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

inhibiting the mutant enzyme would make these tumors behave like their more aggressive WT counterparts. The differences in survival most likely stem from the fact that IDH1- mutant and -WT tumors arise from distinct lineages and ontogenies and thus represent entirely different neoplastic disease processes. Because gliomas acquire the IDH1 mutation very early in their development, akin to BRAF mutations in dysplastic nevi and melanoma, we envisage that it similarly represents a targetable dependency. From a surgical standpoint, it will be important to determine

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Nicholas F. Marko and Robert J. Weil

chromosomes 1, 15, 20, and 22. 152 Many molecular features that are commonly observed in other WHO Grade II gliomas are generally absent in PXAs. TP53 mutations are uncommon; 35 , 75 , 110 , 126 , 204 EGFR overexpression is absent; 50 LOH on chromosome 1, 8p, 9p, 10, 17, 19q, and 22q are only rarely observed; 75 , 126 and deletions or epigenomic inactivation involving CDKN2A or CDKN2B are inconsistent (although potentially functionally significant). 75 , 191 Conversely, BRAF mutations (particularly at the V600E “hot spot”) are common in PXA, 25 , 111 , 154

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Darryl Lau, Stephen T. Magill and Manish K. Aghi

C , Hu X , Rosenblum MK , Koutcher JA , Holland EC : Dose-dependent effects of platelet-derived growth factor-B on glial tumorigenesis . Cancer Res 64 : 4783 – 4789 , 2004 95 Smalley KS , Xiao M , Villanueva J , Nguyen TK , Flaherty KT , Letrero R , : CRAF inhibition induces apoptosis in melanoma cells with non-V600E BRAF mutations . Oncogene 28 : 85 – 94 , 2009 96 Stommel JM , Kimmelman AC , Ying H , Nabioullin R , Ponugoti AH , Wiedemeyer R , : Coactivation of receptor tyrosine kinases affects the

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Pamela S. Jones, Daniel P. Cahill, Priscilla K. Brastianos, Keith T. Flaherty and William T. Curry

information was obtained: date of birth; sex; date of primary melanoma diagnosis; number of cerebral metastases; date(s) of craniotomy; date(s) and dose(s) of ipilimumab; radiation therapy type, dose(s), and date(s); neurological examination findings; operative note(s); pathology, including BRAF mutation status; and neurosurgical and oncological visit notes. Improvements in performance status were noted as “no change,” “improved,” or “worsened,” based on comparison of preoperative and postoperative notes. Corticosteroid dependence was determined by duration and magnitude

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Michael Karsy, Jian Guan, Walavan Sivakumar, Jayson A. Neil, Meic H. Schmidt and Mark A. Mahan

novel factor in human breast cancer cells with metastatic potential . Cancer Res 59 : 4675 – 4680 , 1999 87 Ren X , Wang J , Hu M , Jiang H , Yang J , Jiang Z : Clinical, radiological, and pathological features of 26 intracranial and intraspinal malignant peripheral nerve sheath tumors . J Neurosurg 119 : 695 – 708 , 2013 88 Robert C , Long GV , Brady B , Dutriaux C , Maio M , Mortier L , : Nivolumab in previously untreated melanoma without BRAF mutation . N Engl J Med 372 : 320 – 330 , 2015 89 Robertson KA

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Juan Carlos Martinez-Gutierrez, Megan R. D'Andrea, Daniel P. Cahill, Sandro Santagata, Fred G. Barker II and Priscilla K. Brastianos

= acute myelogenous leukemia; CLL = chronic lymphocytic leukemia; cranio = craniopharyngioma; DLBCL = diffuse large B-cell lymphoma; GBM = glioblastoma multiforme; LUAD = lung adenocarcinoma; LUSC = lung squamous cell carcinoma. B: Location of CTNNB1 and BRAF mutations detected by whole-exome sequencing study of adamantinomatous and papillary craniopharyngiomas in their corresponding protein sequences. All CTNNB1 mutations were located in exon 3 exclusively. All BRAF mutations were activating V600E mutations. Both images reproduced with permission from

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Christina Stache, Christiane Bils, Rudolf Fahlbusch, Jörg Flitsch, Michael Buchfelder, Harald Stefanits, Thomas Czech, Udo Gaipl, Benjamin Frey, Rolf Buslei and Annett Hölsken

ACP5 40, M Codon 33/Ser>Cys Wild type ACP6 45, M Codon 41/Thr>Ile Wild type ACP7 39, M Codon 33/Ser>Cys Wild type ACP8 16, F Codon 32/Asp>Asn Wild type ACP9 53, F Codon 33/Ser>Cys Wild type ACP10 28, F Not analyzed Not analyzed * List of patient ACP samples, provided by collaborating neurosurgery departments, used for generation of primary cell cultures. Age represents the age of the patient at the time of tumor surgery. Samples were screened for CTNNB1 and BRAF mutations. Immunohistochemical

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Nelson Moussazadeh, Vishaal Prabhu, Evan D. Bander, Ryan C. Cusic, Apostolos John Tsiouris, Vijay K. Anand and Theodore H. Schwartz

, Taylor-Weiner A , Manley PE , Jones RT , Dias-Santagata D , Thorner AR , : Exome sequencing identifies BRAF mutations in papillary craniopharyngiomas . Nat Genet 46 : 161 – 165 , 2014 3 Bunin GR , Surawicz TS , Witman PA , Preston-Martin S , Davis F , Bruner JM : The descriptive epidemiology of craniopharyngioma . J Neurosurg 89 : 547 – 551 , 1998 4 Cavallo LM , de Divitiis O , Aydin S , Messina A , Esposito F , Iaconetta G , : Extended endoscopic endonasal transsphenoidal approach to the suprasellar area

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Mazda K. Turel, Georgios Tsermoulas, Lior Gonen, George Klironomos, Joao Paulo Almeida, Gelareh Zadeh and Fred Gentili

(range 40–90; Table 2 ). Discussion The recurrence rate of craniopharyngiomas is reported as 0%–62% at 10 years, even after apparent GTR. 14 , 16 , 23 The challenges encountered in the management of recurrent and residual craniopharyngiomas have resulted in various treatment options being used for these tumors. Several therapeutic modalities such as RT, stereotactic catheter placement, intratumoral bleomycin, intracystic radiotherapy, and more recently, targeted chemotherapy in patients with BRAF mutations have been employed to obtain tumor control. 1 , 2

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John Richard Apps and Juan Pedro Martinez-Barbera

metabolites in the blood, CSF, cystic fluid, or urine A marker could be from the tumor itself or reflect damage, e.g., to the hypothalamus BRAF mutation detectable in plasma of patients with PCP (Brastianos et al., 2016) Identification of matrix metalloproteinases in urine of patient with recurrent ACP (Smith et al., 2007) Risk stratification for surgery Risk stratification of risk of relapse Assessment of response to radiotherapy Early detection of relapse Novel solid tumor therapies Targeting pathways in the tumor tissue or targeting the host