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Andrej Paľa, Jan Coburger, Moritz Scherer, Hajrullah Ahmeti, Constantin Roder, Florian Gessler, Christine Jungk, Angelika Scheuerle, Christian Senft, Marcos Tatagiba, Michael Synowitz, Christian Rainer Wirtz, Bernd Schmitz, and Andreas W. Unterberg

adjuvant treatment do not provide sufficient evidence to produce an algorithm for clinical practice in WHO grade II lesions. Additionally, the molecular characteristics of LGG, including isocitrate dehydrogenase (IDH) mutation status and 1p/19q codeletion, resulted in a new era of classification and decision-making for further LGG treatment protocols. 11 In the randomized EORTC (European Organization for Research and Treatment of Cancer) 22845 trial, a significant advantage in progression-free survival (PFS) was observed in a mixed series of glioma patients with a

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Catherine Gozé, Lamisse Mansour, Valérie Rigau, and Hugues Duffau

D iffuse WHO Grade II gliomas are slow-growing tumors that migrate within the brain, with an ineluctable risk of anaplastic transformation. 9 However, spontaneous evolution of these lesions is very heterogeneous, despite an identical initial pathological diagnosis. 28 Some genetic alterations, especially 1p19q codeletion and IDH1/IDH2 mutations, are believed to have an influence on the biological behavior of tumors, and the impact of these alterations on the prognosis of gliomas has extensively been investigated. The 1p19q codeletion has always been

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Jason K. Hsieh, Christopher S. Hong, Sunil Manjila, Mark L. Cohen, Simon Lo, Lisa Rogers, and Andrew E. Sloan

I socitrate dehydrogenase-1 ( IDH1 ) mutations were first identified in glioblastoma by Parsons and colleagues in 2008, 30 and were discovered to be particularly prevalent in younger patients and secondary glioblastomas. Notably, patients with IDH1 mutation-positive gliomas demonstrated strikingly increased overall survival compared with those with IDH1 wild-type tumors, a finding corroborated in 2 seminal studies 35 , 41 among many others. Subsequent work has demonstrated that IDH1 mutations occur early in tumorigenesis, preceding further genetic

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Cemaliye B. Akyerli, Şirin Yüksel, Özge Can, E. Zeynep Erson-Omay, Yavuz Oktay, Erdal Coşgun, Ege Ülgen, Yiğit Erdemgil, Aydın Sav, Andreas von Deimling, Murat Günel, M. Cengiz Yakıcıer, M. Necmettin Pamir, and Koray Özduman

R ecent large integrated analyses have clearly established that oncogenic molecular changes closely correlate with clinical behavior in diffuse gliomas. 3–6 , 19 Most of these oncogenic changes are stochastic, but some recur enough to be used as molecular markers to define clinical subsets. 7 Today, there is compelling evidence that isocitrate dehydrogenase 1 and/or 2 (IDH) mutations (IDH-mut) are indicative of a specific disease group. 3–6 , 19 Similarly, 1p/19q codeletions have become synonymous with oligodendrogliomas. Other authors have demonstrated that

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Vincent C. Ye, Alexander P. Landry, Teresa Purzner, Aristotelis Kalyvas, Nilesh Mohan, Philip J. O’Halloran, Andrew Gao, and Gelareh Zadeh

Interestingly, on the one hand, outcomes in H3K27M-mutant midline gliomas have been reported as similar in pediatric and adult populations, 8 suggesting overlapping biology in this subtype of tumor. Isocitrate dehydrogenase (IDH) mutations, on the other hand, are uncommon in brainstem gliomas and are more common in (but not exclusive to) the adult population. 9 , 10 Mutations in IDH, a rate-limiting enzyme in the Krebs cycle, are known to be associated with gliomagenesis. 11 A survey of The Cancer Genome Atlas cancer database reveals that 80% of adult

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Pamela S. Jones, Gavin P. Dunn, Fred G. Barker II, William T. Curry, Fred H. Hochberg, and Daniel P. Cahill

refinement of traditional classification between low- and high-grade gliomas. Over the past 4 years, several recurring mutations have been identified in low-grade gliomas that, together, have transformed our understanding of this disease. Recently identified gene mutations include those found in the family of isocitrate dehydrogenase (IDH) genes, enzymes involved in citrate metabolism. The IDH1 mutation was first reported in 2008, when it was discovered in 12% of sequenced glioblastoma genomes. 21 Further research has shown that IDH gene mutations are found in a

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Gavin P. Dunn, Ovidiu C. Andronesi, and Daniel P. Cahill

set the stage for a reevaluation of their clinical management. A prototypic example has been the recent identification of mutations in the IDH1 gene, 65 a stunning and unexpected discovery that has led to new insights into glioma and cancer biology, has fueled new interest in studies of cancer metabolism, and has clear clinical implications. Today, neurooncologists and neurosurgeons increasingly stratify glial neoplasms into IDH1 -mutant or IDH1 -WT disease. 24 , 92 Indeed, the divergent clinical characteristics of histopathologically identical primary ( IDH

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Shuyu Hao, Christopher S. Hong, Jie Feng, Chunzhang Yang, Prashant Chittiboina, Junting Zhang, and Zhengping Zhuang

and Ollier disease harbor somatic mosaicism of mutations in isocitrate dehydrogenase 1 (IDH1) or isocitrate dehydrogenase 2 (IDH2) . 1 Maffucci syndrome was originally characterized as enchondromatosis with hemangioma. However, additional tumors have been reported in these patients, including lymphangiomas, pancreatic adenocarcinomas, biliary adenocarcinomas, osteosarcomas, and mesenchymal ovarian tumors. 2 , 13 , 17 , 29 Additionally, intracranial tumors including astrocytomas, olfactory neuroblastomas, malignant chordomas, spindle cell hemangioendotheliomas

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Tal Gonen, Rachel Grossman, Razi Sitt, Erez Nossek, Raneen Yanaki, Emanuela Cagnano, Akiva Korn, Daniel Hayat, and Zvi Ram

. Preliminary observations in our patients have suggested a high occurrence of intraoperative seizures in patients with tumors located in the SMA region, and this was further investigated in this study. Interestingly, an association between seizures as a presenting symptom in patients with diffuse LGGs and the isocitrate dehydrogenase 1 (IDH1) mutation has recently been reported, 21 with the IDH1 mutation occurring mostly in tumors located in the insula and in frontal regions. 21 In this study, we have evaluated the association between tumor location, specifically in

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Takahide Nejo, Shota Tanaka, Masako Ikemura, Masashi Nomura, Shunsaku Takayanagi, Masahiro Shin, Tetsuo Ushiku, Junji Shibahara, Nobuhito Saito, and Akitake Mukasa

I n 2008, Parsons et al. first reported a mutation in the isocitrate dehydrogenase 1 ( IDH1 ) gene in glioblastomas and showed that it was associated with a favorable prognosis. 17 This mutation, along with a rare mutation in the isocitrate dehydrogenase 2 ( IDH2 ) gene, turned out to be a hallmark of grade II and III gliomas and secondary glioblastomas. 11 , 23 , 24 Subsequent studies revealed that IDH1/2 mutations were also found in several other types of tumors. 24 Among them, cartilaginous tumors are known to have a high frequency of IDH1/2 mutations