genes in human clear cell renal cell carcinoma. Information on corresponding somatic mutations in each sample can be found at http://www.sanger.ac.uk/genetics/CGP/Studies/.
Systematic sequencing of renal carcinoma reveals inactivation of histone modifying genes.
No sample metadata fields
View SamplesPBRM1 was found to be mutated in a high percentage of clear cell RCCs. We performed knockdown of PBRM1 via siRNA and compared with scrambled control in three different RCC cell lines.
Exome sequencing identifies frequent mutation of the SWI/SNF complex gene PBRM1 in renal carcinoma.
Specimen part, Cell line, Treatment
View SamplesTranscriptional crosstalk between mammary gland, liver and adipose tissue
Homeorhetic adaptation to lactation: comparative transcriptome analysis of mammary, liver, and adipose tissue during the transition from pregnancy to lactation in rats.
No sample metadata fields
View SamplesFumarate hydratase (FH) mutation causes hereditary type 2 papillary renal cell carcinoma (HLRCC, Hereditary Leiomyomatosis and Renal Cell Cancer (MM ID # 605839)). The main effect of FH mutation is fumarate accumulation. The current paradigm posits that the main consequence of fumarate accumulation is HIF-a stabilization. Paradoxically, FH mutation differs from other HIF-a stabilizing mutations, such as VHL and SDH mutations, in its associated tumor types. We identified that fumarate can directly up-regulate antioxidant response element (ARE)-controlled genes. We demonstrated that AKR1B10 is an ARE-controlled gene and is up-regulated upon FH knockdown as well as in FH-null cell lines. AKR1B10 overexpression is also a prominent feature in both hereditary and sporadic PRCC2. This phenotype better explains the similarities between hereditary and sporadic PRCC2.
An antioxidant response phenotype shared between hereditary and sporadic type 2 papillary renal cell carcinoma.
Disease, Disease stage
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.
No sample metadata fields
View SamplesHypoxia signature in Clear cell RCC
Regulation of endocytosis via the oxygen-sensing pathway.
Specimen part, Disease, Disease stage
View SamplesWe used microarrays to analyze the global expression patterns for 22 commercially available pancreatic cancer cell lines
Glycogene expression alterations associated with pancreatic cancer epithelial-mesenchymal transition in complementary model systems.
Specimen part, Cell line
View SamplesMature NK and T-cell lymphomas are occasionally encountered in Asia but are very rare in Western populations. In part due to its rarity, little is known about this group of neoplasms, and despite being rather different disease entities, they are all treated similarly but with diverse clinical outcomes. Novel biomarkers (at both the genetic and protein levels) are needed to resolve diagnostic difficulties, improve prognostication and develop targeted therapies. To rectify this deficiency, we interrogated the transcriptome of several NK and mature T-cell lymphomas by whole-genome expression profiling for new markers that may further stratify this diverse group of conditions. Our initial efforts have identified a promising candidate marker that appears to differentiate NKTL lymphoma from other forms of T-cell neoplasms, and this finding has been validated by immunohistochemistry on archival material in a large number of patient cases.
Nuclear expression of MATK is a novel marker of type II enteropathy-associated T-cell lymphoma.
Specimen part, Cell line
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
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