Succinate dehydrogenase mutation underlies global epigenomic divergence in gastrointestinal stromal tumor.

نویسندگان

  • J Keith Killian
  • Su Young Kim
  • Markku Miettinen
  • Carly Smith
  • Maria Merino
  • Maria Tsokos
  • Martha Quezado
  • William I Smith
  • Mona S Jahromi
  • Paraskevi Xekouki
  • Eva Szarek
  • Robert L Walker
  • Jerzy Lasota
  • Mark Raffeld
  • Brandy Klotzle
  • Zengfeng Wang
  • Laura Jones
  • Yuelin Zhu
  • Yonghong Wang
  • Joshua J Waterfall
  • Maureen J O'Sullivan
  • Marina Bibikova
  • Karel Pacak
  • Constantine Stratakis
  • Katherine A Janeway
  • Joshua D Schiffman
  • Jian-Bing Fan
  • Lee Helman
  • Paul S Meltzer
چکیده

Gastrointestinal stromal tumors (GIST) harbor driver mutations of signal transduction kinases such as KIT, or, alternatively, manifest loss-of-function defects in the mitochondrial succinate dehydrogenase (SDH) complex, a component of the Krebs cycle and electron transport chain. We have uncovered a striking divergence between the DNA methylation profiles of SDH-deficient GIST (n = 24) versus KIT tyrosine kinase pathway-mutated GIST (n = 39). Infinium 450K methylation array analysis of formalin-fixed paraffin-embedded tissues disclosed an order of magnitude greater genomic hypermethylation relative to SDH-deficient GIST versus the KIT-mutant group (84.9 K vs. 8.4 K targets). Epigenomic divergence was further found among SDH-mutant paraganglioma/pheochromocytoma (n = 29), a developmentally distinct SDH-deficient tumor system. Comparison of SDH-mutant GIST with isocitrate dehydrogenase-mutant glioma, another Krebs cycle-defective tumor type, revealed comparable measures of global hypo- and hypermethylation. These data expose a vital connection between succinate metabolism and genomic DNA methylation during tumorigenesis, and generally implicate the mitochondrial Krebs cycle in nuclear epigenomic maintenance.

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منابع مشابه

Divergence in Gastrointestinal Stromal Tumor Succinate Dehydrogenase Mutation Underlies Global Epigenomic

Gastrointestinal stromal tumors (GIST) harbor driver mutations of signal transduction kinases such as KIT, or, alternatively, manifest loss-of-function defects in the mitochondrial succinate dehydrogenase (SDH) complex, a component of the Krebs cycle and electron transport chain. We have uncovered a striking divergence between the DNA methylation profi les of SDH-defi cient GIST ( n = 24) versu...

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Clinicopathologic study of succinate-dehydrogenase-deficient gastrointestinal stromal tumors

Gastrointestinal stromal tumors (GISTs) that are not driven by kinase mutations, as are most GISTs, often show loss of function of the succinate dehydrogenase (SDH) complex and are considered SDH-deficient GISTs. SDH-deficient GISTs share many distinct characteristics compared with conventional GISTs. However, data regarding these characteristics, particularly among Asian people, are relatively...

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Author's response to reviews Title: SDHA Loss of Function Mutations in a Subset of Young Adult Wild-type Gastrointestinal Stromal Tumors Authors: ANTOINE ITALIANO ([email protected])

Background: KIT/PDGFRA wild-type gastrointestinal stromal tumors (WT GIST) have been associated with alteration of the succinate dehydrogenase (SDH) complex II function. A recent report identified, in two cases of young adults WT GIST, a germline mutation in SDHA encoding the main subunit of the SDH complex II. Methods: Next generation sequencing was applied on five pediatric and one young adul...

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عنوان ژورنال:
  • Cancer discovery

دوره 3 6  شماره 

صفحات  -

تاریخ انتشار 2013