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3. Targeting integrated epigenetic and metabolic pathways in lethal childhood PFA ependymomas

Author

Panwalkar, Pooja, Tamrazi, Benita, Dang, Derek, Chung, Chan, Sweha, Stefan, Natarajan, Siva Kumar, Pun, Matthew, Bayliss, Jill, Ogrodzinski, Martin P, Pratt, Drew, Mullan, Brendan, Hawes, Debra, Yang, Fusheng, Lu, Chao, Sabari, Benjamin R, Achreja, Abhinav, Heon, Jin, Animasahun, Olamide, Cieslik, Marcin, Dunham, Christopher, Yip, Stephen, Hukin, Juliette, Phillips, Joanna J, Bornhorst, Miriam, Griesinger, Andrea M, Donson, Andrew M, Foreman, Nicholas K, Garton, Hugh JL, Heth, Jason, Muraszko, Karin, Nazarian, Javad, Koschmann, Carl, Jiang, Li, Filbin, Mariella G, Nagrath, Deepak, Kool, Marcel, Korshunov, Andrey, Pfister, Stefan M, Gilbertson, Richard J, Allis, C David, Chinnaiyan, Arul M, Lunt, Sophia Y, Blüml, Stefan, Judkins, Alexander R, and Venneti, Sriram

Subjects
Cancer, Biotechnology, Genetics, Rare Diseases, Orphan Drug, Neurosciences, Brain Disorders, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Animals, Child, Ependymoma, Epigenesis, Genetic, Epigenomics, Histones, Humans, Metabolic Networks and Pathways, Mice, Biological Sciences, Medical and Health Sciences
Abstract

Childhood posterior fossa group A ependymomas (PFAs) have limited treatment options and bear dismal prognoses compared to group B ependymomas (PFBs). PFAs overexpress the oncohistone-like protein EZHIP (enhancer of Zeste homologs inhibitory protein), causing global reduction of repressive histone H3 lysine 27 trimethylation (H3K27me3), similar to the oncohistone H3K27M. Integrated metabolic analyses in patient-derived cells and tumors, single-cell RNA sequencing of tumors, and noninvasive metabolic imaging in patients demonstrated enhanced glycolysis and tricarboxylic acid (TCA) cycle metabolism in PFAs. Furthermore, high glycolytic gene expression in PFAs was associated with a poor outcome. PFAs demonstrated high EZHIP expression associated with poor prognosis and elevated activating mark histone H3 lysine 27 acetylation (H3K27ac). Genomic H3K27ac was enriched in PFAs at key glycolytic and TCA cycle–related genes including hexokinase-2 and pyruvate dehydrogenase. Similarly, mouse neuronal stem cells (NSCs) expressing wild-type EZHIP (EZHIP-WT) versus catalytically attenuated EZHIP-M406K demonstrated H3K27ac enrichment at hexokinase-2 and pyruvate dehydrogenase, accompanied by enhanced glycolysis and TCA cycle metabolism. AMPKα-2, a key component of the metabolic regulator AMP-activated protein kinase (AMPK), also showed H3K27ac enrichment in PFAs and EZHIP-WT NSCs. The AMPK activator metformin lowered EZHIP protein concentrations, increased H3K27me3, suppressed TCA cycle metabolism, and showed therapeutic efficacy in vitro and in vivo in patient-derived PFA xenografts in mice. Our data indicate that PFAs and EZHIP-WT–expressing NSCs are characterized by enhanced glycolysis and TCA cycle metabolism. Repurposing the antidiabetic drug metformin lowered pathogenic EZHIP, increased H3K27me3, and suppressed tumor growth, suggesting that targeting integrated metabolic/epigenetic pathways is a potential therapeutic strategy for treating childhood ependymomas.

Published
2021

5. Human fetal cerebellar cell atlas informs medulloblastoma origin and oncogenesis

Author

Luo, Zaili, Xia, Mingyang, Shi, Wei, Zhao, Chuntao, Wang, Jiajia, Xin, Dazhuan, Dong, Xinran, Xiong, Yu, Zhang, Feng, Berry, Kalen, Ogurek, Sean, Liu, Xuezhao, Rao, Rohit, Xing, Rui, Wu, Lai Man Natalie, Cui, Siying, Xu, Lingli, Lin, Yifeng, Ma, Wenkun, Tian, Shuaiwei, Xie, Qi, Zhang, Li, Xin, Mei, Wang, Xiaotao, Yue, Feng, Zheng, Haizi, Liu, Yaping, Stevenson, Charles B., de Blank, Peter, Perentesis, John P., Gilbertson, Richard J., Li, Hao, Ma, Jie, Zhou, Wenhao, Taylor, Michael D., and Lu, Q. Richard

Published
2022
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6. The NALCN channel regulates metastasis and nonmalignant cell dissemination

Author

Rahrmann, Eric P., Shorthouse, David, Jassim, Amir, Hu, Linda P., Ortiz, Mariaestela, Mahler-Araujo, Betania, Vogel, Peter, Paez-Ribes, Marta, Fatemi, Atefeh, Hannon, Gregory J., Iyer, Radhika, Blundon, Jay A., Lourenço, Filipe C., Kay, Jonathan, Nazarian, Rosalynn M., Hall, Benjamin A., Zakharenko, Stanislav S., Winton, Douglas J., Zhu, Liqin, and Gilbertson, Richard J.

Published
2022
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7. Spectrum and prevalence of genetic predisposition in medulloblastoma: a retrospective genetic study and prospective validation in a clinical trial cohort.

Author

Waszak, Sebastian M, Northcott, Paul A, Buchhalter, Ivo, Robinson, Giles W, Sutter, Christian, Groebner, Susanne, Grund, Kerstin B, Brugières, Laurence, Jones, David TW, Pajtler, Kristian W, Morrissy, A Sorana, Kool, Marcel, Sturm, Dominik, Chavez, Lukas, Ernst, Aurelie, Brabetz, Sebastian, Hain, Michael, Zichner, Thomas, Segura-Wang, Maia, Weischenfeldt, Joachim, Rausch, Tobias, Mardin, Balca R, Zhou, Xin, Baciu, Cristina, Lawerenz, Christian, Chan, Jennifer A, Varlet, Pascale, Guerrini-Rousseau, Lea, Fults, Daniel W, Grajkowska, Wiesława, Hauser, Peter, Jabado, Nada, Ra, Young-Shin, Zitterbart, Karel, Shringarpure, Suyash S, De La Vega, Francisco M, Bustamante, Carlos D, Ng, Ho-Keung, Perry, Arie, MacDonald, Tobey J, Hernáiz Driever, Pablo, Bendel, Anne E, Bowers, Daniel C, McCowage, Geoffrey, Chintagumpala, Murali M, Cohn, Richard, Hassall, Timothy, Fleischhack, Gudrun, Eggen, Tone, Wesenberg, Finn, Feychting, Maria, Lannering, Birgitta, Schüz, Joachim, Johansen, Christoffer, Andersen, Tina V, Röösli, Martin, Kuehni, Claudia E, Grotzer, Michael, Kjaerheim, Kristina, Monoranu, Camelia M, Archer, Tenley C, Duke, Elizabeth, Pomeroy, Scott L, Shelagh, Redmond, Frank, Stephan, Sumerauer, David, Scheurlen, Wolfram, Ryzhova, Marina V, Milde, Till, Kratz, Christian P, Samuel, David, Zhang, Jinghui, Solomon, David A, Marra, Marco, Eils, Roland, Bartram, Claus R, von Hoff, Katja, Rutkowski, Stefan, Ramaswamy, Vijay, Gilbertson, Richard J, Korshunov, Andrey, Taylor, Michael D, Lichter, Peter, Malkin, David, Gajjar, Amar, Korbel, Jan O, and Pfister, Stefan M

Subjects
Humans, Medulloblastoma, Cerebellar Neoplasms, Genetic Predisposition to Disease, Risk Factors, Retrospective Studies, Prospective Studies, Reproducibility of Results, Predictive Value of Tests, Gene Expression Profiling, Pedigree, DNA Mutational Analysis, DNA Methylation, Heredity, Phenotype, Germ-Line Mutation, Models, Genetic, Adolescent, Adult, Child, Child, Preschool, Infant, Female, Male, Young Adult, Genetic Testing, Transcriptome, Biomarkers, Tumor, Progression-Free Survival, Exome Sequencing, Brain Cancer, Genetics, Cancer, Human Genome, Pediatric, Pediatric Cancer, Rare Diseases, Brain Disorders, Aetiology, 2.1 Biological and endogenous factors, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

BackgroundMedulloblastoma is associated with rare hereditary cancer predisposition syndromes; however, consensus medulloblastoma predisposition genes have not been defined and screening guidelines for genetic counselling and testing for paediatric patients are not available. We aimed to assess and define these genes to provide evidence for future screening guidelines.MethodsIn this international, multicentre study, we analysed patients with medulloblastoma from retrospective cohorts (International Cancer Genome Consortium [ICGC] PedBrain, Medulloblastoma Advanced Genomics International Consortium [MAGIC], and the CEFALO series) and from prospective cohorts from four clinical studies (SJMB03, SJMB12, SJYC07, and I-HIT-MED). Whole-genome sequences and exome sequences from blood and tumour samples were analysed for rare damaging germline mutations in cancer predisposition genes. DNA methylation profiling was done to determine consensus molecular subgroups: WNT (MBWNT), SHH (MBSHH), group 3 (MBGroup3), and group 4 (MBGroup4). Medulloblastoma predisposition genes were predicted on the basis of rare variant burden tests against controls without a cancer diagnosis from the Exome Aggregation Consortium (ExAC). Previously defined somatic mutational signatures were used to further classify medulloblastoma genomes into two groups, a clock-like group (signatures 1 and 5) and a homologous recombination repair deficiency-like group (signatures 3 and 8), and chromothripsis was investigated using previously established criteria. Progression-free survival and overall survival were modelled for patients with a genetic predisposition to medulloblastoma.FindingsWe included a total of 1022 patients with medulloblastoma from the retrospective cohorts (n=673) and the four prospective studies (n=349), from whom blood samples (n=1022) and tumour samples (n=800) were analysed for germline mutations in 110 cancer predisposition genes. In our rare variant burden analysis, we compared these against 53 105 sequenced controls from ExAC and identified APC, BRCA2, PALB2, PTCH1, SUFU, and TP53 as consensus medulloblastoma predisposition genes according to our rare variant burden analysis and estimated that germline mutations accounted for 6% of medulloblastoma diagnoses in the retrospective cohort. The prevalence of genetic predispositions differed between molecular subgroups in the retrospective cohort and was highest for patients in the MBSHH subgroup (20% in the retrospective cohort). These estimates were replicated in the prospective clinical cohort (germline mutations accounted for 5% of medulloblastoma diagnoses, with the highest prevalence [14%] in the MBSHH subgroup). Patients with germline APC mutations developed MBWNT and accounted for most (five [71%] of seven) cases of MBWNT that had no somatic CTNNB1 exon 3 mutations. Patients with germline mutations in SUFU and PTCH1 mostly developed infant MBSHH. Germline TP53 mutations presented only in childhood patients in the MBSHH subgroup and explained more than half (eight [57%] of 14) of all chromothripsis events in this subgroup. Germline mutations in PALB2 and BRCA2 were observed across the MBSHH, MBGroup3, and MBGroup4 molecular subgroups and were associated with mutational signatures typical of homologous recombination repair deficiency. In patients with a genetic predisposition to medulloblastoma, 5-year progression-free survival was 52% (95% CI 40-69) and 5-year overall survival was 65% (95% CI 52-81); these survival estimates differed significantly across patients with germline mutations in different medulloblastoma predisposition genes.InterpretationGenetic counselling and testing should be used as a standard-of-care procedure in patients with MBWNT and MBSHH because these patients have the highest prevalence of damaging germline mutations in known cancer predisposition genes. We propose criteria for routine genetic screening for patients with medulloblastoma based on clinical and molecular tumour characteristics.FundingGerman Cancer Aid; German Federal Ministry of Education and Research; German Childhood Cancer Foundation (Deutsche Kinderkrebsstiftung); European Research Council; National Institutes of Health; Canadian Institutes for Health Research; German Cancer Research Center; St Jude Comprehensive Cancer Center; American Lebanese Syrian Associated Charities; Swiss National Science Foundation; European Molecular Biology Organization; Cancer Research UK; Hertie Foundation; Alexander and Margaret Stewart Trust; V Foundation for Cancer Research; Sontag Foundation; Musicians Against Childhood Cancer; BC Cancer Foundation; Swedish Council for Health, Working Life and Welfare; Swedish Research Council; Swedish Cancer Society; the Swedish Radiation Protection Authority; Danish Strategic Research Council; Swiss Federal Office of Public Health; Swiss Research Foundation on Mobile Communication; Masaryk University; Ministry of Health of the Czech Republic; Research Council of Norway; Genome Canada; Genome BC; Terry Fox Research Institute; Ontario Institute for Cancer Research; Pediatric Oncology Group of Ontario; The Family of Kathleen Lorette and the Clark H Smith Brain Tumour Centre; Montreal Children's Hospital Foundation; The Hospital for Sick Children: Sonia and Arthur Labatt Brain Tumour Research Centre, Chief of Research Fund, Cancer Genetics Program, Garron Family Cancer Centre, MDT's Garron Family Endowment; BC Childhood Cancer Parents Association; Cure Search Foundation; Pediatric Brain Tumor Foundation; Brainchild; and the Government of Ontario.

Published
2018

8. Natural language processing charts transcriptome evolution to design combination cancer therapies

Author

Jassim, Amir, primary, Nimmervoll, Birgit V., additional, Terranova, Sabrina, additional, Nathan, Erica, additional, Masih, Katherine E., additional, Ruff, Lisa, additional, Duarte, Matilde, additional, Cooper, Elizabeth, additional, Hu, Linda P., additional, Katyal, Gunjan, additional, Akhbari, Melika, additional, Gilbertson, Reuben J., additional, Terhune, Colton, additional, Balmus, Gabriel, additional, Jackson, Stephen P., additional, Filbin, Mariella G., additional, Hill, Anthony, additional, Patrizi, Anarita, additional, Dani, Neil, additional, Regev, Aviv, additional, Lehtinen, Maria K., additional, and Gilbertson, Richard J., additional

Published
2024
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10. Vismodegib Exerts Targeted Efficacy Against Recurrent Sonic Hedgehog–Subgroup Medulloblastoma: Results From Phase II Pediatric Brain Tumor Consortium Studies PBTC-025B and PBTC-032

Author

Robinson, Giles W, Orr, Brent A, Wu, Gang, Gururangan, Sridharan, Lin, Tong, Qaddoumi, Ibrahim, Packer, Roger J, Goldman, Stewart, Prados, Michael D, Desjardins, Annick, Chintagumpala, Murali, Takebe, Naoko, Kaste, Sue C, Rusch, Michael, Allen, Sariah J, Onar-Thomas, Arzu, Stewart, Clinton F, Fouladi, Maryam, Boyett, James M, Gilbertson, Richard J, Curran, Tom, Ellison, David W, and Gajjar, Amar

Subjects
Rare Diseases, Neurosciences, Pediatric Research Initiative, Brain Cancer, Cancer, Clinical Research, Pediatric, Brain Disorders, Pediatric Cancer, Genetics, Human Genome, Adult, Anilides, Brain Neoplasms, Female, Hedgehog Proteins, Humans, Male, Medulloblastoma, Middle Aged, Pyridines, Young Adult, Clinical Sciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

PurposeTwo phase II studies assessed the efficacy of vismodegib, a sonic hedgehog (SHH) pathway inhibitor that binds smoothened (SMO), in pediatric and adult recurrent medulloblastoma (MB).Patients and methodsAdult patients enrolled onto PBTC-025B and pediatric patients enrolled onto PBTC-032 were treated with vismodegib (150 to 300 mg/d). Protocol-defined response, which had to be sustained for 8 weeks, was confirmed by central neuroimaging review. Molecular tests to identify patterns of response and insensitivity were performed when tissue was available.ResultsA total of 31 patients were enrolled onto PBTC-025B, and 12 were enrolled onto PBTC-032. Three patients in PBTC-025B and one in PBTC-032, all with SHH-subgroup MB (SHH-MB), exhibited protocol-defined responses. Progression-free survival (PFS) was longer in those with SHH-MB than in those with non-SHH-MB, and prolonged disease stabilization occurred in 41% of patient cases of SHH-MB. Among those with SHH-MB, loss of heterozygosity of PTCH1 was associated with prolonged PFS, and diffuse staining of P53 was associated with reduced PFS. Whole-exome sequencing identified mutations in SHH genes downstream from SMO in four of four tissue samples from nonresponders and upstream of SMO in two of four patients with favorable responses.ConclusionVismodegib exhibits activity against adult recurrent SHH-MB but not against recurrent non-SHH-MB. Inadequate accrual of pediatric patients precluded conclusions in this population. Molecular analyses support the hypothesis that SMO inhibitor activity depends on the genomic aberrations within the tumor. Such inhibitors should be advanced in SHH-MB studies; however, molecular and genomic work remains imperative to identify target populations that will truly benefit.

Published
2015

13. DDX3X acts as a live-or-die checkpoint in stressed cells by regulating NLRP3 inflammasome

Author

Samir, Parimal, Kesavardhana, Sannula, Patmore, Deanna M., Gingras, Sebastien, Malireddi, R. K. Subbarao, Karki, Rajendra, Guy, Clifford S., Briard, Benoit, Place, David E., Bhattacharya, Anannya, Sharma, Bhesh Raj, Nourse, Amanda, King, Sharon V., Pitre, Aaron, Burton, Amanda R., Pelletier, Stephane, Gilbertson, Richard J., and Kanneganti, Thirumala-Devi

Published
2019
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14. Challenges to curing primary brain tumours

Author

Aldape, Kenneth, Brindle, Kevin M., Chesler, Louis, Chopra, Rajesh, Gajjar, Amar, Gilbert, Mark R., Gottardo, Nicholas, Gutmann, David H., Hargrave, Darren, Holland, Eric C., Jones, David T. W., Joyce, Johanna A., Kearns, Pamela, Kieran, Mark W., Mellinghoff, Ingo K., Merchant, Melinda, Pfister, Stefan M., Pollard, Steven M., Ramaswamy, Vijay, Rich, Jeremy N., Robinson, Giles W., Rowitch, David H., Sampson, John H., Taylor, Michael D., Workman, Paul, and Gilbertson, Richard J.

Published
2019
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15. Dual and opposing roles of primary cilia in medulloblastoma development.

Author

Han, Young-Goo, Kim, Hong Joo, Dlugosz, Andrzej A, Ellison, David W, Gilbertson, Richard J, and Alvarez-Buylla, Arturo

Subjects
Cilia, Animals, Mice, Transgenic, Humans, Mice, Mice, Mutant Strains, Medulloblastoma, Cerebellar Neoplasms, Glial Fibrillary Acidic Protein, Receptors, G-Protein-Coupled, Nerve Tissue Proteins, Nuclear Proteins, Signal Transduction, Child, Wnt Proteins, Kruppel-Like Transcription Factors, Hedgehog Proteins, Smoothened Receptor, Zinc Finger Protein Gli2, Kinesins, Cancer, Brain Disorders, Brain Cancer, Rare Diseases, Pediatric, Medical and Health Sciences, Immunology
Abstract

Recent work has shown that primary cilia are essential for Hedgehog (Hh) signaling during mammalian development. It is also known that aberrant Hh signaling can lead to cancer, but the role of primary cilia in oncogenesis is not known. Cerebellar granule neuron precursors (GNPs) can give rise to medulloblastomas, the most common malignant brain tumor in children. The primary cilium and Hh signaling are required for GNP proliferation. We asked whether primary cilia in GNPs have a role in medulloblastoma growth in mice. Genetic ablation of primary cilia blocked medulloblastoma formation when this tumor was driven by a constitutively active Smoothened protein (Smo), an upstream activator of Hh signaling. In contrast, removal of cilia was required for medulloblastoma growth by a constitutively active glioma-associated oncogene family zinc finger-2 (GLI2), a downstream transcription factor. Thus, primary cilia are either required for or inhibit medulloblastoma formation, depending on the initiating oncogenic event. Remarkably, the presence or absence of cilia was associated with specific variants of human medulloblastomas; primary cilia were found in medulloblastomas with activation in HH or WNT signaling but not in most medulloblastomas in other distinct molecular subgroups. Primary cilia could serve as a diagnostic tool and provide new insights into the mechanism of tumorigenesis.

Published
2009

18. Primary cilia control translation and the cell cycle in medulloblastoma

Author

Youn, Yong Ha, Hou, Shirui, Wu, Chang-Chih, Kawauchi, Daisuke, Orr, Brent A, Robinson, Giles W, Finkelstein, David, Taketo, Makoto M, Gilbertson, Richard J, Roussel, Martine F, Han, Young-Goo, Han, Young-Goo [0000-0002-4008-294X], and Apollo - University of Cambridge Repository

Subjects
WNT, Mice, Brain Neoplasms, Cell Cycle, Genetics, translation, Animals, Humans, Cilia, Cerebellar Neoplasms, Medulloblastoma, Developmental Biology
Abstract

The primary cilium, a signaling organelle projecting from the surface of a cell, controls cellular physiology and behavior. The presence or absence of primary cilia is a distinctive feature of a given tumor type; however, whether and how the primary cilium contributes to tumorigenesis are unknown for most tumors. Medulloblastoma (MB) is a common pediatric brain cancer comprising four groups: SHH, WNT, group 3 (G3), and group 4 (G4). From 111 cases of MB, we show that primary cilia are abundant in SHH and WNT MBs but rare in G3 and G4 MBs. Using WNT and G3 MB mouse models, we show that primary cilia promote WNT MB by facilitating translation of mRNA encoding β-catenin, a major oncoprotein driving WNT MB, whereas cilium loss promotes G3 MB by disrupting cell cycle control and destabilizing the genome. Our findings reveal tumor type-specific ciliary functions and underlying molecular mechanisms. Moreover, we expand the function of primary cilia to translation control and reveal a molecular mechanism by which cilia regulate cell cycle progression, thereby providing new frameworks for studying cilium function in normal and pathologic conditions.

Published
2022

19. Data from Cross-Species Genomics Reveals Oncogenic Dependencies in ZFTA/C11orf95 Fusion–Positive Supratentorial Ependymomas

Author

Zheng, Tuyu, primary, Ghasemi, David R., primary, Okonechnikov, Konstantin, primary, Korshunov, Andrey, primary, Sill, Martin, primary, Maass, Kendra K., primary, Benites Goncalves da Silva, Patricia, primary, Ryzhova, Marina, primary, Gojo, Johannes, primary, Stichel, Damian, primary, Arabzade, Amir, primary, Kupp, Robert, primary, Benzel, Julia, primary, Taya, Shinichiro, primary, Adachi, Toma, primary, Shiraishi, Ryo, primary, Gerber, Nicolas U., primary, Sturm, Dominik, primary, Ecker, Jonas, primary, Sievers, Philipp, primary, Selt, Florian, primary, Chapman, Rebecca, primary, Haberler, Christine, primary, Figarella-Branger, Dominique, primary, Reifenberger, Guido, primary, Fleischhack, Gudrun, primary, Rutkowski, Stefan, primary, Donson, Andrew M., primary, Ramaswamy, Vijay, primary, Capper, David, primary, Ellison, David W., primary, Herold-Mende, Christel C., primary, Schüller, Ulrich, primary, Brandner, Sebastian, primary, Driever, Pablo Hernáiz, primary, Kros, Johan M., primary, Snuderl, Matija, primary, Milde, Till, primary, Grundy, Richard G., primary, Hoshino, Mikio, primary, Mack, Stephen C., primary, Gilbertson, Richard J., primary, Jones, David T.W., primary, Kool, Marcel, primary, von Deimling, Andreas, primary, Pfister, Stefan M., primary, Sahm, Felix, primary, Kawauchi, Daisuke, primary, and Pajtler, Kristian W., primary

Published
2023
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20. Table S2 from ZFTA Translocations Constitute Ependymoma Chromatin Remodeling and Transcription Factors

Author

Kupp, Robert, primary, Ruff, Lisa, primary, Terranova, Sabrina, primary, Nathan, Erica, primary, Ballereau, Stephane, primary, Stark, Rory, primary, Sekhar Reddy Chilamakuri, Chandra, primary, Hoffmann, Nadin, primary, Wickham-Rahrmann, Katherine, primary, Widdess, Marcus, primary, Arabzade, Amir, primary, Zhao, Yanhua, primary, Varadharajan, Srinidhi, primary, Zheng, Tuyu, primary, Murugesan, Mohankumar, primary, Pfister, Stefan M., primary, Kawauchi, Daisuke, primary, Pajtler, Kristian W., primary, Deneen, Benjamin, primary, Mack, Stephen C., primary, Masih, Katherine E., primary, Gryder, Berkley E., primary, Khan, Javed, primary, and Gilbertson, Richard J., primary

Published
2023
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21. Figure S2 from ZFTA–RELA Dictates Oncogenic Transcriptional Programs to Drive Aggressive Supratentorial Ependymoma

Author

Arabzade, Amir, primary, Zhao, Yanhua, primary, Varadharajan, Srinidhi, primary, Chen, Hsiao-Chi, primary, Jessa, Selin, primary, Rivas, Bryan, primary, Stuckert, Austin J., primary, Solis, Minerva, primary, Kardian, Alisha, primary, Tlais, Dana, primary, Golbourn, Brian J., primary, Stanton, Ann-Catherine J., primary, Chan, Yuen San, primary, Olson, Calla, primary, Karlin, Kristen L., primary, Kong, Kathleen, primary, Kupp, Robert, primary, Hu, Baoli, primary, Injac, Sarah G., primary, Ngo, Madeline, primary, Wang, Peter R., primary, De León, Luz A., primary, Sahm, Felix, primary, Kawauchi, Daisuke, primary, Pfister, Stefan M., primary, Lin, Charles Y., primary, Hodges, H. Courtney, primary, Singh, Irtisha, primary, Westbrook, Thomas F., primary, Chintagumpala, Murali M., primary, Blaney, Susan M., primary, Parsons, Donald W., primary, Pajtler, Kristian W., primary, Agnihotri, Sameer, primary, Gilbertson, Richard J., primary, Yi, Joanna, primary, Jabado, Nada, primary, Kleinman, Claudia L., primary, Bertrand, Kelsey C., primary, Deneen, Benjamin, primary, and Mack, Stephen C., primary

Published
2023
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22. Table S2 from ZFTA–RELA Dictates Oncogenic Transcriptional Programs to Drive Aggressive Supratentorial Ependymoma

Author

Arabzade, Amir, primary, Zhao, Yanhua, primary, Varadharajan, Srinidhi, primary, Chen, Hsiao-Chi, primary, Jessa, Selin, primary, Rivas, Bryan, primary, Stuckert, Austin J., primary, Solis, Minerva, primary, Kardian, Alisha, primary, Tlais, Dana, primary, Golbourn, Brian J., primary, Stanton, Ann-Catherine J., primary, Chan, Yuen San, primary, Olson, Calla, primary, Karlin, Kristen L., primary, Kong, Kathleen, primary, Kupp, Robert, primary, Hu, Baoli, primary, Injac, Sarah G., primary, Ngo, Madeline, primary, Wang, Peter R., primary, De León, Luz A., primary, Sahm, Felix, primary, Kawauchi, Daisuke, primary, Pfister, Stefan M., primary, Lin, Charles Y., primary, Hodges, H. Courtney, primary, Singh, Irtisha, primary, Westbrook, Thomas F., primary, Chintagumpala, Murali M., primary, Blaney, Susan M., primary, Parsons, Donald W., primary, Pajtler, Kristian W., primary, Agnihotri, Sameer, primary, Gilbertson, Richard J., primary, Yi, Joanna, primary, Jabado, Nada, primary, Kleinman, Claudia L., primary, Bertrand, Kelsey C., primary, Deneen, Benjamin, primary, and Mack, Stephen C., primary

Published
2023
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23. Data from ZFTA–RELA Dictates Oncogenic Transcriptional Programs to Drive Aggressive Supratentorial Ependymoma

Author

Arabzade, Amir, primary, Zhao, Yanhua, primary, Varadharajan, Srinidhi, primary, Chen, Hsiao-Chi, primary, Jessa, Selin, primary, Rivas, Bryan, primary, Stuckert, Austin J., primary, Solis, Minerva, primary, Kardian, Alisha, primary, Tlais, Dana, primary, Golbourn, Brian J., primary, Stanton, Ann-Catherine J., primary, Chan, Yuen San, primary, Olson, Calla, primary, Karlin, Kristen L., primary, Kong, Kathleen, primary, Kupp, Robert, primary, Hu, Baoli, primary, Injac, Sarah G., primary, Ngo, Madeline, primary, Wang, Peter R., primary, De León, Luz A., primary, Sahm, Felix, primary, Kawauchi, Daisuke, primary, Pfister, Stefan M., primary, Lin, Charles Y., primary, Hodges, H. Courtney, primary, Singh, Irtisha, primary, Westbrook, Thomas F., primary, Chintagumpala, Murali M., primary, Blaney, Susan M., primary, Parsons, Donald W., primary, Pajtler, Kristian W., primary, Agnihotri, Sameer, primary, Gilbertson, Richard J., primary, Yi, Joanna, primary, Jabado, Nada, primary, Kleinman, Claudia L., primary, Bertrand, Kelsey C., primary, Deneen, Benjamin, primary, and Mack, Stephen C., primary

Published
2023
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24. Supplementary Table S4 from Cross-Species Genomics Reveals Oncogenic Dependencies in ZFTA/C11orf95 Fusion–Positive Supratentorial Ependymomas

Author

Zheng, Tuyu, primary, Ghasemi, David R., primary, Okonechnikov, Konstantin, primary, Korshunov, Andrey, primary, Sill, Martin, primary, Maass, Kendra K., primary, Benites Goncalves da Silva, Patricia, primary, Ryzhova, Marina, primary, Gojo, Johannes, primary, Stichel, Damian, primary, Arabzade, Amir, primary, Kupp, Robert, primary, Benzel, Julia, primary, Taya, Shinichiro, primary, Adachi, Toma, primary, Shiraishi, Ryo, primary, Gerber, Nicolas U., primary, Sturm, Dominik, primary, Ecker, Jonas, primary, Sievers, Philipp, primary, Selt, Florian, primary, Chapman, Rebecca, primary, Haberler, Christine, primary, Figarella-Branger, Dominique, primary, Reifenberger, Guido, primary, Fleischhack, Gudrun, primary, Rutkowski, Stefan, primary, Donson, Andrew M., primary, Ramaswamy, Vijay, primary, Capper, David, primary, Ellison, David W., primary, Herold-Mende, Christel C., primary, Schüller, Ulrich, primary, Brandner, Sebastian, primary, Driever, Pablo Hernáiz, primary, Kros, Johan M., primary, Snuderl, Matija, primary, Milde, Till, primary, Grundy, Richard G., primary, Hoshino, Mikio, primary, Mack, Stephen C., primary, Gilbertson, Richard J., primary, Jones, David T.W., primary, Kool, Marcel, primary, von Deimling, Andreas, primary, Pfister, Stefan M., primary, Sahm, Felix, primary, Kawauchi, Daisuke, primary, and Pajtler, Kristian W., primary

Published
2023
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25. Data from ZFTA Translocations Constitute Ependymoma Chromatin Remodeling and Transcription Factors

Author

Kupp, Robert, primary, Ruff, Lisa, primary, Terranova, Sabrina, primary, Nathan, Erica, primary, Ballereau, Stephane, primary, Stark, Rory, primary, Sekhar Reddy Chilamakuri, Chandra, primary, Hoffmann, Nadin, primary, Wickham-Rahrmann, Katherine, primary, Widdess, Marcus, primary, Arabzade, Amir, primary, Zhao, Yanhua, primary, Varadharajan, Srinidhi, primary, Zheng, Tuyu, primary, Murugesan, Mohankumar, primary, Pfister, Stefan M., primary, Kawauchi, Daisuke, primary, Pajtler, Kristian W., primary, Deneen, Benjamin, primary, Mack, Stephen C., primary, Masih, Katherine E., primary, Gryder, Berkley E., primary, Khan, Javed, primary, and Gilbertson, Richard J., primary

Published
2023
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26. Figure S2 from ZFTA Translocations Constitute Ependymoma Chromatin Remodeling and Transcription Factors

Author

Kupp, Robert, primary, Ruff, Lisa, primary, Terranova, Sabrina, primary, Nathan, Erica, primary, Ballereau, Stephane, primary, Stark, Rory, primary, Sekhar Reddy Chilamakuri, Chandra, primary, Hoffmann, Nadin, primary, Wickham-Rahrmann, Katherine, primary, Widdess, Marcus, primary, Arabzade, Amir, primary, Zhao, Yanhua, primary, Varadharajan, Srinidhi, primary, Zheng, Tuyu, primary, Murugesan, Mohankumar, primary, Pfister, Stefan M., primary, Kawauchi, Daisuke, primary, Pajtler, Kristian W., primary, Deneen, Benjamin, primary, Mack, Stephen C., primary, Masih, Katherine E., primary, Gryder, Berkley E., primary, Khan, Javed, primary, and Gilbertson, Richard J., primary

Published
2023
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27. Supplementary Methods from ZFTA Translocations Constitute Ependymoma Chromatin Remodeling and Transcription Factors

Author

Kupp, Robert, primary, Ruff, Lisa, primary, Terranova, Sabrina, primary, Nathan, Erica, primary, Ballereau, Stephane, primary, Stark, Rory, primary, Sekhar Reddy Chilamakuri, Chandra, primary, Hoffmann, Nadin, primary, Wickham-Rahrmann, Katherine, primary, Widdess, Marcus, primary, Arabzade, Amir, primary, Zhao, Yanhua, primary, Varadharajan, Srinidhi, primary, Zheng, Tuyu, primary, Murugesan, Mohankumar, primary, Pfister, Stefan M., primary, Kawauchi, Daisuke, primary, Pajtler, Kristian W., primary, Deneen, Benjamin, primary, Mack, Stephen C., primary, Masih, Katherine E., primary, Gryder, Berkley E., primary, Khan, Javed, primary, and Gilbertson, Richard J., primary

Published
2023
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28. Supplementary Data from Cross-Species Genomics Reveals Oncogenic Dependencies in ZFTA/C11orf95 Fusion–Positive Supratentorial Ependymomas

Author

Zheng, Tuyu, primary, Ghasemi, David R., primary, Okonechnikov, Konstantin, primary, Korshunov, Andrey, primary, Sill, Martin, primary, Maass, Kendra K., primary, Benites Goncalves da Silva, Patricia, primary, Ryzhova, Marina, primary, Gojo, Johannes, primary, Stichel, Damian, primary, Arabzade, Amir, primary, Kupp, Robert, primary, Benzel, Julia, primary, Taya, Shinichiro, primary, Adachi, Toma, primary, Shiraishi, Ryo, primary, Gerber, Nicolas U., primary, Sturm, Dominik, primary, Ecker, Jonas, primary, Sievers, Philipp, primary, Selt, Florian, primary, Chapman, Rebecca, primary, Haberler, Christine, primary, Figarella-Branger, Dominique, primary, Reifenberger, Guido, primary, Fleischhack, Gudrun, primary, Rutkowski, Stefan, primary, Donson, Andrew M., primary, Ramaswamy, Vijay, primary, Capper, David, primary, Ellison, David W., primary, Herold-Mende, Christel C., primary, Schüller, Ulrich, primary, Brandner, Sebastian, primary, Driever, Pablo Hernáiz, primary, Kros, Johan M., primary, Snuderl, Matija, primary, Milde, Till, primary, Grundy, Richard G., primary, Hoshino, Mikio, primary, Mack, Stephen C., primary, Gilbertson, Richard J., primary, Jones, David T.W., primary, Kool, Marcel, primary, von Deimling, Andreas, primary, Pfister, Stefan M., primary, Sahm, Felix, primary, Kawauchi, Daisuke, primary, and Pajtler, Kristian W., primary

Published
2023
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29. Supplementary Fig 5 from Myc and Loss of p53 Cooperate to Drive Formation of Choroid Plexus Carcinoma

Author

Wang, Jun, primary, Merino, Diana M., primary, Light, Nicholas, primary, Murphy, Brian L., primary, Wang, Yong-Dong, primary, Guo, Xiaohui, primary, Hodges, Andrew P., primary, Chau, Lianne Q., primary, Liu, Kun-Wei, primary, Dhall, Girish, primary, Asgharzadeh, Shahab, primary, Kiehna, Erin N., primary, Shirey, Ryan J., primary, Janda, Kim D., primary, Taylor, Michael D., primary, Malkin, David, primary, Ellison, David W., primary, VandenBerg, Scott R., primary, Eberhart, Charles G., primary, Sears, Rosalie C., primary, Roussel, Martine F., primary, Gilbertson, Richard J., primary, and Wechsler-Reya, Robert J., primary

Published
2023
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30. Supplementary Figure Legends from Myc and Loss of p53 Cooperate to Drive Formation of Choroid Plexus Carcinoma

Author

Wang, Jun, primary, Merino, Diana M., primary, Light, Nicholas, primary, Murphy, Brian L., primary, Wang, Yong-Dong, primary, Guo, Xiaohui, primary, Hodges, Andrew P., primary, Chau, Lianne Q., primary, Liu, Kun-Wei, primary, Dhall, Girish, primary, Asgharzadeh, Shahab, primary, Kiehna, Erin N., primary, Shirey, Ryan J., primary, Janda, Kim D., primary, Taylor, Michael D., primary, Malkin, David, primary, Ellison, David W., primary, VandenBerg, Scott R., primary, Eberhart, Charles G., primary, Sears, Rosalie C., primary, Roussel, Martine F., primary, Gilbertson, Richard J., primary, and Wechsler-Reya, Robert J., primary

Published
2023
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31. Supplementary Figure Legends 1-3 from Copy Number Gain of 1q25 Predicts Poor Progression-Free Survival for Pediatric Intracranial Ependymomas and Enables Patient Risk Stratification: A Prospective European Clinical Trial Cohort Analysis on Behalf of the Children's Cancer Leukaemia Group (CCLG), Société Française d'Oncologie Pédiatrique (SFOP), and International Society for Pediatric Oncology (SIOP)

Author

Kilday, John-Paul, primary, Mitra, Biswaroop, primary, Domerg, Caroline, primary, Ward, Jennifer, primary, Andreiuolo, Felipe, primary, Osteso-Ibanez, Teresa, primary, Mauguen, Audrey, primary, Varlet, Pascale, primary, Le Deley, Marie-Cecile, primary, Lowe, James, primary, Ellison, David W., primary, Gilbertson, Richard J., primary, Coyle, Beth, primary, Grill, Jacques, primary, and Grundy, Richard G., primary

Published
2023
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32. Figure S4 from Molecular Characterization of Choroid Plexus Tumors Reveals Novel Clinically Relevant Subgroups

Author

Merino, Diana M., primary, Shlien, Adam, primary, Villani, Anita, primary, Pienkowska, Malgorzata, primary, Mack, Stephen, primary, Ramaswamy, Vijay, primary, Shih, David, primary, Tatevossian, Ruth, primary, Novokmet, Ana, primary, Choufani, Sanaa, primary, Dvir, Rina, primary, Ben-Arush, Myran, primary, Harris, Brent T., primary, Hwang, Eugene I., primary, Lulla, Rishi, primary, Pfister, Stefan M., primary, Achatz, Maria Isabel, primary, Jabado, Nada, primary, Finlay, Jonathan L., primary, Weksberg, Rosanna, primary, Bouffet, Eric, primary, Hawkins, Cynthia, primary, Taylor, Michael D., primary, Tabori, Uri, primary, Ellison, David W., primary, Gilbertson, Richard J., primary, and Malkin, David, primary

Published
2023
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33. Appendix from Molecular Characterization of Choroid Plexus Tumors Reveals Novel Clinically Relevant Subgroups

Author

Merino, Diana M., primary, Shlien, Adam, primary, Villani, Anita, primary, Pienkowska, Malgorzata, primary, Mack, Stephen, primary, Ramaswamy, Vijay, primary, Shih, David, primary, Tatevossian, Ruth, primary, Novokmet, Ana, primary, Choufani, Sanaa, primary, Dvir, Rina, primary, Ben-Arush, Myran, primary, Harris, Brent T., primary, Hwang, Eugene I., primary, Lulla, Rishi, primary, Pfister, Stefan M., primary, Achatz, Maria Isabel, primary, Jabado, Nada, primary, Finlay, Jonathan L., primary, Weksberg, Rosanna, primary, Bouffet, Eric, primary, Hawkins, Cynthia, primary, Taylor, Michael D., primary, Tabori, Uri, primary, Ellison, David W., primary, Gilbertson, Richard J., primary, and Malkin, David, primary

Published
2023
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34. Supplementary Fig 1 from Myc and Loss of p53 Cooperate to Drive Formation of Choroid Plexus Carcinoma

Author

Wang, Jun, primary, Merino, Diana M., primary, Light, Nicholas, primary, Murphy, Brian L., primary, Wang, Yong-Dong, primary, Guo, Xiaohui, primary, Hodges, Andrew P., primary, Chau, Lianne Q., primary, Liu, Kun-Wei, primary, Dhall, Girish, primary, Asgharzadeh, Shahab, primary, Kiehna, Erin N., primary, Shirey, Ryan J., primary, Janda, Kim D., primary, Taylor, Michael D., primary, Malkin, David, primary, Ellison, David W., primary, VandenBerg, Scott R., primary, Eberhart, Charles G., primary, Sears, Rosalie C., primary, Roussel, Martine F., primary, Gilbertson, Richard J., primary, and Wechsler-Reya, Robert J., primary

Published
2023
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35. Supplementary Tables 1 - 3 from Phase I Study of Vismodegib in Children with Recurrent or Refractory Medulloblastoma: A Pediatric Brain Tumor Consortium Study

Author

Gajjar, Amar, primary, Stewart, Clinton F., primary, Ellison, David W., primary, Kaste, Sue, primary, Kun, Larry E., primary, Packer, Roger J., primary, Goldman, Stewart, primary, Chintagumpala, Murali, primary, Wallace, Dana, primary, Takebe, Naoko, primary, Boyett, James M., primary, Gilbertson, Richard J., primary, and Curran, Tom, primary

Published
2023
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36. Supplementary Figure 3 from Copy Number Gain of 1q25 Predicts Poor Progression-Free Survival for Pediatric Intracranial Ependymomas and Enables Patient Risk Stratification: A Prospective European Clinical Trial Cohort Analysis on Behalf of the Children's Cancer Leukaemia Group (CCLG), Société Française d'Oncologie Pédiatrique (SFOP), and International Society for Pediatric Oncology (SIOP)

Author

Kilday, John-Paul, primary, Mitra, Biswaroop, primary, Domerg, Caroline, primary, Ward, Jennifer, primary, Andreiuolo, Felipe, primary, Osteso-Ibanez, Teresa, primary, Mauguen, Audrey, primary, Varlet, Pascale, primary, Le Deley, Marie-Cecile, primary, Lowe, James, primary, Ellison, David W., primary, Gilbertson, Richard J., primary, Coyle, Beth, primary, Grill, Jacques, primary, and Grundy, Richard G., primary

Published
2023
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37. supplemental figure and table legend from Molecular Characterization of Choroid Plexus Tumors Reveals Novel Clinically Relevant Subgroups

Author

Merino, Diana M., primary, Shlien, Adam, primary, Villani, Anita, primary, Pienkowska, Malgorzata, primary, Mack, Stephen, primary, Ramaswamy, Vijay, primary, Shih, David, primary, Tatevossian, Ruth, primary, Novokmet, Ana, primary, Choufani, Sanaa, primary, Dvir, Rina, primary, Ben-Arush, Myran, primary, Harris, Brent T., primary, Hwang, Eugene I., primary, Lulla, Rishi, primary, Pfister, Stefan M., primary, Achatz, Maria Isabel, primary, Jabado, Nada, primary, Finlay, Jonathan L., primary, Weksberg, Rosanna, primary, Bouffet, Eric, primary, Hawkins, Cynthia, primary, Taylor, Michael D., primary, Tabori, Uri, primary, Ellison, David W., primary, Gilbertson, Richard J., primary, and Malkin, David, primary

Published
2023
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38. Supplementary Fig 2 from Myc and Loss of p53 Cooperate to Drive Formation of Choroid Plexus Carcinoma

Author

Wang, Jun, primary, Merino, Diana M., primary, Light, Nicholas, primary, Murphy, Brian L., primary, Wang, Yong-Dong, primary, Guo, Xiaohui, primary, Hodges, Andrew P., primary, Chau, Lianne Q., primary, Liu, Kun-Wei, primary, Dhall, Girish, primary, Asgharzadeh, Shahab, primary, Kiehna, Erin N., primary, Shirey, Ryan J., primary, Janda, Kim D., primary, Taylor, Michael D., primary, Malkin, David, primary, Ellison, David W., primary, VandenBerg, Scott R., primary, Eberhart, Charles G., primary, Sears, Rosalie C., primary, Roussel, Martine F., primary, Gilbertson, Richard J., primary, and Wechsler-Reya, Robert J., primary

Published
2023
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39. Supplementary Fig 7 from Myc and Loss of p53 Cooperate to Drive Formation of Choroid Plexus Carcinoma

Author

Wang, Jun, primary, Merino, Diana M., primary, Light, Nicholas, primary, Murphy, Brian L., primary, Wang, Yong-Dong, primary, Guo, Xiaohui, primary, Hodges, Andrew P., primary, Chau, Lianne Q., primary, Liu, Kun-Wei, primary, Dhall, Girish, primary, Asgharzadeh, Shahab, primary, Kiehna, Erin N., primary, Shirey, Ryan J., primary, Janda, Kim D., primary, Taylor, Michael D., primary, Malkin, David, primary, Ellison, David W., primary, VandenBerg, Scott R., primary, Eberhart, Charles G., primary, Sears, Rosalie C., primary, Roussel, Martine F., primary, Gilbertson, Richard J., primary, and Wechsler-Reya, Robert J., primary

Published
2023
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40. Supplementary Fig 3 from Myc and Loss of p53 Cooperate to Drive Formation of Choroid Plexus Carcinoma

Author

Wang, Jun, primary, Merino, Diana M., primary, Light, Nicholas, primary, Murphy, Brian L., primary, Wang, Yong-Dong, primary, Guo, Xiaohui, primary, Hodges, Andrew P., primary, Chau, Lianne Q., primary, Liu, Kun-Wei, primary, Dhall, Girish, primary, Asgharzadeh, Shahab, primary, Kiehna, Erin N., primary, Shirey, Ryan J., primary, Janda, Kim D., primary, Taylor, Michael D., primary, Malkin, David, primary, Ellison, David W., primary, VandenBerg, Scott R., primary, Eberhart, Charles G., primary, Sears, Rosalie C., primary, Roussel, Martine F., primary, Gilbertson, Richard J., primary, and Wechsler-Reya, Robert J., primary

Published
2023
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41. Supplementary Data from Rapid Diagnosis of Medulloblastoma Molecular Subgroups

Author

Schwalbe, Ed C., primary, Lindsey, Janet C., primary, Straughton, Debbie, primary, Hogg, Twala L., primary, Cole, Michael, primary, Megahed, Hisham, primary, Ryan, Sarra L., primary, Lusher, Meryl E., primary, Taylor, Michael D., primary, Gilbertson, Richard J., primary, Ellison, David W., primary, Bailey, Simon, primary, and Clifford, Steven C., primary

Published
2023
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42. Figure S1 from Establishing a Preclinical Multidisciplinary Board for Brain Tumors

Author

Nimmervoll, Birgit V., primary, Boulos, Nidal, primary, Bianski, Brandon, primary, Dapper, Jason, primary, DeCuypere, Michael, primary, Shelat, Anang, primary, Terranova, Sabrina, primary, Terhune, Hope E., primary, Gajjar, Amar, primary, Patel, Yogesh T., primary, Freeman, Burgess B., primary, Onar-Thomas, Arzu, primary, Stewart, Clinton F., primary, Roussel, Martine F., primary, Guy, R. Kipling, primary, Merchant, Thomas E., primary, Calabrese, Christopher, primary, Wright, Karen D., primary, and Gilbertson, Richard J., primary

Published
2023
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43. Table S1-S3 from Molecular Characterization of Choroid Plexus Tumors Reveals Novel Clinically Relevant Subgroups

Author

Merino, Diana M., primary, Shlien, Adam, primary, Villani, Anita, primary, Pienkowska, Malgorzata, primary, Mack, Stephen, primary, Ramaswamy, Vijay, primary, Shih, David, primary, Tatevossian, Ruth, primary, Novokmet, Ana, primary, Choufani, Sanaa, primary, Dvir, Rina, primary, Ben-Arush, Myran, primary, Harris, Brent T., primary, Hwang, Eugene I., primary, Lulla, Rishi, primary, Pfister, Stefan M., primary, Achatz, Maria Isabel, primary, Jabado, Nada, primary, Finlay, Jonathan L., primary, Weksberg, Rosanna, primary, Bouffet, Eric, primary, Hawkins, Cynthia, primary, Taylor, Michael D., primary, Tabori, Uri, primary, Ellison, David W., primary, Gilbertson, Richard J., primary, and Malkin, David, primary

Published
2023
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44. Supplementary Materials and Methods from Copy Number Gain of 1q25 Predicts Poor Progression-Free Survival for Pediatric Intracranial Ependymomas and Enables Patient Risk Stratification: A Prospective European Clinical Trial Cohort Analysis on Behalf of the Children's Cancer Leukaemia Group (CCLG), Société Française d'Oncologie Pédiatrique (SFOP), and International Society for Pediatric Oncology (SIOP)

Author

Kilday, John-Paul, primary, Mitra, Biswaroop, primary, Domerg, Caroline, primary, Ward, Jennifer, primary, Andreiuolo, Felipe, primary, Osteso-Ibanez, Teresa, primary, Mauguen, Audrey, primary, Varlet, Pascale, primary, Le Deley, Marie-Cecile, primary, Lowe, James, primary, Ellison, David W., primary, Gilbertson, Richard J., primary, Coyle, Beth, primary, Grill, Jacques, primary, and Grundy, Richard G., primary

Published
2023
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45. Supplementary Fig 6 from Myc and Loss of p53 Cooperate to Drive Formation of Choroid Plexus Carcinoma

Author

Wang, Jun, primary, Merino, Diana M., primary, Light, Nicholas, primary, Murphy, Brian L., primary, Wang, Yong-Dong, primary, Guo, Xiaohui, primary, Hodges, Andrew P., primary, Chau, Lianne Q., primary, Liu, Kun-Wei, primary, Dhall, Girish, primary, Asgharzadeh, Shahab, primary, Kiehna, Erin N., primary, Shirey, Ryan J., primary, Janda, Kim D., primary, Taylor, Michael D., primary, Malkin, David, primary, Ellison, David W., primary, VandenBerg, Scott R., primary, Eberhart, Charles G., primary, Sears, Rosalie C., primary, Roussel, Martine F., primary, Gilbertson, Richard J., primary, and Wechsler-Reya, Robert J., primary

Published
2023
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46. Data from Myc and Loss of p53 Cooperate to Drive Formation of Choroid Plexus Carcinoma

Author

Wang, Jun, primary, Merino, Diana M., primary, Light, Nicholas, primary, Murphy, Brian L., primary, Wang, Yong-Dong, primary, Guo, Xiaohui, primary, Hodges, Andrew P., primary, Chau, Lianne Q., primary, Liu, Kun-Wei, primary, Dhall, Girish, primary, Asgharzadeh, Shahab, primary, Kiehna, Erin N., primary, Shirey, Ryan J., primary, Janda, Kim D., primary, Taylor, Michael D., primary, Malkin, David, primary, Ellison, David W., primary, VandenBerg, Scott R., primary, Eberhart, Charles G., primary, Sears, Rosalie C., primary, Roussel, Martine F., primary, Gilbertson, Richard J., primary, and Wechsler-Reya, Robert J., primary

Published
2023
Full Text
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47. Supplementary Figures 1 - 2 from Phase I Study of Vismodegib in Children with Recurrent or Refractory Medulloblastoma: A Pediatric Brain Tumor Consortium Study

Author

Gajjar, Amar, primary, Stewart, Clinton F., primary, Ellison, David W., primary, Kaste, Sue, primary, Kun, Larry E., primary, Packer, Roger J., primary, Goldman, Stewart, primary, Chintagumpala, Murali, primary, Wallace, Dana, primary, Takebe, Naoko, primary, Boyett, James M., primary, Gilbertson, Richard J., primary, and Curran, Tom, primary

Published
2023
Full Text
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48. Supplementary Table 2 from Copy Number Gain of 1q25 Predicts Poor Progression-Free Survival for Pediatric Intracranial Ependymomas and Enables Patient Risk Stratification: A Prospective European Clinical Trial Cohort Analysis on Behalf of the Children's Cancer Leukaemia Group (CCLG), Société Française d'Oncologie Pédiatrique (SFOP), and International Society for Pediatric Oncology (SIOP)

Author

Kilday, John-Paul, primary, Mitra, Biswaroop, primary, Domerg, Caroline, primary, Ward, Jennifer, primary, Andreiuolo, Felipe, primary, Osteso-Ibanez, Teresa, primary, Mauguen, Audrey, primary, Varlet, Pascale, primary, Le Deley, Marie-Cecile, primary, Lowe, James, primary, Ellison, David W., primary, Gilbertson, Richard J., primary, Coyle, Beth, primary, Grill, Jacques, primary, and Grundy, Richard G., primary

Published
2023
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49. Supplementary Fig 4 from Myc and Loss of p53 Cooperate to Drive Formation of Choroid Plexus Carcinoma

Author

Wang, Jun, primary, Merino, Diana M., primary, Light, Nicholas, primary, Murphy, Brian L., primary, Wang, Yong-Dong, primary, Guo, Xiaohui, primary, Hodges, Andrew P., primary, Chau, Lianne Q., primary, Liu, Kun-Wei, primary, Dhall, Girish, primary, Asgharzadeh, Shahab, primary, Kiehna, Erin N., primary, Shirey, Ryan J., primary, Janda, Kim D., primary, Taylor, Michael D., primary, Malkin, David, primary, Ellison, David W., primary, VandenBerg, Scott R., primary, Eberhart, Charles G., primary, Sears, Rosalie C., primary, Roussel, Martine F., primary, Gilbertson, Richard J., primary, and Wechsler-Reya, Robert J., primary

Published
2023
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50. Supplementary Figure 1 from Copy Number Gain of 1q25 Predicts Poor Progression-Free Survival for Pediatric Intracranial Ependymomas and Enables Patient Risk Stratification: A Prospective European Clinical Trial Cohort Analysis on Behalf of the Children's Cancer Leukaemia Group (CCLG), Société Française d'Oncologie Pédiatrique (SFOP), and International Society for Pediatric Oncology (SIOP)

Author

Kilday, John-Paul, primary, Mitra, Biswaroop, primary, Domerg, Caroline, primary, Ward, Jennifer, primary, Andreiuolo, Felipe, primary, Osteso-Ibanez, Teresa, primary, Mauguen, Audrey, primary, Varlet, Pascale, primary, Le Deley, Marie-Cecile, primary, Lowe, James, primary, Ellison, David W., primary, Gilbertson, Richard J., primary, Coyle, Beth, primary, Grill, Jacques, primary, and Grundy, Richard G., primary

Published
2023
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