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Journal of the National Cancer Institute Advance Access originally published online on August 26, 2008
JNCI Journal of the National Cancer Institute 2008 100(17):1193-1195; doi:10.1093/jnci/djn263
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© The Author 2008. Published by Oxford University Press.

EDITORIAL

SDHB—A Gene for All Tumors?

Charis Eng

Affiliation of author: Genomic Medicine Institute, Lerner Research Institute and Taussig Cancer Institute, Cleveland Clinic Foundation, Cleveland, OH; Department of Genetics and CASE Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, OH

Correspondence to: Charis Eng, MD, PhD, Genomic Medicine Institute, Cleveland Clinic, 9500 Euclid Ave, NE-50, Cleveland, OH 44195 (e-mail: engc@ccf.org).

The first 150 words of the full text of this article appear below.

Succinate dehydrogenase (SDH) or mitochondrial complex II, comprising four subunits (A–D) in the inner mitochondrial membrane, lies at the crossroads of electron transport and the Krebs tricarboxylic acid cycle (1). SDH, whose subunits are encoded by autosomal genes, catalyzes the conversion of succinate to fumarate. In turn, the fumarate to malate conversation is catalyzed by fumarate hydratase (FH). It is well documented that germline homozygous or compound heterozygous mutations of SDH genes (typically SDHA) and of genes encoding other mitochondrial complexes cause a group of recessive syndromes (eg, Leigh syndrome) that are characterized by relatively severe encephalomyelopathy, myopathy, cardiomyopathies, and/or hepatopathies, typically resulting in death in childhood (1). Similarly, germline homozygous or compound heterozygous mutations in FH also result in severe neurodegeneration and early death. Thus, it came as a surprise to both those with interest in mitochondrial metabolism and the oncology community when germline . . . [Full Text of this Article]


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