IDH1 and IDH2 mutations are frequent events in central chondrosarcoma and central and periosteal chondromas but not in other mesenchymal tumours
By M. F. Amary, K. Bácsi, F. Maggiani, S. Damato, D. Halai, F. Berisha, R. Pollock, P. O'Donnell, A. Grigoriadis, T. Diss and 6 more. Journal of Pathology, 2011
971 citations recorded by the source corpus.
Subfields: Cancer Research, Pulmonary and Respiratory Medicine, Rheumatology
View Paper: https://www.semanticscholar.org/paper/8b38d1c2d2979f242f7bc553ba6f625c651456ec
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In Cancer Research
- H. Ohgaki
- P. Kleihues
- K. Guan
- Craig B. Thompson
- M. V. Vander Heiden
- Ralph J. Deberardinis
- David M. Sabatini
- Alec C. Kimmelman
In Pulmonary and Respiratory Medicine
In Rheumatology
Citations in the corpus
- Frequent mutation of isocitrate dehydrogenase (IDH)1 and IDH2 in cholangiocarcinoma identified through broad-based tumor genotyping. (2012, background): “Consistent with reports that IDH1 and IDH2 gene mutations are rare in tumor types other than gliomas, AML, and cartilaginous tumors [20, 36, 38 – 40], we identified IDH1 mutations in only 2% of the total gastrointestinal cohort (Table 3).”
- Metabolic regulation of epigenetics (2012, background): “…isocitrate dehydrogenase 1 (IDH1) and IDH2 were found to be frequently mutated in low-grade gliomas (Yan et al., 2009), adult de novo acute myeloid leukemias (AMLs) (Mardis et al., 2009; Ward et al., 2010) and subsets of chondrosarcomas and lymphomas (Amary et al., 2011; Cairns et al., 2012).”
- The Definition of Primary and Secondary Glioblastoma (2012, background): “Exceptions are central chondrosarcomas (~55%) (16), intrahepatic cholangio-carcinomas (23%) (17), acute myeloid leukemia (AML; 15–20%) (18-23), angioimmunoblastic T-cell lymphoma (AITL; ~20%) (24) malignant melanoma (~10%) (25), and anaplastic thyroid cancer (~10%) (26).”
- Inhibition of α-KG-dependent histone and DNA demethylases by fumarate and succinate that are accumulated in mutations of FH and SDH tumor suppressors. (2012, background): “…IDH1 and IDH2 are frequently mutated in >75% of glioma (Parsons et al. 2008), ;20% of acute myeloid leukaemia (AML) (Mardis et al. 2009), and several additional tumors at different frequencies (Hemerly et al. 2010; Murugan et al. 2010; Amary et al. 2011; Damato et al. 2012; Oermann et al. 2012).”