Spontaneous loss of heterozygosity leading to homozygous R132H in a patient-derived IDH1 mutant cell line

Neuro-Oncology

Volumn 15, Issue 8, 2013, Pages 979-980

  Luchman, H Artee ^a,b   Chesnelong, Charles ^a,b   Cairncross, J Gregory ^a,b   Weiss, Samuel ^a,b  

^a UNIVERSITY OF CALGARY   (Canada)

^b UNIVERSITY OF CALGARY   (Canada)

Author keywords

[No Author keywords available]

Indexed keywords

2 HYDROXYGLUTARIC ACID; GENOMIC DNA; ISOCITRATE DEHYDROGENASE 1; RIBONUCLEASE P;

CARCINOGENICITY; CELL MUTANT; CELL PROLIFERATION; EXON; FOLLOW UP; GENE LOCUS; GENE LOSS; GENE MUTATION; GENE SEQUENCE; GLIOMA; HETEROZYGOSITY LOSS; HOMOZYGOSITY; HUMAN; IN VITRO STUDY; IN VIVO STUDY; LETTER; PHENOTYPE; QUANTITATIVE ANALYSIS; REAL TIME POLYMERASE CHAIN REACTION; WILD TYPE;

ANIMALS; BRAIN NEOPLASMS; GLIOMA; HUMANS; ISOCITRATE DEHYDROGENASE; MALE; POINT MUTATION;

EID: 84880676555     PISSN: 15228517     EISSN: 15235866     Source Type: Journal    
DOI: 10.1093/neuonc/not064     Document Type: Letter

References (4)

1. Luchman HA, Stechishin OD, Dang NH, et al. An in vivo patient-derived model of endogenous IDH1-mutant glioma. Neuro Oncol. 2012;14:184-191.
2. American Type Culture Collection cat#ACS-1018.
3. Jin G, Reitman ZJ, Duncan CG, et al. Disruption of wild-type IDH1 suppresses D-2-hydroxyglutarate production in IDH1-mutated gliomas. Cancer Res. 2013;73:496-501.
4. Ward PS, Lu C, Cross JR, et al. The potential for isocitrate dehydrogenase mutations to produce 2-hydroxyglutarate depends on allele specificity and subcellular compartmentalization. J Biol Chem. 2013;288(6):3804-3815.