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E-GEOD-26574 - An antioxidant response phenotype is shared between hereditary and sporadic type 2 papillary renal cell carcinoma

Released on 17 October 2011, last updated on 17 November 2011
Homo sapiens
Samples (67)
Array (1)
Protocols (6)
Fumarate 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. Expression profiling renal normal and tumor tissue
Experiment type
transcription profiling by array 
Karl Dykema
An Antioxidant Response Phenotype Shared between Hereditary and Sporadic Type 2 Papillary Renal Cell Carcinoma. Ooi A, Wong JC, Petillo D, Roossien D, Perrier-Trudova V, Whitten D, Min BW, Tan MH, Zhang Z, Yang XJ, Zhou M, Gardie B, Molinié V, Richard S, Tan PH, Teh BT, Furge KA. , PMID:22014576
Investigation descriptionE-GEOD-26574.idf.txt
Sample and data relationshipE-GEOD-26574.sdrf.txt
Raw data (2),
Processed data (1)
Array designA-GEOD-11433.adf.txt
R ExpressionSetE-GEOD-26574.eSet.r