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Rupesh Kotecha, Jacob A. Miller, Vyshak A. Venur, Alireza M. Mohammadi, Samuel T. Chao, John H. Suh, Gene H. Barnett, Erin S. Murphy, Pauline Funchain, Jennifer S. Yu, Michael A. Vogelbaum, Lilyana Angelov and Manmeet S. Ahluwalia

P atients with metastatic melanoma have the highest predisposition for developing brain metastasis, and autopsy studies have demonstrated brain metastases in up to 55%–75% of patients with metastatic melanoma. 28 Melanoma is associated with a number of somatic mutations and aberrations, the most common of which is the BRAF mutation. 22 The BRAF inhibitors (BRAFi), including vemurafenib and dabrafenib, and immune-based therapies, including ipilimumab, have demonstrated intracranial efficacy and improved survival in Phase II studies in patients with active

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David Ly, Hilary P. Bagshaw, Christopher J. Anker, Jonathan D. Tward, Kenneth F. Grossmann, Randy L. Jensen and Dennis C. Shrieve

survival and intracranial response. BRAF is a protein kinase that has been implicated in cell proliferation and differentiation and is mutated in 70% of patients with melanoma. 8 Mutation in the BRAF gene protects cells from apoptosis. 22 Targeted therapies for the BRAF V600E mutation have been developed. Vemurafenib was shown in a randomized controlled trial 7 to prolong overall survival. In addition, dabrafenib has been shown to improve progression-free survival. 17 The use of BRAF inhibitors was studied in patients with melanoma brain metastases after case

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Zhiyuan Xu, Cheng-Chia Lee, Arjun Ramesh, Adam C. Mueller, David Schlesinger, Or Cohen-Inbar, Han-Hsun Shih and Jason P. Sheehan

melanoma BM and the role of BRAF mutation status as a prognostic factor after the development of BMs. Methods Patient Selection The institutional review board approved this retrospective study. In 2011, ipilimumab and vemurafenib were approved by the US FDA for treating patients harboring metastatic melanomas. Therefore, we selected patients who had developed cutaneous melanoma BM between June of 2010 and August of 2014. The inclusion criteria were set as patients with melanoma whose BRAF V600E mutation status of the metastatic melanoma was confirmed

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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

inhibitor vemurafenib. 2 However, the patient in that case was not concurrently treated with a MEK inhibitor, and the tumor progressed after 6 weeks of treatment. Although this suggests the importance of MEK inhibition in the targeted treatment of BRAF mutated tumors, the role of BRAF monotherapy versus BRAF and MEK combination therapy needs to be prospectively studied. Due to the genetic simplicity of craniopharyngiomas, there is great potential for targeted therapy as treatment for these neoplasms. While BRAF inhibitors such as vemurafenib and dabrafenib are

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Benjamin T. Himes, Michael W. Ruff, Jaimie J. Van Gompel, Sean S. Park, Evanthia Galanis, Timothy J. Kaufmann and Joon H. Uhm

signaling and regulation. Mutations in BRAF that transform the BRAF kinase into a constitutively active form result in cell proliferation and tumor growth. The BRAF V600E mutation has been described in 7% of human cancers. 7 It is targeted in malignant melanoma and non–small cell lung cancer using inhibitors such as vemurafenib and dabrafenib, but these agents have also been used as targeted therapy for other tumor types with BRAF V600E mutations, including pleomorphic xanthoastrocytoma, ganglioglioma, and a BRAF V600E–mutant glioblastoma with systemic metastases

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Benjamin T. Himes, Michael W. Ruff, Jaimie J. Van Gompel, Sean S. Park, Evanthia Galanis, Timothy J. Kaufmann and Joon H. Uhm

signaling and regulation. Mutations in BRAF that transform the BRAF kinase into a constitutively active form result in cell proliferation and tumor growth. The BRAF V600E mutation has been described in 7% of human cancers. 7 It is targeted in malignant melanoma and non–small cell lung cancer using inhibitors such as vemurafenib and dabrafenib, but these agents have also been used as targeted therapy for other tumor types with BRAF V600E mutations, including pleomorphic xanthoastrocytoma, ganglioglioma, and a BRAF V600E–mutant glioblastoma with systemic metastases

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Qi Yue, Yang Yu, Zhifeng Shi, Yongfei Wang, Wei Zhu, Zunguo Du, Zhenwei Yao, Liang Chen and Ying Mao

to being seen in craniopharyngiomas, CTNNB1 mutation is also seen in calcifying odontogenic cysts. 23 These data partially explain the heterogeneous composition of CTNNB1 -mutated craniopharyngiomas, which include cholesterol, triglycerides, protein, and desquamated epithelium. The tumors free of both BRAF and CTNNB1 mutations in our study showed a tendency toward a more irregular shape, but further investigation of molecular mechanisms is needed. The development of BRAF mutation inhibitors, including vemurafenib and dabrafenib, has strikingly advanced

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to a secondgeneration selective BRAF inhibitor that, unlike vemurafenib, does not induce activation of wild-type BRAF. Conclusion Our data support the development of targeted treatment paradigms for BRAF-altered pediatric astrocytomas and also demonstrate that therapies must be tailored to the specific mutational context and distinct mechanisms of action of the mutant kinase

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Xiaolei Hao, Ruie Feng, Yalan Bi, Yuhan Liu, Chunde Li, Tao Lu and Yongji Tian

of BRAF mutations in ECD and LCH. 1 , 6 Currently, regimens including BRAF inhibitors are under investigation. In the Cohen Aubart et al. and Diamond et al. studies, vemurafenib demonstrated clinically meaningful, long-term efficacy in adult patients with BRAF V600E mutant–isolated ECD and –isolated LCH. 2 , 4 In previous mixed ECD and LCH cases, BRAF V600E–positive LCH lesions sometimes occurred concomitant with BRAF V600E–positive ECD lesions. 8 In this condition, the effect of BRAF inhibitors has not been identified, especially for children

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

. 12 , 22 Despite ongoing research and advancements in care, melanoma has typically been resistant to radiotherapy and cytotoxic chemotherapy. 18 In the central nervous system (CNS), treatment options include surgery, stereotactic radiosurgery (SRS), and whole-brain radiation therapy (WBRT), depending on the size and number of lesions. Temozolomide has been the most widely used systemic treatment for brain metastases, with only 10% clinical response. 1 Recently, however, promising new therapies for advanced melanoma have emerged. Vemurafenib is an inhibitor of