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51. Author Correction: Failure of human rhombic lip differentiation underlies medulloblastoma formation

Author

Hendrikse, Liam D., Haldipur, Parthiv, Saulnier, Olivier, Millman, Jake, Sjoboen, Alexandria H., Erickson, Anders W., Ong, Winnie, Gordon, Victor, Coudière-Morrison, Ludivine, Mercier, Audrey L., Shokouhian, Mohammad, Suárez, Raúl A., Ly, Michelle, Borlase, Stephanie, Scott, David S., Vladoiu, Maria C., Farooq, Hamza, Sirbu, Olga, Nakashima, Takuma, Nambu, Shohei, Funakoshi, Yusuke, Bahcheli, Alec, Diaz-Mejia, J. Javier, Golser, Joseph, Bach, Kathleen, Phuong-Bao, Tram, Skowron, Patryk, Wang, Evan Y., Kumar, Sachin A., Balin, Polina, Visvanathan, Abhirami, Lee, John J. Y., Ayoub, Ramy, Chen, Xin, Chen, Xiaodi, Mungall, Karen L., Luu, Betty, Bérubé, Pierre, Wang, Yu C., Pfister, Stefan M., Kim, Seung-Ki, Delattre, Olivier, Bourdeaut, Franck, Doz, François, Masliah-Planchon, Julien, Grajkowska, Wieslawa A., Loukides, James, Dirks, Peter, Fèvre-Montange, Michelle, Jouvet, Anne, French, Pim J., Kros, Johan M., Zitterbart, Karel, Bailey, Swneke D., Eberhart, Charles G., Rao, Amulya A. N., Giannini, Caterina, Olson, James M., Garami, Miklós, Hauser, Peter, Phillips, Joanna J., Ra, Young S., de Torres, Carmen, Mora, Jaume, Li, Kay K. W., Ng, Ho-Keung, Poon, Wai S., Pollack, Ian F., López-Aguilar, Enrique, Gillespie, G. Yancey, Van Meter, Timothy E., Shofuda, Tomoko, Vibhakar, Rajeev, Thompson, Reid C., Cooper, Michael K., Rubin, Joshua B., Kumabe, Toshihiro, Jung, Shin, Lach, Boleslaw, Iolascon, Achille, Ferrucci, Veronica, de Antonellis, Pasqualino, Zollo, Massimo, Cinalli, Giuseppe, Robinson, Shenandoah, Stearns, Duncan S., Van Meir, Erwin G., Porrati, Paola, Finocchiaro, Gaetano, Massimino, Maura, Carlotti, Carlos G., Faria, Claudia C., Roussel, Martine F., Boop, Frederick, Chan, Jennifer A., Aldinger, Kimberly A., Razavi, Ferechte, Silvestri, Evelina, McLendon, Roger E., Thompson, Eric M., Ansari, Marc, Garre, Maria L., Chico, Fernando, Eguía, Pilar, Pérezpeña, Mario, Morrissy, A. Sorana, Cavalli, Florence M. G., Wu, Xiaochong, Daniels, Craig, Rich, Jeremy N., Jones, Steven J. M., Moore, Richard A., Marra, Marco A., Huang, Xi, Reimand, Jüri, Sorensen, Poul H., Wechsler-Reya, Robert J., Weiss, William A., Pugh, Trevor J., Garzia, Livia, Kleinman, Claudia L., Stein, Lincoln D., Jabado, Nada, Malkin, David, Ayrault, Olivier, Golden, Jeffrey A., Ellison, David W., Doble, Brad, Ramaswamy, Vijay, Werbowetski-Ogilvie, Tamra E., Suzuki, Hiromichi, Millen, Kathleen J., and Taylor, Michael D.

Published
2022
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52. Therapeutic Impact of Cytoreductive Surgery and Irradiation of Posterior Fossa Ependymoma in the Molecular Era: A Retrospective Multicohort Analysis.

Author

Ramaswamy, Vijay, Hielscher, Thomas, Mack, Stephen C, Lassaletta, Alvaro, Lin, Tong, Pajtler, Kristian W, Jones, David TW, Luu, Betty, Cavalli, Florence MG, Aldape, Kenneth, Remke, Marc, Mynarek, Martin, Rutkowski, Stefan, Gururangan, Sridharan, McLendon, Roger E, Lipp, Eric S, Dunham, Christopher, Hukin, Juliette, Eisenstat, David D, Fulton, Dorcas, van Landeghem, Frank KH, Santi, Mariarita, van Veelen, Marie-Lise C, Van Meir, Erwin G, Osuka, Satoru, Fan, Xing, Muraszko, Karin M, Tirapelli, Daniela PC, Oba-Shinjo, Sueli M, Marie, Suely KN, Carlotti, Carlos G, Lee, Ji Yeoun, Rao, Amulya A Nageswara, Giannini, Caterina, Faria, Claudia C, Nunes, Sofia, Mora, Jaume, Hamilton, Ronald L, Hauser, Peter, Jabado, Nada, Petrecca, Kevin, Jung, Shin, Massimi, Luca, Zollo, Massimo, Cinalli, Giuseppe, Bognár, László, Klekner, Almos, Hortobágyi, Tibor, Leary, Sarah, Ermoian, Ralph P, Olson, James M, Leonard, Jeffrey R, Gardner, Corrine, Grajkowska, Wieslawa A, Chambless, Lola B, Cain, Jason, Eberhart, Charles G, Ahsan, Sama, Massimino, Maura, Giangaspero, Felice, Buttarelli, Francesca R, Packer, Roger J, Emery, Lyndsey, Yong, William H, Soto, Horacio, Liau, Linda M, Everson, Richard, Grossbach, Andrew, Shalaby, Tarek, Grotzer, Michael, Karajannis, Matthias A, Zagzag, David, Wheeler, Helen, von Hoff, Katja, Alonso, Marta M, Tuñon, Teresa, Schüller, Ulrich, Zitterbart, Karel, Sterba, Jaroslav, Chan, Jennifer A, Guzman, Miguel, Elbabaa, Samer K, Colman, Howard, Dhall, Girish, Fisher, Paul G, Fouladi, Maryam, Gajjar, Amar, Goldman, Stewart, Hwang, Eugene, Kool, Marcel, Ladha, Harshad, Vera-Bolanos, Elizabeth, Wani, Khalida, Lieberman, Frank, Mikkelsen, Tom, Omuro, Antonio M, Pollack, Ian F, Prados, Michael, Robins, H Ian, and Soffietti, Riccardo

Subjects
Humans, Ependymoma, Infratentorial Neoplasms, Combined Modality Therapy, Retrospective Studies, Cohort Studies, Adolescent, Adult, Child, Child, Preschool, Infant, Female, Male, Cytoreduction Surgical Procedures, Rare Diseases, Pediatric Cancer, Cancer, Pediatric, Patient Safety, Clinical Sciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

PurposePosterior fossa ependymoma comprises two distinct molecular variants termed EPN_PFA and EPN_PFB that have a distinct biology and natural history. The therapeutic value of cytoreductive surgery and radiation therapy for posterior fossa ependymoma after accounting for molecular subgroup is not known.MethodsFour independent nonoverlapping retrospective cohorts of posterior fossa ependymomas (n = 820) were profiled using genome-wide methylation arrays. Risk stratification models were designed based on known clinical and newly described molecular biomarkers identified by multivariable Cox proportional hazards analyses.ResultsMolecular subgroup is a powerful independent predictor of outcome even when accounting for age or treatment regimen. Incompletely resected EPN_PFA ependymomas have a dismal prognosis, with a 5-year progression-free survival ranging from 26.1% to 56.8% across all four cohorts. Although first-line (adjuvant) radiation is clearly beneficial for completely resected EPN_PFA, a substantial proportion of patients with EPN_PFB can be cured with surgery alone, and patients with relapsed EPN_PFB can often be treated successfully with delayed external-beam irradiation.ConclusionThe most impactful biomarker for posterior fossa ependymoma is molecular subgroup affiliation, independent of other demographic or treatment variables. However, both EPN_PFA and EPN_PFB still benefit from increased extent of resection, with the survival rates being particularly poor for subtotally resected EPN_PFA, even with adjuvant radiation therapy. Patients with EPN_PFB who undergo gross total resection are at lower risk for relapse and should be considered for inclusion in a randomized clinical trial of observation alone with radiation reserved for those who experience recurrence.

Published
2016

53. Prognostic value of medulloblastoma extent of resection after accounting for molecular subgroup: a retrospective integrated clinical and molecular analysis

Author

Thompson, Eric M, Hielscher, Thomas, Bouffet, Eric, Remke, Marc, Luu, Betty, Gururangan, Sridharan, McLendon, Roger E, Bigner, Darell D, Lipp, Eric S, Perreault, Sebastien, Cho, Yoon-Jae, Grant, Gerald, Kim, Seung-Ki, Lee, Ji Yeoun, Rao, Amulya A Nageswara, Giannini, Caterina, Li, Kay Ka Wai, Ng, Ho-Keung, Yao, Yu, Kumabe, Toshihiro, Tominaga, Teiji, Grajkowska, Wieslawa A, Perek-Polnik, Marta, Low, David CY, Seow, Wan Tew, Chang, Kenneth TE, Mora, Jaume, Pollack, Ian F, Hamilton, Ronald L, Leary, Sarah, Moore, Andrew S, Ingram, Wendy J, Hallahan, Andrew R, Jouvet, Anne, Fèvre-Montange, Michelle, Vasiljevic, Alexandre, Faure-Conter, Cecile, Shofuda, Tomoko, Kagawa, Naoki, Hashimoto, Naoya, Jabado, Nada, Weil, Alexander G, Gayden, Tenzin, Wataya, Takafumi, Shalaby, Tarek, Grotzer, Michael, Zitterbart, Karel, Sterba, Jaroslav, Kren, Leos, Hortobágyi, Tibor, Klekner, Almos, László, Bognár, Pócza, Tímea, Hauser, Peter, Schüller, Ulrich, Jung, Shin, Jang, Woo-Youl, French, Pim J, Kros, Johan M, van Veelen, Marie-Lise C, Massimi, Luca, Leonard, Jeffrey R, Rubin, Joshua B, Vibhakar, Rajeev, Chambless, Lola B, Cooper, Michael K, Thompson, Reid C, Faria, Claudia C, Carvalho, Alice, Nunes, Sofia, Pimentel, José, Fan, Xing, Muraszko, Karin M, López-Aguilar, Enrique, Lyden, David, Garzia, Livia, Shih, David JH, Kijima, Noriyuki, Schneider, Christian, Adamski, Jennifer, Northcott, Paul A, Kool, Marcel, Jones, David TW, Chan, Jennifer A, Nikolic, Ana, Garre, Maria Luisa, Van Meir, Erwin G, Osuka, Satoru, Olson, Jeffrey J, Jahangiri, Arman, Castro, Brandyn A, Gupta, Nalin, Weiss, William A, Moxon-Emre, Iska, Mabbott, Donald J, Lassaletta, Alvaro, Hawkins, Cynthia E, Tabori, Uri, Drake, James, and Kulkarni, Abhaya

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Oncology and Carcinogenesis, Brain Disorders, Rare Diseases, Brain Cancer, Pediatric Research Initiative, Pediatric, Cancer, Adult, Brain Neoplasms, Canada, Child, Child, Preschool, Combined Modality Therapy, Disease Progression, Disease-Free Survival, Female, Humans, Infant, Magnetic Resonance Imaging, Male, Medulloblastoma, Prognosis, Retrospective Studies, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

BackgroundPatients with incomplete surgical resection of medulloblastoma are controversially regarded as having a marker of high-risk disease, which leads to patients undergoing aggressive surgical resections, so-called second-look surgeries, and intensified chemoradiotherapy. All previous studies assessing the clinical importance of extent of resection have not accounted for molecular subgroup. We analysed the prognostic value of extent of resection in a subgroup-specific manner.MethodsWe retrospectively identified patients who had a histological diagnosis of medulloblastoma and complete data about extent of resection and survival from centres participating in the Medulloblastoma Advanced Genomics International Consortium. We collected from resections done between April, 1997, and February, 2013, at 35 international institutions. We established medulloblastoma subgroup affiliation by gene expression profiling on frozen or formalin-fixed paraffin-embedded tissues. We classified extent of resection on the basis of postoperative imaging as gross total resection (no residual tumour), near-total resection (30 Gy vs no craniospinal irradiation). The primary analysis outcome was the effect of extent of resection by molecular subgroup and the effects of other clinical variables on overall and progression-free survival.FindingsWe included 787 patients with medulloblastoma (86 with WNT tumours, 242 with SHH tumours, 163 with group 3 tumours, and 296 with group 4 tumours) in our multivariable Cox models of progression-free and overall survival. We found that the prognostic benefit of increased extent of resection for patients with medulloblastoma is attenuated after molecular subgroup affiliation is taken into account. We identified a progression-free survival benefit for gross total resection over sub-total resection (hazard ratio [HR] 1·45, 95% CI 1·07-1·96, p=0·16) but no overall survival benefit (HR 1·23, 0·87-1·72, p=0·24). We saw no progression-free survival or overall survival benefit for gross total resection compared with near-total resection (HR 1·05, 0·71-1·53, p=0·8158 for progression-free survival and HR 1·14, 0·75-1·72, p=0·55 for overall survival). No significant survival benefit existed for greater extent of resection for patients with WNT, SHH, or group 3 tumours (HR 1·03, 0·67-1·58, p=0·89 for sub-total resection vs gross total resection). For patients with group 4 tumours, gross total resection conferred a benefit to progression-free survival compared with sub-total resection (HR 1·97, 1·22-3·17, p=0·0056), especially for those with metastatic disease (HR 2·22, 1·00-4·93, p=0·050). However, gross total resection had no effect on overall survival compared with sub-total resection in patients with group 4 tumours (HR 1·67, 0·93-2·99, p=0·084).InterpretationThe prognostic benefit of increased extent of resection for patients with medulloblastoma is attenuated after molecular subgroup affiliation is taken into account. Although maximum safe surgical resection should remain the standard of care, surgical removal of small residual portions of medulloblastoma is not recommended when the likelihood of neurological morbidity is high because there is no definitive benefit to gross total resection compared with near-total resection.FundingCanadian Cancer Society Research Institute, Terry Fox Research Institute, Canadian Institutes of Health Research, National Institutes of Health, Pediatric Brain Tumor Foundation, and the Garron Family Chair in Childhood Cancer Research.

Published
2016

55. Pontine gliomas a 10-year population-based study: a report from The Canadian Paediatric Brain Tumour Consortium (CPBTC)

Author

Fonseca, Adriana, Afzal, Samina, Bowes, Lynette, Crooks, Bruce, Larouche, Valerie, Jabado, Nada, Perreault, Sebastien, Johnston, Donna L., Zelcer, Shayna, Fleming, Adam, Scheinemann, Katrin, Silva, Mariana, Vanan, Magimairajan Issai, Mpofu, Chris, Wilson, Beverly, Eisenstat, David D., Lafay-Cousin, Lucie, Hukin, Juliette, Hawkins, Cynthia, Bartels, Ute, and Bouffet, Eric

Published
2020
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56. Pineoblastoma segregates into molecular sub-groups with distinct clinico-pathologic features: a Rare Brain Tumor Consortium registry study

Author

Li, Bryan K., Vasiljevic, Alexandre, Dufour, Christelle, Yao, Fupan, Ho, Ben L. B., Lu, Mei, Hwang, Eugene I., Gururangan, Sridharan, Hansford, Jordan R., Fouladi, Maryam, Nobusawa, Sumihito, Laquerriere, Annie, Delisle, Marie-Bernadette, Fangusaro, Jason, Forest, Fabien, Toledano, Helen, Solano-Paez, Palma, Leary, Sarah, Birks, Diane, Hoffman, Lindsey M., Szathmari, Alexandru, Faure-Conter, Cécile, Fan, Xing, Catchpoole, Daniel, Zhou, Li, Schultz, Kris Ann P., Ichimura, Koichi, Gauchotte, Guillaume, Jabado, Nada, Jones, Chris, Loussouarn, Delphine, Mokhtari, Karima, Rousseau, Audrey, Ziegler, David S., Tanaka, Shinya, Pomeroy, Scott L., Gajjar, Amar, Ramaswamy, Vijay, Hawkins, Cynthia, Grundy, Richard G., Hill, D. Ashley, Bouffet, Eric, Huang, Annie, and Jouvet, Anne

Published
2020
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57. YAP1-fusions in pediatric NF2-wildtype meningioma

Author

Sievers, Philipp, Chiang, Jason, Schrimpf, Daniel, Stichel, Damian, Paramasivam, Nagarajan, Sill, Martin, Gayden, Tenzin, Casalini, Belen, Reuss, David E., Dalton, James, Pajtler, Kristian W., Hänggi, Daniel, Herold-Mende, Christel, Rushing, Elisabeth, Korshunov, Andrey, Mawrin, Christian, Weller, Michael, Schlesner, Matthias, Wick, Wolfgang, Jabado, Nada, Jones, David T. W., Pfister, Stefan M., von Deimling, Andreas, Ellison, David W., and Sahm, Felix

Published
2020
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58. Spinal Myxopapillary Ependymomas Demonstrate a Warburg Phenotype

Author

Mack, Stephen C, Agnihotri, Sameer, Bertrand, Kelsey C, Wang, Xin, Shih, David J, Witt, Hendrik, Hill, Nadia, Zayne, Kory, Barszczyk, Mark, Ramaswamy, Vijay, Remke, Marc, Thompson, Yuan, Ryzhova, Marina, Massimi, Luca, Grajkowska, Wieslawa, Lach, Boleslaw, Gupta, Nalin, Weiss, William A, Guha, Abhijit, Hawkins, Cynthia, Croul, Sidney, Rutka, James T, Pfister, Stefan M, Korshunov, Andrey, Pekmezci, Melike, Tihan, Tarik, Philips, Joanna J, Jabado, Nada, Zadeh, Gelareh, and Taylor, Michael D

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Biotechnology, Genetics, Cancer, Brain Disorders, Adult, Aged, DNA Copy Number Variations, Ependymoma, Female, Gene Expression Regulation, Neoplastic, Hexokinase, Humans, Hypoxia-Inducible Factor 1, alpha Subunit, Male, Middle Aged, Neoplasm Metastasis, Protein Serine-Threonine Kinases, Pyruvate Dehydrogenase Acetyl-Transferring Kinase, Spinal Cord, Spinal Neoplasms, Transcriptome, Oncology and Carcinogenesis, Oncology & Carcinogenesis, Clinical sciences, Oncology and carcinogenesis
Abstract

PurposeMyxopapillary ependymoma (MPE) is a distinct histologic variant of ependymoma arising commonly in the spinal cord. Despite an overall favorable prognosis, distant metastases, subarachnoid dissemination, and late recurrences have been reported. Currently, the only effective treatment for MPE is gross-total resection. We characterized the genomic and transcriptional landscape of spinal ependymomas in an effort to delineate the genetic basis of this disease and identify new leads for therapy.Experimental designGene expression profiling was performed on 35 spinal ependymomas, and copy number profiling was done on an overlapping cohort of 46 spinal ependymomas. Functional validation experiments were performed on tumor lysates consisting of assays measuring pyruvate kinase M activity (PKM), hexokinase activity (HK), and lactate production.ResultsAt a gene expression level, we demonstrate that spinal grade II and MPE are molecularly and biologically distinct. These are supported by specific copy number alterations occurring in each histologic variant. Pathway analysis revealed that MPE are characterized by increased cellular metabolism, associated with upregulation of HIF1α. These findings were validated by Western blot analysis demonstrating increased protein expression of HIF1α, HK2, PDK1, and phosphorylation of PDHE1A. Functional assays were performed on MPE lysates, which demonstrated decreased PKM activity, increased HK activity, and elevated lactate production.ConclusionsOur findings suggest that MPE may be driven by a Warburg metabolic phenotype. The key enzymes promoting the Warburg phenotype: HK2, PKM2, and PDK are targetable by small-molecule inhibitors/activators, and should be considered for evaluation in future clinical trials for MPE.

Published
2015

59. Stalled developmental programs at the root of pediatric brain tumors

Author

Jessa, Selin, Blanchet-Cohen, Alexis, Krug, Brian, Vladoiu, Maria, Coutelier, Marie, Faury, Damien, Poreau, Brice, De Jay, Nicolas, Hébert, Steven, Monlong, Jean, Farmer, W. Todd, Donovan, Laura K., Hu, Yixing, McConechy, Melissa K., Cavalli, Florence M. G., Mikael, Leonie G., Ellezam, Benjamin, Richer, Maxime, Allaire, Andréa, Weil, Alexander G., Atkinson, Jeffrey, Farmer, Jean-Pierre, Dudley, Roy W. R., Larouche, Valerie, Crevier, Louis, Albrecht, Steffen, Filbin, Mariella G., Sartelet, Hervé, Lutz, Pierre-Eric, Nagy, Corina, Turecki, Gustavo, Costantino, Santiago, Dirks, Peter B., Murai, Keith K., Bourque, Guillaume, Ragoussis, Jiannis, Garzia, Livia, Taylor, Michael D., Jabado, Nada, and Kleinman, Claudia L.

Published
2019
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60. The molecular landscape of ETMR at diagnosis and relapse

Author

Lambo, Sander, Gröbner, Susanne N., Rausch, Tobias, Waszak, Sebastian M., Schmidt, Christin, Gorthi, Aparna, Romero, July Carolina, Mauermann, Monika, Brabetz, Sebastian, Krausert, Sonja, Buchhalter, Ivo, Koster, Jan, Zwijnenburg, Danny A., Sill, Martin, Hübner, Jens-Martin, Mack, Norman, Schwalm, Benjamin, Ryzhova, Marina, Hovestadt, Volker, Papillon-Cavanagh, Simon, Chan, Jennifer A., Landgraf, Pablo, Ho, Ben, Milde, Till, Witt, Olaf, Ecker, Jonas, Sahm, Felix, Sumerauer, David, Ellison, David W., Orr, Brent A., Darabi, Anna, Haberler, Christine, Figarella-Branger, Dominique, Wesseling, Pieter, Schittenhelm, Jens, Remke, Marc, Taylor, Michael D., Gil-da-Costa, Maria J., Łastowska, Maria, Grajkowska, Wiesława, Hasselblatt, Martin, Hauser, Peter, Pietsch, Torsten, Uro-Coste, Emmanuelle, Bourdeaut, Franck, Masliah-Planchon, Julien, Rigau, Valérie, Alexandrescu, Sanda, Wolf, Stephan, Li, Xiao-Nan, Schüller, Ulrich, Snuderl, Matija, Karajannis, Matthias A., Giangaspero, Felice, Jabado, Nada, von Deimling, Andreas, Jones, David T. W., Korbel, Jan O., von Hoff, Katja, Lichter, Peter, Huang, Annie, Bishop, Alexander J. R., Pfister, Stefan M., Korshunov, Andrey, and Kool, Marcel

Published
2019
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61. Brainstem Tumors

Author

Freeman, Carolyn R., Farmer, Jean-Pierre, Jabado, Nada, Mahajan, Anita, editor, and Paulino, Arnold, editor

Published
2018
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62. Author Correction: Loss of MAT2A compromises methionine metabolism and represents a vulnerability in H3K27M mutant glioma by modulating the epigenome

Author

Golbourn, Brian J., Halbert, Matthew E., Halligan, Katharine, Varadharajan, Srinidhi, Krug, Brian, Mbah, Nneka E., Kabir, Nisha, Stanton, Ann-Catherine J., Locke, Abigail L., Casillo, Stephanie M., Zhao, Yanhua, Sanders, Lauren M., Cheney, Allison, Mullett, Steven J., Chen, Apeng, Wassell, Michelle, Andren, Anthony, Perez, Jennifer, Jane, Esther P., Premkumar, Daniel R. David, Koncar, Robert F., Mirhadi, Shideh, McCarl, Lauren H., Chang, Yue-Fang, Wu, Yijen L., Gatesman, Taylor A., Cruz, Andrea F., Zapotocky, Michal, Hu, Baoli, Kohanbash, Gary, Wang, Xiuxing, Vartanian, Alenoush, Moran, Michael F., Lieberman, Frank, Amankulor, Nduka M., Wendell, Stacy G., Vaske, Olena M., Panigrahy, Ashok, Felker, James, Bertrand, Kelsey C., Kleinman, Claudia L., Rich, Jeremy N., Friedlander, Robert M., Broniscer, Alberto, Lyssiotis, Costas, Jabado, Nada, Pollack, Ian F., Mack, Stephen C., and Agnihotri, Sameer

Published
2022
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63. Recurrent somatic mutations in ACVR1 in pediatric midline high-grade astrocytoma.

Author

Fontebasso, Adam, Papillon-Cavanagh, Simon, Schwartzentruber, Jeremy, Nikbakht, Hamid, Gerges, Noha, Fiset, Pierre-Olivier, Bechet, Denise, Faury, Damien, De Jay, Nicolas, Ramkissoon, Lori, Corcoran, Aoife, Jones, David, Sturm, Dominik, Johann, Pascal, Tomita, Tadanori, Goldman, Stewart, Nagib, Mahmoud, Bendel, Anne, Goumnerova, Liliana, Bowers, Daniel, Leonard, Jeffrey, Rubin, Joshua, Alden, Tord, Browd, Samuel, Geyer, J, Leary, Sarah, Jallo, George, Cohen, Kenneth, Carret, Anne-Sophie, Ellezam, Benjamin, Crevier, Louis, Klekner, Almos, Bognar, Laszlo, Hauser, Peter, Garami, Miklos, Myseros, John, Dong, Zhifeng, Siegel, Peter, Malkin, Hayley, Ligon, Azra, Albrecht, Steffen, Pfister, Stefan, Ligon, Keith, Majewski, Jacek, Jabado, Nada, Kieran, Mark, Prados, Michael, and Gupta, Nalin

Subjects
Activin Receptors, Type I, Animals, Astrocytoma, Base Sequence, Bone Morphogenetic Proteins, Brain Neoplasms, Child, DNA Copy Number Variations, DNA Methylation, Gene Expression Regulation, Neoplastic, Genome, Human, Humans, Immunohistochemistry, In Situ Hybridization, Fluorescence, Molecular Sequence Data, Mutation, Sequence Analysis, DNA, Smad Proteins
Abstract

Pediatric midline high-grade astrocytomas (mHGAs) are incurable with few treatment targets identified. Most tumors harbor mutations encoding p.Lys27Met in histone H3 variants. In 40 treatment-naive mHGAs, 39 analyzed by whole-exome sequencing, we find additional somatic mutations specific to tumor location. Gain-of-function mutations in ACVR1 occur in tumors of the pons in conjunction with histone H3.1 p.Lys27Met substitution, whereas FGFR1 mutations or fusions occur in thalamic tumors associated with histone H3.3 p.Lys27Met substitution. Hyperactivation of the bone morphogenetic protein (BMP)-ACVR1 developmental pathway in mHGAs harboring ACVR1 mutations led to increased levels of phosphorylated SMAD1, SMAD5 and SMAD8 and upregulation of BMP downstream early-response genes in tumor cells. Global DNA methylation profiles were significantly associated with the p.Lys27Met alteration, regardless of the mutant histone H3 variant and irrespective of tumor location, supporting the role of this substitution in driving the epigenetic phenotype. This work considerably expands the number of potential treatment targets and further justifies pretreatment biopsy in pediatric mHGA as a means to orient therapeutic efforts in this disease.

Published
2014

64. Cytogenetic prognostication within medulloblastoma subgroups.

Author

Shih, David, Northcott, Paul, Remke, Marc, Korshunov, Andrey, Ramaswamy, Vijay, Kool, Marcel, Luu, Betty, Yao, Yuan, Wang, Xin, Dubuc, Adrian, Garzia, Livia, Peacock, John, Mack, Stephen, Wu, Xiaochong, Rolider, Adi, Morrissy, A, Cavalli, Florence, Jones, David, Zitterbart, Karel, Faria, Claudia, Schüller, Ulrich, Kren, Leos, Kumabe, Toshihiro, Tominaga, Teiji, Shin Ra, Young, Garami, Miklós, Hauser, Peter, Chan, Jennifer, Robinson, Shenandoah, Bognár, László, Klekner, Almos, Saad, Ali, Albrecht, Steffen, Fontebasso, Adam, Cinalli, Giuseppe, De Antonellis, Pasqualino, Zollo, Massimo, Cooper, Michael, Thompson, Reid, Bailey, Simon, Lindsey, Janet, Di Rocco, Concezio, Massimi, Luca, Michiels, Erna, Scherer, Stephen, Lee, Ji-Yeoun, Cho, Byung-Kyu, Kim, Seung-Ki, Wang, Kyu-Chang, Leonard, Jeffrey, Rubin, Joshua, de Torres, Carmen, Lavarino, Cinzia, Mora, Jaume, Cho, Yoon-Jae, Tabori, Uri, Olson, James, Gajjar, Amar, Packer, Roger, Fan, Xing, Muraszko, Karin, Vibhakar, Rajeev, Eberhart, Charles, Fouladi, Maryam, Lach, Boleslaw, Jung, Shin, Wechsler-Reya, Robert, Fèvre-Montange, Michelle, Jouvet, Anne, Jabado, Nada, Pollack, Ian, Rutkowski, Stefan, Pomeroy, Scott, French, Pim, Kloosterhof, Nanne, Kros, Johan, Van Meir, Erwin, Clifford, Steven, Bourdeaut, Franck, Delattre, Olivier, Doz, François, Hawkins, Cynthia, Malkin, David, Grajkowska, Wieslawa, Perek-Polnik, Marta, Bouffet, Eric, Rutka, James, Pfister, Stefan, Taylor, Michael, Gupta, Nalin, Phillips, Joanna, Weiss, William, and Liau, Linda

Subjects
Adolescent, Biomarkers, Tumor, Child, Child, Preschool, Chromosomes, Human, Pair 11, Chromosomes, Human, Pair 14, Cytogenetics, Female, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Hedgehog Proteins, Humans, In Situ Hybridization, Fluorescence, Infant, Kruppel-Like Transcription Factors, Male, Medulloblastoma, Nuclear Proteins, Predictive Value of Tests, Prognosis, Proportional Hazards Models, Proto-Oncogene Proteins c-myc, Reproducibility of Results, Risk Assessment, Risk Factors, Tissue Array Analysis, Wnt Proteins, Young Adult, Zinc Finger Protein Gli2
Abstract

PURPOSE: Medulloblastoma comprises four distinct molecular subgroups: WNT, SHH, Group 3, and Group 4. Current medulloblastoma protocols stratify patients based on clinical features: patient age, metastatic stage, extent of resection, and histologic variant. Stark prognostic and genetic differences among the four subgroups suggest that subgroup-specific molecular biomarkers could improve patient prognostication. PATIENTS AND METHODS: Molecular biomarkers were identified from a discovery set of 673 medulloblastomas from 43 cities around the world. Combined risk stratification models were designed based on clinical and cytogenetic biomarkers identified by multivariable Cox proportional hazards analyses. Identified biomarkers were tested using fluorescent in situ hybridization (FISH) on a nonoverlapping medulloblastoma tissue microarray (n = 453), with subsequent validation of the risk stratification models. RESULTS: Subgroup information improves the predictive accuracy of a multivariable survival model compared with clinical biomarkers alone. Most previously published cytogenetic biomarkers are only prognostic within a single medulloblastoma subgroup. Profiling six FISH biomarkers (GLI2, MYC, chromosome 11 [chr11], chr14, 17p, and 17q) on formalin-fixed paraffin-embedded tissues, we can reliably and reproducibly identify very low-risk and very high-risk patients within SHH, Group 3, and Group 4 medulloblastomas. CONCLUSION: Combining subgroup and cytogenetic biomarkers with established clinical biomarkers substantially improves patient prognostication, even in the context of heterogeneous clinical therapies. The prognostic significance of most molecular biomarkers is restricted to a specific subgroup. We have identified a small panel of cytogenetic biomarkers that reliably identifies very high-risk and very low-risk groups of patients, making it an excellent tool for selecting patients for therapy intensification and therapy de-escalation in future clinical trials.

Published
2014

65. Genome Sequencing of SHH Medulloblastoma Predicts Genotype-Related Response to Smoothened Inhibition

Author

Kool, Marcel, Jones, David TW, Jäger, Natalie, Northcott, Paul A, Pugh, Trevor J, Hovestadt, Volker, Piro, Rosario M, Esparza, L Adriana, Markant, Shirley L, Remke, Marc, Milde, Till, Bourdeaut, Franck, Ryzhova, Marina, Sturm, Dominik, Pfaff, Elke, Stark, Sebastian, Hutter, Sonja, Şeker-Cin, Huriye, Johann, Pascal, Bender, Sebastian, Schmidt, Christin, Rausch, Tobias, Shih, David, Reimand, Jüri, Sieber, Laura, Wittmann, Andrea, Linke, Linda, Witt, Hendrik, Weber, Ursula D, Zapatka, Marc, König, Rainer, Beroukhim, Rameen, Bergthold, Guillaume, van Sluis, Peter, Volckmann, Richard, Koster, Jan, Versteeg, Rogier, Schmidt, Sabine, Wolf, Stephan, Lawerenz, Chris, Bartholomae, Cynthia C, von Kalle, Christof, Unterberg, Andreas, Herold-Mende, Christel, Hofer, Silvia, Kulozik, Andreas E, von Deimling, Andreas, Scheurlen, Wolfram, Felsberg, Jörg, Reifenberger, Guido, Hasselblatt, Martin, Crawford, John R, Grant, Gerald A, Jabado, Nada, Perry, Arie, Cowdrey, Cynthia, Croul, Sydney, Zadeh, Gelareh, Korbel, Jan O, Doz, Francois, Delattre, Olivier, Bader, Gary D, McCabe, Martin G, Collins, V Peter, Kieran, Mark W, Cho, Yoon-Jae, Pomeroy, Scott L, Witt, Olaf, Brors, Benedikt, Taylor, Michael D, Schüller, Ulrich, Korshunov, Andrey, Eils, Roland, Wechsler-Reya, Robert J, Lichter, Peter, Pfister, Stefan M, and Project, on behalf of the ICGC PedBrain Tumor

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Clinical Sciences, Neurosciences, Pediatric Research Initiative, Genetics, Rare Diseases, Cancer, Pediatric, Brain Cancer, Pediatric Cancer, Brain Disorders, Adolescent, Adult, Animals, Base Sequence, Biphenyl Compounds, Cerebellar Neoplasms, Child, Child, Preschool, DEAD-box RNA Helicases, DNA Copy Number Variations, Drug Resistance, Neoplasm, Female, Gene Expression Profiling, Hedgehog Proteins, High-Throughput Nucleotide Sequencing, Humans, Infant, Kruppel-Like Transcription Factors, Male, Medulloblastoma, Mice, Mice, Inbred NOD, Mice, SCID, Molecular Sequence Data, N-Myc Proto-Oncogene Protein, Neoplasm Transplantation, Nuclear Proteins, Oncogene Proteins, Patched Receptors, Patched-1 Receptor, Phosphatidylinositol 3-Kinases, Promoter Regions, Genetic, Proto-Oncogene Proteins c-akt, Pyridines, Receptors, Cell Surface, Receptors, G-Protein-Coupled, Repressor Proteins, Signal Transduction, Smoothened Receptor, Telomerase, Tumor Suppressor Protein p53, Young Adult, Zinc Finger Protein Gli2, ICGC PedBrain Tumor Project, Oncology and Carcinogenesis, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Smoothened (SMO) inhibitors recently entered clinical trials for sonic-hedgehog-driven medulloblastoma (SHH-MB). Clinical response is highly variable. To understand the mechanism(s) of primary resistance and identify pathways cooperating with aberrant SHH signaling, we sequenced and profiled a large cohort of SHH-MBs (n = 133). SHH pathway mutations involved PTCH1 (across all age groups), SUFU (infants, including germline), and SMO (adults). Children >3 years old harbored an excess of downstream MYCN and GLI2 amplifications and frequent TP53 mutations, often in the germline, all of which were rare in infants and adults. Functional assays in different SHH-MB xenograft models demonstrated that SHH-MBs harboring a PTCH1 mutation were responsive to SMO inhibition, whereas tumors harboring an SUFU mutation or MYCN amplification were primarily resistant.

Published
2014

66. Paediatric and adult glioblastoma: multiform (epi)genomic culprits emerge

Author

Sturm, Dominik, Bender, Sebastian, Jones, David TW, Lichter, Peter, Grill, Jacques, Becher, Oren, Hawkins, Cynthia, Majewski, Jacek, Jones, Chris, Costello, Joseph F, Iavarone, Antonio, Aldape, Kenneth, Brennan, Cameron W, Jabado, Nada, and Pfister, Stefan M

Subjects
Biomedical and Clinical Sciences, Biotechnology, Cancer, Human Genome, Brain Cancer, Genetics, Brain Disorders, Neurosciences, Rare Diseases, Age Factors, Epigenomics, Glioblastoma, Humans, Neoplasms, Nerve Tissue, Medical and Health Sciences, Oncology & Carcinogenesis, Biomedical and clinical sciences, Health sciences
Abstract

We have extended our understanding of the molecular biology that underlies adult glioblastoma over many years. By contrast, high-grade gliomas in children and adolescents have remained a relatively under-investigated disease. The latest large-scale genomic and epigenomic profiling studies have yielded an unprecedented abundance of novel data and provided deeper insights into gliomagenesis across all age groups, which has highlighted key distinctions but also some commonalities. As we are on the verge of dissecting glioblastomas into meaningful biological subgroups, this Review summarizes the hallmark genetic alterations that are associated with distinct epigenetic features and patient characteristics in both paediatric and adult disease, and examines the complex interplay between the glioblastoma genome and epigenome.

Published
2014

68. H3K27me3 spreading organizes canonical PRC1 chromatin architecture to regulate developmental programs

Author

Krug, Brian, primary, Hu, Bo, additional, Chen, Haifen, additional, Ptack, Adam, additional, Chen, Xiao, additional, Gretarsson, Kristjan H., additional, Deshmukh, Shriya, additional, Kabir, Nisha, additional, Faria Andrade, Augusto, additional, Jabbour, Elias, additional, Harutyunyan, Ashot S., additional, Lee, John J. Y., additional, Hulswit, Maud, additional, Faury, Damien, additional, Russo, Caterina, additional, Xu, Xinjing, additional, Johnston, Michael J., additional, Baguette, Audrey, additional, Dahl, Nathan A., additional, Weil, Alexander G., additional, Ellezam, Benjamin, additional, Dali, Rola, additional, Blanchette, Mathieu, additional, Wilson, Khadija, additional, Garcia, Benjamin A., additional, Soni, Rajesh Kumar, additional, Gallo, Marco, additional, Taylor, Michael D., additional, Kleinman, Claudia L., additional, Majewski, Jacek, additional, Jabado, Nada, additional, and Lu, Chao, additional

Published
2023
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69. The type II RAF inhibitor tovorafenib in relapsed/refractory pediatric low-grade glioma: the phase 2 FIREFLY-1 trial

Author

Kilburn, Lindsay B., primary, Khuong-Quang, Dong-Anh, additional, Hansford, Jordan R., additional, Landi, Daniel, additional, van der Lugt, Jasper, additional, Leary, Sarah E. S., additional, Driever, Pablo Hernáiz, additional, Bailey, Simon, additional, Perreault, Sébastien, additional, McCowage, Geoffrey, additional, Waanders, Angela J., additional, Ziegler, David S., additional, Witt, Olaf, additional, Baxter, Patricia A., additional, Kang, Hyoung Jin, additional, Hassall, Timothy E., additional, Han, Jung Woo, additional, Hargrave, Darren, additional, Franson, Andrea T., additional, Yalon Oren, Michal, additional, Toledano, Helen, additional, Larouche, Valérie, additional, Kline, Cassie, additional, Abdelbaki, Mohamed S., additional, Jabado, Nada, additional, Gottardo, Nicholas G., additional, Gerber, Nicolas U., additional, Whipple, Nicholas S., additional, Segal, Devorah, additional, Chi, Susan N., additional, Oren, Liat, additional, Tan, Enrica E. K., additional, Mueller, Sabine, additional, Cornelio, Izzy, additional, McLeod, Lisa, additional, Zhao, Xin, additional, Walter, Ashley, additional, Da Costa, Daniel, additional, Manley, Peter, additional, Blackman, Samuel C., additional, Packer, Roger J., additional, and Nysom, Karsten, additional

Published
2023
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70. Supplementary Figures 1-27 from A Compendium of Syngeneic, Transplantable Pediatric High-Grade Glioma Models Reveals Subtype-Specific Therapeutic Vulnerabilities

Author

McNicholas, Michael, primary, De Cola, Antonella, primary, Bashardanesh, Zahedeh, primary, Foss, Amelia, primary, Lloyd, Cameron B., primary, Hébert, Steven, primary, Faury, Damien, primary, Andrade, Augusto Faria, primary, Jabado, Nada, primary, Kleinman, Claudia L., primary, and Pathania, Manav, primary

Published
2023
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71. Supplementary Tables 1-3, 7-9 from A Compendium of Syngeneic, Transplantable Pediatric High-Grade Glioma Models Reveals Subtype-Specific Therapeutic Vulnerabilities

Author

McNicholas, Michael, primary, De Cola, Antonella, primary, Bashardanesh, Zahedeh, primary, Foss, Amelia, primary, Lloyd, Cameron B., primary, Hébert, Steven, primary, Faury, Damien, primary, Andrade, Augusto Faria, primary, Jabado, Nada, primary, Kleinman, Claudia L., primary, and Pathania, Manav, primary

Published
2023
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72. Figure 6 from A Compendium of Syngeneic, Transplantable Pediatric High-Grade Glioma Models Reveals Subtype-Specific Therapeutic Vulnerabilities

Author

McNicholas, Michael, primary, De Cola, Antonella, primary, Bashardanesh, Zahedeh, primary, Foss, Amelia, primary, Lloyd, Cameron B., primary, Hébert, Steven, primary, Faury, Damien, primary, Andrade, Augusto Faria, primary, Jabado, Nada, primary, Kleinman, Claudia L., primary, and Pathania, Manav, primary

Published
2023
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73. Data from A Compendium of Syngeneic, Transplantable Pediatric High-Grade Glioma Models Reveals Subtype-Specific Therapeutic Vulnerabilities

Author

McNicholas, Michael, primary, De Cola, Antonella, primary, Bashardanesh, Zahedeh, primary, Foss, Amelia, primary, Lloyd, Cameron B., primary, Hébert, Steven, primary, Faury, Damien, primary, Andrade, Augusto Faria, primary, Jabado, Nada, primary, Kleinman, Claudia L., primary, and Pathania, Manav, primary

Published
2023
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74. TMIC-04. IMMUNE PROFILING OF PEDIATRIC ONCOHISTONE GLIOMAS REVEALS DIVERSE MYELOID POPULATIONS AND TUMOR-PROMOTING BEHAVIORS

Author

Andrade, Augusto Faria, primary, Topouza, Danai, additional, McNicholas, Michael, additional, Gonzalez Santiago, Eduardo G, additional, De Cola, Antonella, additional, Gehlhaar, Arne, additional, Jessa, Selin, additional, Chandarana, Bhavyaa, additional, Russo, Caterina, additional, Faury, Damien, additional, Danieau, Geoffroy, additional, Zeinieh, Michele, additional, Krug, Brian, additional, Wei, Yuhong, additional, Wu, Qing, additional, Nakada, Emily M, additional, Juretic, Nikoleta, additional, Larouche, Valerie, additional, Weil, Alexander G, additional, Dudley, Roy, additional, Karamchandani, Jason, additional, Agnihotri, Sameer, additional, Ellezam, Benjamin, additional, Quail, Daniela, additional, Konnikova, Yelizaveta, additional, Kleinman, Claudia, additional, Walsh, Logan, additional, Pathania, Manav, additional, and Jabado, Nada, additional

Published
2023
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75. Comprehensive genomic analysis of cemento-ossifying fibroma

Author

Gomez, Ricardo Santiago, primary, El Mouatani, Ahmed, additional, Duarte-Andrade, Filipe Fideles, additional, Pereira, Thais dos Santos Fontes, additional, Guimarães, Letícia Martins, additional, Gayden, Tenzin, additional, Faury, Damien, additional, Nakada, Emily M., additional, Langlois, Sylvie, additional, Sinnett, Daniel, additional, Henriques de Castro, Wagner, additional, Diniz, Marina Gonçalves, additional, Jabado, Nada, additional, and Gomes, Carolina Cavalieri, additional

Published
2023
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76. CTNI-24. CLINICAL ACTIVITY AND SAFETY OF THE RAF INHIBITOR TOVORAFENIB IN PATIENTS WITH OPTIC PATHWAY GLIOMAS IN THE REGISTRATIONAL PEDIATRIC LOW-GRADE GLIOMA ARM OF THE PHASE 2 FIREFLY-1 (PNOC026) STUDY

Author

Nysom, Karsten, primary, Kilburn, Lindsay, additional, Leary, Sarah, additional, Landi, Daniel, additional, de Vos-Kerkhof, E, additional, Perreault, Sébastien, additional, Witt, Olaf, additional, Ziegler, David, additional, Driever, Pablo Hernáiz, additional, Franson, Andrea, additional, Baxter, Patricia, additional, Whipple, Nicholas S, additional, Kline, Cassie, additional, Segal, Devorah, additional, Jabado, Nada, additional, Bailey, Simon, additional, McCowage, Geoffrey, additional, Hansford, Jordan, additional, Khuong-Quang, Dong-Anh, additional, Gottardo, Nicholas, additional, Hassall, Timothy, additional, Han, Jung Woo, additional, Oren, Michal Yalon, additional, Chi, Susan, additional, Lee, Vai, additional, McLeod, Lisa, additional, Qiu, Jiaheng, additional, Walter, Ashley, additional, Manley, Peter, additional, and Hargrave, Darren, additional

Published
2023
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77. MODL-08. A COMPENDIUM OF SYNGENEIC, TRANSPLANTABLE PEDIATRIC HIGH-GRADE GLIOMA MODELS REVEALS SUBTYPE-SPECIFIC THERAPEUTIC VULNERABILITIES

Author

McNicholas, Michael, primary, De Cola, Antonella, additional, Bashardanesh, Zahedeh, additional, Foss, Amelia, additional, Lloyd, Cameron, additional, Hebert, Steven, additional, Faury, Damien, additional, Andrade, Augusto Faria, additional, Jabado, Nada, additional, Kleinman, Claudia, additional, and Pathania, Manav, additional

Published
2023
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79. Adaptive rewiring of purine metabolism promotes treatment resistance in H3K27M-mutant diffuse midline glioma

Author

Peterson, Erik R., primary, Sajjakulnukit, Peter, additional, Scott, Andrew J., additional, Heaslip, Caleb, additional, Andren, Anthony, additional, Wilder-Romans, Kari, additional, Zhou, Weihua, additional, Palavalasa, Sravya, additional, Korimerla, Navyateja, additional, Lin, Angelica, additional, Obrien, Alexandra, additional, Kothari, Ayesha, additional, Zhao, Zitong, additional, Zhang, Li, additional, Morgan, Meredith A., additional, Venneti, Sriram, additional, Koschmann, Carl, additional, Jabado, Nada, additional, Lyssiotis, Costas A., additional, Castro, Maria G., additional, and Wahl, Daniel R., additional

Published
2023
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80. TERT promoter mutations are highly recurrent in SHH subgroup medulloblastoma.

Author

Remke, Marc, Ramaswamy, Vijay, Peacock, John, Shih, David, Koelsche, Christian, Northcott, Paul, Hill, Nadia, Cavalli, Florence, Kool, Marcel, Wang, Xin, Mack, Stephen, Barszczyk, Mark, Morrissy, A, Wu, Xiaochong, Agnihotri, Sameer, Luu, Betty, Jones, David, Garzia, Livia, Dubuc, Adrian, Zhukova, Nataliya, Vanner, Robert, Kros, Johan, French, Pim, Van Meir, Erwin, Vibhakar, Rajeev, Zitterbart, Karel, Chan, Jennifer, Bognár, László, Klekner, Almos, Lach, Boleslaw, Jung, Shin, Saad, Ali, Albrecht, Steffen, Zollo, Massimo, Cooper, Michael, Thompson, Reid, Delattre, Oliver, Bourdeaut, Franck, Doz, François, Garami, Miklós, Hauser, Peter, Carlotti, Carlos, Van Meter, Timothy, Massimi, Luca, Fults, Daniel, Pomeroy, Scott, Kumabe, Toshiro, Ra, Young, Leonard, Jeffrey, Elbabaa, Samer, Mora, Jaume, Rubin, Joshua, Cho, Yoon-Jae, McLendon, Roger, Bigner, Darell, Eberhart, Charles, Fouladi, Maryam, Wechsler-Reya, Robert, Faria, Claudia, Croul, Sidney, Huang, Annie, Bouffet, Eric, Hawkins, Cynthia, Dirks, Peter, Schüller, Ulrich, Pollack, Ian, Rutkowski, Stefan, Meyronet, David, Jouvet, Anne, Fèvre-Montange, Michelle, Jabado, Nada, Perek-Polnik, Marta, Grajkowska, Wieslawa, Kim, Seung-Ki, Rutka, James, Malkin, David, Tabori, Uri, Pfister, Stefan, Korshunov, Andrey, von Deimling, Andreas, Taylor, Michael, Weiss, William, and Liau, Linda

Subjects
Adolescent, Adult, Brain Neoplasms, Child, Child, Preschool, DNA Mutational Analysis, Female, Gene Expression Profiling, Genotype, Humans, Infant, Male, Medulloblastoma, Middle Aged, Mutation, Prognosis, Promoter Regions, Genetic, Telomerase
Abstract

Telomerase reverse transcriptase (TERT) promoter mutations were recently shown to drive telomerase activity in various cancer types, including medulloblastoma. However, the clinical and biological implications of TERT mutations in medulloblastoma have not been described. Hence, we sought to describe these mutations and their impact in a subgroup-specific manner. We analyzed the TERT promoter by direct sequencing and genotyping in 466 medulloblastomas. The mutational distributions were determined according to subgroup affiliation, demographics, and clinical, prognostic, and molecular features. Integrated genomics approaches were used to identify specific somatic copy number alterations in TERT promoter-mutated and wild-type tumors. Overall, TERT promoter mutations were identified in 21 % of medulloblastomas. Strikingly, the highest frequencies of TERT mutations were observed in SHH (83 %; 55/66) and WNT (31 %; 4/13) medulloblastomas derived from adult patients. Group 3 and Group 4 harbored this alteration in

Published
2013

82. Subgroup-specific prognostic implications of TP53 mutation in medulloblastoma.

Author

Zhukova, Nataliya, Ramaswamy, Vijay, Remke, Marc, Pfaff, Elke, Shih, David, Martin, Dianna, Castelo-Branco, Pedro, Baskin, Berivan, Ray, Peter, Bouffet, Eric, von Bueren, André, Jones, David, Northcott, Paul, Kool, Marcel, Sturm, Dominik, Pugh, Trevor, Pomeroy, Scott, Cho, Yoon-Jae, Pietsch, Torsten, Gessi, Marco, Rutkowski, Stefan, Bognar, Laszlo, Klekner, Almos, Cho, Byung-Kyu, Kim, Seung-Ki, Wang, Kyu-Chang, Eberhart, Charles, Fevre-Montange, Michelle, Fouladi, Maryam, French, Pim, Kros, Max, Grajkowska, Wieslawa, Hauser, Peter, Jabado, Nada, Jouvet, Anne, Jung, Shin, Kumabe, Toshihiro, Lach, Boleslaw, Leonard, Jeffrey, Rubin, Joshua, Massimi, Luca, Pollack, Ian, Shin Ra, Young, Van Meir, Erwin, Zitterbart, Karel, Schüller, Ulrich, Hill, Rebecca, Lindsey, Janet, Schwalbe, Ed, Bailey, Simon, Ellison, David, Hawkins, Cynthia, Malkin, David, Clifford, Steven, Korshunov, Andrey, Pfister, Stefan, Taylor, Michael, Tabori, Uri, Gupta, Nalin, Weiss, William, and Liau, Linda

Subjects
Adolescent, Adult, Cerebellar Neoplasms, Child, Child, Preschool, Female, Gene Expression Profiling, Genes, p53, Humans, Infant, Male, Medulloblastoma, Middle Aged, Mutation, Prognosis, Young Adult
Abstract

PURPOSE: Reports detailing the prognostic impact of TP53 mutations in medulloblastoma offer conflicting conclusions. We resolve this issue through the inclusion of molecular subgroup profiles. PATIENTS AND METHODS: We determined subgroup affiliation, TP53 mutation status, and clinical outcome in a discovery cohort of 397 medulloblastomas. We subsequently validated our results on an independent cohort of 156 medulloblastomas. RESULTS: TP53 mutations are enriched in wingless (WNT; 16%) and sonic hedgehog (SHH; 21%) medulloblastomas and are virtually absent in subgroups 3 and 4 tumors (P < .001). Patients with SHH/TP53 mutant tumors are almost exclusively between ages 5 and 18 years, dramatically different from the general SHH distribution (P < .001). Children with SHH/TP53 mutant tumors harbor 56% germline TP53 mutations, which are not observed in children with WNT/TP53 mutant tumors. Five-year overall survival (OS; ± SE) was 41% ± 9% and 81% ± 5% for patients with SHH medulloblastomas with and without TP53 mutations, respectively (P < .001). Furthermore, TP53 mutations accounted for 72% of deaths in children older than 5 years with SHH medulloblastomas. In contrast, 5-year OS rates were 90% ± 9% and 97% ± 3% for patients with WNT tumors with and without TP53 mutations (P = .21). Multivariate analysis revealed that TP53 status was the most important risk factor for SHH medulloblastoma. Survival rates in the validation cohort mimicked the discovery results, revealing that poor survival of TP53 mutations is restricted to patients with SHH medulloblastomas (P = .012) and not WNT tumors. CONCLUSION: Subgroup-specific analysis reconciles prior conflicting publications and confirms that TP53 mutations are enriched among SHH medulloblastomas, in which they portend poor outcome and account for a large proportion of treatment failures in these patients.

Published
2013

83. Recurrent noncoding U1 snRNA mutations drive cryptic splicing in SHH medulloblastoma

Author

Suzuki, Hiromichi, Kumar, Sachin A., Shuai, Shimin, Diaz-Navarro, Ander, Gutierrez-Fernandez, Ana, De Antonellis, Pasqualino, Cavalli, Florence M. G., Juraschka, Kyle, Farooq, Hamza, Shibahara, Ichiyo, Vladoiu, Maria C., Zhang, Jiao, Abeysundara, Namal, Przelicki, David, Skowron, Patryk, Gauer, Nicole, Luu, Betty, Daniels, Craig, Wu, Xiaochong, Forget, Antoine, Momin, Ali, Wang, Jun, Dong, Weifan, Kim, Seung-Ki, Grajkowska, Wieslawa A., Jouvet, Anne, Fèvre-Montange, Michelle, Garrè, Maria Luisa, Nageswara Rao, Amulya A., Giannini, Caterina, Kros, Johan M., French, Pim J., Jabado, Nada, Ng, Ho-Keung, Poon, Wai Sang, Eberhart, Charles G., Pollack, Ian F., Olson, James M., Weiss, William A., Kumabe, Toshihiro, López-Aguilar, Enrique, Lach, Boleslaw, Massimino, Maura, Van Meir, Erwin G., Rubin, Joshua B., Vibhakar, Rajeev, Chambless, Lola B., Kijima, Noriyuki, Klekner, Almos, Bognár, László, Chan, Jennifer A., Faria, Claudia C., Ragoussis, Jiannis, Pfister, Stefan M., Goldenberg, Anna, Wechsler-Reya, Robert J., Bailey, Swneke D., Garzia, Livia, Morrissy, A. Sorana, Marra, Marco A., Huang, Xi, Malkin, David, Ayrault, Olivier, Ramaswamy, Vijay, Puente, Xose S., Calarco, John A., Stein, Lincoln, and Taylor, Michael D.

Published
2019
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84. The histone mark H3K36me2 recruits DNMT3A and shapes the intergenic DNA methylation landscape

Author

Weinberg, Daniel N., Papillon-Cavanagh, Simon, Chen, Haifen, Yue, Yuan, Chen, Xiao, Rajagopalan, Kartik N., Horth, Cynthia, McGuire, John T., Xu, Xinjing, Nikbakht, Hamid, Lemiesz, Agata E., Marchione, Dylan M., Marunde, Matthew R., Meiners, Matthew J., Cheek, Marcus A., Keogh, Michael-Christopher, Bareke, Eric, Djedid, Anissa, Harutyunyan, Ashot S., Jabado, Nada, Garcia, Benjamin A., Li, Haitao, Allis, C. David, Majewski, Jacek, and Lu, Chao

Published
2019
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86. Germline HAVCR2 mutations altering TIM-3 characterize subcutaneous panniculitis-like T cell lymphomas with hemophagocytic lymphohistiocytic syndrome

Author

Gayden, Tenzin, Sepulveda, Fernando E., Khuong-Quang, Dong-Anh, Pratt, Jonathan, Valera, Elvis T., Garrigue, Alexandrine, Kelso, Susan, Sicheri, Frank, Mikael, Leonie G., Hamel, Nancy, Bajic, Andrea, Dali, Rola, Deshmukh, Shriya, Dervovic, Dzana, Schramek, Daniel, Guerin, Frédéric, Taipale, Mikko, Nikbakht, Hamid, Majewski, Jacek, Moshous, Despina, Charlebois, Janie, Abish, Sharon, Bole-Feysot, Christine, Nitschke, Patrick, Bader-Meunier, Brigitte, Mitchell, David, Thieblemont, Catherine, Battistella, Maxime, Gravel, Simon, Nguyen, Van-Hung, Conyers, Rachel, Diana, Jean-Sebastien, McCormack, Chris, Prince, H. Miles, Besnard, Marianne, Blanche, Stephane, Ekert, Paul G., Fraitag, Sylvie, Foulkes, William D., Fischer, Alain, Neven, Bénédicte, Michonneau, David, de Saint Basile, Geneviève, and Jabado, Nada

Published
2018
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87. Subgroup-specific structural variation across 1,000 medulloblastoma genomes.

Author

Northcott, Paul, Shih, David, Peacock, John, Garzia, Livia, Morrissy, A, Zichner, Thomas, Stütz, Adrian, Korshunov, Andrey, Reimand, Jüri, Schumacher, Steven, Beroukhim, Rameen, Ellison, David, Marshall, Christian, Lionel, Anath, Mack, Stephen, Dubuc, Adrian, Yao, Yuan, Ramaswamy, Vijay, Luu, Betty, Rolider, Adi, Cavalli, Florence, Wang, Xin, Remke, Marc, Wu, Xiaochong, Chiu, Readman, Chu, Andy, Chuah, Eric, Corbett, Richard, Hoad, Gemma, Jackman, Shaun, Li, Yisu, Lo, Allan, Mungall, Karen, Nip, Ka, Qian, Jenny, Raymond, Anthony, Thiessen, Nina, Varhol, Richard, Birol, Inanc, Moore, Richard, Mungall, Andrew, Holt, Robert, Kawauchi, Daisuke, Roussel, Martine, Kool, Marcel, Jones, David, Witt, Hendrick, Fernandez-L, Africa, Kenney, Anna, Wechsler-Reya, Robert, Dirks, Peter, Aviv, Tzvi, Grajkowska, Wieslawa, Perek-Polnik, Marta, Haberler, Christine, Delattre, Olivier, Reynaud, Stéphanie, Doz, François, Pernet-Fattet, Sarah, Cho, Byung-Kyu, Kim, Seung-Ki, Wang, Kyu-Chang, Scheurlen, Wolfram, Eberhart, Charles, Fèvre-Montange, Michelle, Jouvet, Anne, Pollack, Ian, Fan, Xing, Muraszko, Karin, Gillespie, G, Di Rocco, Concezio, Massimi, Luca, Michiels, Erna, Kloosterhof, Nanne, French, Pim, Kros, Johan, Olson, James, Ellenbogen, Richard, Zitterbart, Karel, Kren, Leos, Thompson, Reid, Cooper, Michael, Lach, Boleslaw, McLendon, Roger, Bigner, Darell, Fontebasso, Adam, Albrecht, Steffen, Jabado, Nada, Lindsey, Janet, Bailey, Simon, Van Meir, Erwin, Fouladi, Maryam, Nakamura, Hideo, Cinalli, Giuseppe, Garami, Miklós, Hauser, Peter, Saad, Ali, Iolascon, Achille, Jung, Shin, and Carlotti, Carlos

Subjects
Carrier Proteins, Cerebellar Neoplasms, Child, DNA Copy Number Variations, Gene Duplication, Genes, myc, Genome, Human, Genomic Structural Variation, Genomics, Hedgehog Proteins, Humans, Medulloblastoma, NF-kappa B, Nerve Tissue Proteins, Oncogene Proteins, Fusion, Proteins, RNA, Long Noncoding, Signal Transduction, Transforming Growth Factor beta, Translocation, Genetic
Abstract

Medulloblastoma, the most common malignant paediatric brain tumour, is currently treated with nonspecific cytotoxic therapies including surgery, whole-brain radiation, and aggressive chemotherapy. As medulloblastoma exhibits marked intertumoural heterogeneity, with at least four distinct molecular variants, previous attempts to identify targets for therapy have been underpowered because of small samples sizes. Here we report somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas. SCNAs are common in medulloblastoma, and are predominantly subgroup-enriched. The most common region of focal copy number gain is a tandem duplication of SNCAIP, a gene associated with Parkinsons disease, which is exquisitely restricted to Group 4α. Recurrent translocations of PVT1, including PVT1-MYC and PVT1-NDRG1, that arise through chromothripsis are restricted to Group 3. Numerous targetable SCNAs, including recurrent events targeting TGF-β signalling in Group 3, and NF-κB signalling in Group 4, suggest future avenues for rational, targeted therapy.

Published
2012

88. Clonal selection drives genetic divergence of metastatic medulloblastoma.

Author

Wu, Xiaochong, Northcott, Paul A, Dubuc, Adrian, Dupuy, Adam J, Shih, David JH, Witt, Hendrik, Croul, Sidney, Bouffet, Eric, Fults, Daniel W, Eberhart, Charles G, Garzia, Livia, Van Meter, Timothy, Zagzag, David, Jabado, Nada, Schwartzentruber, Jeremy, Majewski, Jacek, Scheetz, Todd E, Pfister, Stefan M, Korshunov, Andrey, Li, Xiao-Nan, Scherer, Stephen W, Cho, Yoon-Jae, Akagi, Keiko, MacDonald, Tobey J, Koster, Jan, McCabe, Martin G, Sarver, Aaron L, Collins, V Peter, Weiss, William A, Largaespada, David A, Collier, Lara S, and Taylor, Michael D

Subjects
Animals, Humans, Mice, Medulloblastoma, Neoplasm Metastasis, Li-Fraumeni Syndrome, Disease Models, Animal, DNA Transposable Elements, Survival Rate, Mutagenesis, Insertional, DNA Methylation, CpG Islands, Germ-Line Mutation, Genes, p53, Clonal Evolution, Disease Models, Animal, Genes, p53, Mutagenesis, Insertional, General Science & Technology
Abstract

Medulloblastoma, the most common malignant paediatric brain tumour, arises in the cerebellum and disseminates through the cerebrospinal fluid in the leptomeningeal space to coat the brain and spinal cord. Dissemination, a marker of poor prognosis, is found in up to 40% of children at diagnosis and in most children at the time of recurrence. Affected children therefore are treated with radiation to the entire developing brain and spinal cord, followed by high-dose chemotherapy, with the ensuing deleterious effects on the developing nervous system. The mechanisms of dissemination through the cerebrospinal fluid are poorly studied, and medulloblastoma metastases have been assumed to be biologically similar to the primary tumour. Here we show that in both mouse and human medulloblastoma, the metastases from an individual are extremely similar to each other but are divergent from the matched primary tumour. Clonal genetic events in the metastases can be demonstrated in a restricted subclone of the primary tumour, suggesting that only rare cells within the primary tumour have the ability to metastasize. Failure to account for the bicompartmental nature of metastatic medulloblastoma could be a major barrier to the development of effective targeted therapies.

Published
2012

89. A Compendium of Syngeneic, Transplantable Pediatric High-Grade Glioma Models Reveals Subtype-Specific Therapeutic Vulnerabilities

Author

McNicholas, Michael, De Cola, Antonella, Bashardanesh, Zahedeh, Foss, Amelia, Lloyd, Cameron B, Hébert, Steven, Faury, Damien, Andrade, Augusto Faria, Jabado, Nada, Kleinman, Claudia L, Pathania, Manav, McNicholas, Michael [0000-0002-6920-9924], De Cola, Antonella [0000-0002-3202-5339], Bashardanesh, Zahedeh [0000-0003-1277-2270], Foss, Amelia [0000-0001-5956-6779], Lloyd, Cameron B [0000-0003-1055-2282], Hébert, Steven [0000-0001-6267-8595], Faury, Damien [0000-0003-1584-599X], Andrade, Augusto Faria [0000-0001-5866-0501], Jabado, Nada [0000-0003-2485-3692], Kleinman, Claudia L [0000-0002-5158-7126], Pathania, Manav [0000-0001-5635-5028], and Apollo - University of Cambridge Repository

Subjects
Histones, Gene Expression Regulation, Neoplastic, Mice, Oncology, Brain Neoplasms, Mutation, Animals, Brain, Glioma
Abstract

UNLABELLED: Pediatric high-grade gliomas (pHGG) are lethal, incurable brain tumors frequently driven by clonal mutations in histone genes. They often harbor a range of additional genetic alterations that correlate with different ages, anatomic locations, and tumor subtypes. We developed models representing 16 pHGG subtypes driven by different combinations of alterations targeted to specific brain regions. Tumors developed with varying latencies and cell lines derived from these models engrafted in syngeneic, immunocompetent mice with high penetrance. Targeted drug screening revealed unexpected selective vulnerabilities-H3.3G34R/PDGFRAC235Y to FGFR inhibition, H3.3K27M/PDGFRAWT to PDGFRA inhibition, and H3.3K27M/PDGFRAWT and H3.3K27M/PPM1DΔC/PIK3CAE545K to combined inhibition of MEK and PIK3CA. Moreover, H3.3K27M tumors with PIK3CA, NF1, and FGFR1 mutations were more invasive and harbored distinct additional phenotypes, such as exophytic spread, cranial nerve invasion, and spinal dissemination. Collectively, these models reveal that different partner alterations produce distinct effects on pHGG cellular composition, latency, invasiveness, and treatment sensitivity. SIGNIFICANCE: Histone-mutant pediatric gliomas are a highly heterogeneous tumor entity. Different histone mutations correlate with different ages of onset, survival outcomes, brain regions, and partner alterations. We have developed models of histone-mutant gliomas that reflect this anatomic and genetic heterogeneity and provide evidence of subtype-specific biology and therapeutic targeting. See related commentary by Lubanszky and Hawkins, p. 1516. This article is highlighted in the In This Issue feature, p. 1501.

Published
2023

90. Phase I trial of panobinostat in children with diffuse intrinsic pontine glioma: A report from the Pediatric Brain Tumor Consortium (PBTC-047)

Author

Monje, Michelle, primary, Cooney, Tabitha, additional, Glod, John, additional, Huang, Jie, additional, Peer, Cody J, additional, Faury, Damien, additional, Baxter, Patricia, additional, Kramer, Kim, additional, Lenzen, Alicia, additional, Robison, Nathan J, additional, Kilburn, Lindsay, additional, Vinitsky, Anna, additional, Figg, William D, additional, Jabado, Nada, additional, Fouladi, Maryam, additional, Fangusaro, Jason, additional, Onar-Thomas, Arzu, additional, Dunkel, Ira J, additional, and Warren, Katherine E, additional

Published
2023
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92. Supplementary Table 6 from A Compendium of Syngeneic, Transplantable Pediatric High-Grade Glioma Models Reveals Subtype-Specific Therapeutic Vulnerabilities

Author

McNicholas, Michael, primary, De Cola, Antonella, primary, Bashardanesh, Zahedeh, primary, Foss, Amelia, primary, Lloyd, Cameron B., primary, Hébert, Steven, primary, Faury, Damien, primary, Andrade, Augusto Faria, primary, Jabado, Nada, primary, Kleinman, Claudia L., primary, and Pathania, Manav, primary

Published
2023
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93. Supplementary Table 4 from A Compendium of Syngeneic, Transplantable Pediatric High-Grade Glioma Models Reveals Subtype-Specific Therapeutic Vulnerabilities

Author

McNicholas, Michael, primary, De Cola, Antonella, primary, Bashardanesh, Zahedeh, primary, Foss, Amelia, primary, Lloyd, Cameron B., primary, Hébert, Steven, primary, Faury, Damien, primary, Andrade, Augusto Faria, primary, Jabado, Nada, primary, Kleinman, Claudia L., primary, and Pathania, Manav, primary

Published
2023
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94. Supplementary Table 5 from A Compendium of Syngeneic, Transplantable Pediatric High-Grade Glioma Models Reveals Subtype-Specific Therapeutic Vulnerabilities

Author

McNicholas, Michael, primary, De Cola, Antonella, primary, Bashardanesh, Zahedeh, primary, Foss, Amelia, primary, Lloyd, Cameron B., primary, Hébert, Steven, primary, Faury, Damien, primary, Andrade, Augusto Faria, primary, Jabado, Nada, primary, Kleinman, Claudia L., primary, and Pathania, Manav, primary

Published
2023
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96. A phase 2 study of trametinib for patients with pediatric glioma or plexiform neurofibroma with refractory tumor and activation of the MAPK/ERK pathway: TRAM-01

Author

Perreault, Sébastien, Larouche, Valérie, Tabori, Uri, Hawkin, Cynthia, Lippé, Sarah, Ellezam, Benjamin, Décarie, Jean-Claude, Théoret, Yves, Métras, Marie-Élaine, Sultan, Serge, Cantin, Édith, Routhier, Marie-Ève, Caru, Maxime, Legault, Geneviève, Bouffet, Éric, Lafay-Cousin, Lucie, Hukin, Juliette, Erker, Craig, and Jabado, Nada

Published
2019
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98. Performance of the eHealth decision support tool, MIPOGG, for recognising children with Li-Fraumeni, DICER1, Constitutional mismatch repair deficiency and Gorlin syndromes.

Author

Hebert, Robyn, Cullinan, Noelle, Armstrong, Linlea, Blood, Katherine A., Brossard, Josee, Brunga, Ledia, Cacciotti, Chantel, Caswell, Kimberly, Cellot, Sonia, Coltin, Hallie, Deyell, Rebecca J., Felton, Kathleen, Fernandez, Conrad V., Fleming, Adam J., Gibson, Paul, Hammad, Rawan, Jabado, Nada, Johnston, Donna L., Lafay-Cousin, Lucie, and Larouche, Valérie

Abstract

Background Cancer predisposition syndromes (CPSs) are responsible for at least 10% of cancer diagnoses in children and adolescents, most of which are not clinically recognised prior to cancer diagnosis. A variety of clinical screening guidelines are used in healthcare settings to help clinicians detect patients who have a higher likelihood of having a CPS. The McGill Interactive Pediatric OncoGenetic Guidelines (MIPOGG) is an electronic health decision support tool that uses algorithms to help clinicians determine if a child/adolescent diagnosed with cancer should be referred to genetics for a CPS evaluation. Methods This study assessed MIPOGG’s performance in identifying Li-Fraumeni, DICER1, Constitutional mismatch repair deficiency and Gorlin (nevoid basal cell carcinoma) syndromes in a retrospective series of 84 children diagnosed with cancer and one of these four CPSs in Canadian hospitals over an 18-year period. Results MIPOGG detected 82 of 83 (98.8%) evaluable patients with any one of these four genetic conditions and demonstrated an appropriate rationale for suggesting CPS evaluation. When compared with syndrome-specific clinical screening criteria, MIPOGG’s ability to correctly identify children with any of the four CPSs was equivalent to, or outperformed, existing clinical criteria respective to each CPS. Conclusion This study adds evidence that MIPOGG is an appropriate tool for CPS screening in clinical practice. MIPOGG’s strength is that it starts with a specific cancer diagnosis and incorporates criteria relevant for associated CPSs, making MIPOGG a more universally accessible diagnostic adjunct that does not require in-depth knowledge of each CPS. [ABSTRACT FROM AUTHOR]

Published
2023
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100. X-linked primary immunodeficiency associated with hemizygous mutations in the moesin (MSN) gene

Author

Lagresle-Peyrou, Chantal, Luce, Sonia, Ouchani, Farid, Soheili, Tayebeh Shabi, Sadek, Hanem, Chouteau, Myriam, Durand, Amandine, Pic, Isabelle, Majewski, Jacek, Brouzes, Chantal, Lambert, Nathalie, Bohineust, Armelle, Verhoeyen, Els, Cosset, François-Loïc, Magerus-Chatinet, Aude, Rieux-Laucat, Frédéric, Gandemer, Virginie, Monnier, Delphine, Heijmans, Catherine, van Gijn, Marielle, Dalm, Virgil A., Mahlaoui, Nizar, Stephan, Jean-Louis, Picard, Capucine, Durandy, Anne, Kracker, Sven, Hivroz, Claire, Jabado, Nada, de Saint Basile, Geneviève, Fischer, Alain, Cavazzana, Marina, and André-Schmutz, Isabelle

Published
2016
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