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IDH mutation status in prostate cancer

Oncogene volume 31, page 3826 (2012)Cite this article

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In a recent Oncogene review, Yen et al.1 summarized the important role of somatic mutations in the cytoplasmic and mitochondrial forms of isocitrate dehydrogenase (IDH1 and IDH2, respectively) in cancer. These glioma- and acute myeloid leukemia-associated mutations occur at IDH1 codon 132 (that is, R132) or in IDH2, at codon 172 or 140 (that is, R172, R140).1 Although cancer-associated IDH1/2 mutations impair the wild-type IDH activity of the enzymes, they activate a novel enzymatic function in converting α-ketoglutarate to 2-hydroxyglutarate, which leads to DNA hypermethylation and increased angiogenesis through stabilization of hypoxia-inducible transcription factor-1α.2 Yen et al.1 highlighted the value of documenting mutant IDH1 and IDH2 enzymes as targets for individualized and novel cancer therapies.

We have determined IDH1/2 mutations in localized prostate cancer (PCa), which has significant heterogeneity in genomic stability, tumor metabolism and clinical outcome.3 Mutational and array comparative genomic hybridization analyses for R132, R172 or R140 mutations as well as IDH1/2 allelic copy number were conducted in 158 PCa DNA samples following IRB consent, as previously described.4 IDH1 and IDH2 mutations were determined using a Sequenom MassARRAY platform and confirmed by direct Sanger sequencing.

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Author notes

  1. A F Ghiam and R A Cairns: These authors contributed equally to this work.

Authors and Affiliations

  1. Ontario Cancer Institute/Princess Margaret Hospital and University of Toronto, Toronto, Ontario, Canada

    A F Ghiam, R A Cairns, J Thoms, A Dal Pra, O Ahmed, A Meng, T W Mak & R G Bristow

Authors
  1. A F Ghiam
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  2. R A Cairns
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  3. J Thoms
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  4. A Dal Pra
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  5. O Ahmed
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  6. A Meng
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  7. T W Mak
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  8. R G Bristow
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Correspondence to R G Bristow.

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The authors declare no conflict of interest.

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Ghiam, A., Cairns, R., Thoms, J. et al. IDH mutation status in prostate cancer. Oncogene 31, 3826 (2012). https://doi.org/10.1038/onc.2011.546

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