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2. 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 JY, 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 AN, Giannini, Caterina, Olson, James M, Garami, Miklós, Hauser, Peter, Phillips, Joanna J, Ra, Young S, de Torres, Carmen, Mora, Jaume, Li, Kay KW, 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, and Thompson, Eric M

Subjects
Stem Cell Research, Brain Disorders, Neurosciences, Rare Diseases, Stem Cell Research - Nonembryonic - Non-Human, Aetiology, 1.1 Normal biological development and functioning, Underpinning research, 2.1 Biological and endogenous factors, Cell Differentiation, Cell Lineage, Cerebellar Neoplasms, Cerebellum, Core Binding Factor alpha Subunits, Hedgehog Proteins, Histone Demethylases, Humans, Ki-67 Antigen, Medulloblastoma, Metencephalon, Muscle Proteins, Mutation, Otx Transcription Factors, Repressor Proteins, T-Box Domain Proteins, Transcription Factors, General Science & Technology
Abstract

Medulloblastoma (MB) comprises a group of heterogeneous paediatric embryonal neoplasms of the hindbrain with strong links to early development of the hindbrain1-4. Mutations that activate Sonic hedgehog signalling lead to Sonic hedgehog MB in the upper rhombic lip (RL) granule cell lineage5-8. By contrast, mutations that activate WNT signalling lead to WNT MB in the lower RL9,10. However, little is known about the more commonly occurring group 4 (G4) MB, which is thought to arise in the unipolar brush cell lineage3,4. Here we demonstrate that somatic mutations that cause G4 MB converge on the core binding factor alpha (CBFA) complex and mutually exclusive alterations that affect CBFA2T2, CBFA2T3, PRDM6, UTX and OTX2. CBFA2T2 is expressed early in the progenitor cells of the cerebellar RL subventricular zone in Homo sapiens, and G4 MB transcriptionally resembles these progenitors but are stalled in developmental time. Knockdown of OTX2 in model systems relieves this differentiation blockade, which allows MB cells to spontaneously proceed along normal developmental differentiation trajectories. The specific nature of the split human RL, which is destined to generate most of the neurons in the human brain, and its high level of susceptible EOMES+KI67+ unipolar brush cell progenitor cells probably predisposes our species to the development of G4 MB.

Published
2022

3. Aligning the Central Brain Tumor Registry of the United States (CBTRUS) histology groupings with current definitions.

Author

Waite, Kristin A, Cioffi, Gino, Kruchko, Carol, Patil, Nirav, Brat, Daniel J, Bruner, Janet M, McLendon, Roger E, Tihan, Tarik, Ostrom, Quinn T, and Barnholtz-Sloan, Jill S

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Rare Diseases, Cancer, Neurosciences, brain tumors, epidemiology, histology, CBTRUS, Oncology and carcinogenesis
Abstract

BackgroundThe Central Brain Tumor Registry of the United States (CBTRUS) uses a histology grouping model based on the World Health Organization (WHO) classifications to group records for clinically relevant statistical reporting. Newly identified genetic markers more accurately stratify patients than histology alone and were incorporated into the 2016 update to the WHO Classification.MethodsCBTRUS and consulting neuropathologists reviewed and aligned histology groupings with the 2016 WHO update. "Obsolete" (terms not currently in use) histology nomenclature along with their International Classification of Disease, Oncology 3rd edition (ICD-O-3) codes were identified, some histologies were reclassified to 2016 WHO, and new codes found in 2016 WHO were incorporated. An evaluation of the frequency of histology codes affected in the realignment process, and incidence and survival pre- and post-realignment was conducted.ResultsAfter review, 67 codes were noted as obsolete, 51 codes were reclassified, and 12 new codes were incorporated. Histology groups most affected were mesenchymal tumors and neuronal/mixed neuronal-glial tumors. Reorganization resulted in 2588 (0.65%) cases with grouping reassignment or reporting change, indicating that the 2016 WHO Classification revision has impacted the collection and reporting of primary brain and other CNS tumors.ConclusionThis work demonstrates the need to be responsive to changes in classification and coding in order to ensure the most up-to-date and accurate statistics for brain and CNS tumors. This will require collaboration from all stakeholders within the brain tumor community, so to have the ability to reconcile clinical practices and surveillance requirements.

Published
2022

4. The transcriptional landscape of Shh medulloblastoma.

Author

Skowron, Patryk, Farooq, Hamza, Cavalli, Florence MG, Morrissy, A Sorana, Ly, Michelle, Hendrikse, Liam D, Wang, Evan Y, Djambazian, Haig, Zhu, Helen, Mungall, Karen L, Trinh, Quang M, Zheng, Tina, Dai, Shizhong, Stucklin, Ana S Guerreiro, Vladoiu, Maria C, Fong, Vernon, Holgado, Borja L, Nor, Carolina, Wu, Xiaochong, Abd-Rabbo, Diala, Bérubé, Pierre, Wang, Yu Chang, Luu, Betty, Suarez, Raul A, Rastan, Avesta, Gillmor, Aaron H, Lee, John JY, Zhang, Xiao Yun, Daniels, Craig, Dirks, Peter, Malkin, David, Bouffet, Eric, Tabori, Uri, Loukides, James, Doz, François P, Bourdeaut, Franck, Delattre, Olivier O, Masliah-Planchon, Julien, Ayrault, Olivier, Kim, Seung-Ki, Meyronet, David, Grajkowska, Wieslawa A, Carlotti, Carlos G, de Torres, Carmen, Mora, Jaume, Eberhart, Charles G, Van Meir, Erwin G, Kumabe, Toshihiro, French, Pim J, Kros, Johan M, Jabado, Nada, Lach, Boleslaw, Pollack, Ian F, Hamilton, Ronald L, Rao, Amulya A Nageswara, Giannini, Caterina, Olson, James M, Bognár, László, Klekner, Almos, Zitterbart, Karel, Phillips, Joanna J, Thompson, Reid C, Cooper, Michael K, Rubin, Joshua B, Liau, Linda M, Garami, Miklós, Hauser, Peter, Li, Kay Ka Wai, Ng, Ho-Keung, Poon, Wai Sang, Yancey Gillespie, G, Chan, Jennifer A, Jung, Shin, McLendon, Roger E, Thompson, Eric M, Zagzag, David, Vibhakar, Rajeev, Ra, Young Shin, Garre, Maria Luisa, Schüller, Ulrich, Shofuda, Tomoko, Faria, Claudia C, López-Aguilar, Enrique, Zadeh, Gelareh, Hui, Chi-Chung, Ramaswamy, Vijay, Bailey, Swneke D, Jones, Steven J, Mungall, Andrew J, Moore, Richard A, Calarco, John A, Stein, Lincoln D, Bader, Gary D, Reimand, Jüri, Ragoussis, Jiannis, Weiss, William A, Marra, Marco A, Suzuki, Hiromichi, and Taylor, Michael D

Subjects
Humans, Medulloblastoma, Cerebellar Neoplasms, Signal Transduction, Gene Expression Regulation, Neoplastic, Adolescent, Adult, Middle Aged, Child, Child, Preschool, Infant, Female, Male, Hedgehog Proteins, Gene Regulatory Networks, Genetic Variation, Young Adult, Transcriptome, Pediatric Research Initiative, Brain Cancer, Pediatric, Rare Diseases, Genetics, Pediatric Cancer, Clinical Research, Brain Disorders, Neurosciences, Biotechnology, Human Genome, Cancer, 2.1 Biological and endogenous factors
Abstract

Sonic hedgehog medulloblastoma encompasses a clinically and molecularly diverse group of cancers of the developing central nervous system. Here, we use unbiased sequencing of the transcriptome across a large cohort of 250 tumors to reveal differences among molecular subtypes of the disease, and demonstrate the previously unappreciated importance of non-coding RNA transcripts. We identify alterations within the cAMP dependent pathway (GNAS, PRKAR1A) which converge on GLI2 activity and show that 18% of tumors have a genetic event that directly targets the abundance and/or stability of MYCN. Furthermore, we discover an extensive network of fusions in focally amplified regions encompassing GLI2, and several loss-of-function fusions in tumor suppressor genes PTCH1, SUFU and NCOR1. Molecular convergence on a subset of genes by nucleotide variants, copy number aberrations, and gene fusions highlight the key roles of specific pathways in the pathogenesis of Sonic hedgehog medulloblastoma and open up opportunities for therapeutic intervention.

Published
2021

5. Pattern of Relapse and Treatment Response in WNT-Activated Medulloblastoma

Author

Nobre, Liana, Zapotocky, Michal, Khan, Sara, Fukuoka, Kohei, Fonseca, Adriana, McKeown, Tara, Sumerauer, David, Vicha, Ales, Grajkowska, Wieslawa A, Trubicka, Joanna, Li, Kay Ka Wai, Ng, Ho-Keung, Massimi, Luca, Lee, Ji Yeoun, Kim, Seung-Ki, Zelcer, Shayna, Vasiljevic, Alexandre, Faure-Conter, Cécile, Hauser, Peter, Lach, Boleslaw, van Veelen-Vincent, Marie-Lise, French, Pim J, Van Meir, Erwin G, Weiss, William A, Gupta, Nalin, Pollack, Ian F, Hamilton, Ronald L, Rao, Amulya A Nageswara, Giannini, Caterina, Rubin, Joshua B, Moore, Andrew S, Chambless, Lola B, Vibhakar, Rajeev, Ra, Young Shin, Massimino, Maura, McLendon, Roger E, Wheeler, Helen, Zollo, Massimo, Ferruci, Veronica, Kumabe, Toshihiro, Faria, Claudia C, Sterba, Jaroslav, Jung, Shin, López-Aguilar, Enrique, Mora, Jaume, Carlotti, Carlos G, Olson, James M, Leary, Sarah, Cain, Jason, Krskova, Lenka, Zamecnik, Josef, Hawkins, Cynthia E, Tabori, Uri, Huang, Annie, Bartels, Ute, Northcott, Paul A, Taylor, Michael D, Yip, Stephen, Hansford, Jordan R, Bouffet, Eric, and Ramaswamy, Vijay

Subjects
Cancer, Clinical Research, Evaluation of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Adolescent, Antineoplastic Combined Chemotherapy Protocols, Biomarkers, Tumor, Cerebellar Neoplasms, Child, Cyclophosphamide, Female, Humans, Ifosfamide, Male, Medulloblastoma, Middle Aged, Neoplasm Recurrence, Local, Progression-Free Survival, medulloblastoma, WNT, genomics, cyclophosphamide, chemotherapy, prognosis, survival
Abstract

Over the past decade, wingless-activated (WNT) medulloblastoma has been identified as a candidate for therapy de-escalation based on excellent survival; however, a paucity of relapses has precluded additional analyses of markers of relapse. To address this gap in knowledge, an international cohort of 93 molecularly confirmed WNT MB was assembled, where 5-year progression-free survival is 0.84 (95%, 0.763-0.925) with 15 relapsed individuals identified. Maintenance chemotherapy is identified as a strong predictor of relapse, with individuals receiving high doses of cyclophosphamide or ifosphamide having only one very late molecularly confirmed relapse (p = 0.032). The anatomical location of recurrence is metastatic in 12 of 15 relapses, with 8 of 12 metastatic relapses in the lateral ventricles. Maintenance chemotherapy, specifically cumulative cyclophosphamide doses, is a significant predictor of relapse across WNT MB. Future efforts to de-escalate therapy need to carefully consider not only the radiation dose but also the chemotherapy regimen and the propensity for metastatic relapses.

Published
2020

6. Subgroup and subtype-specific outcomes in adult medulloblastoma

Author

Coltin, Hallie, Sundaresan, Lakshmikirupa, Smith, Kyle S., Skowron, Patryk, Massimi, Luca, Eberhart, Charles G., Schreck, Karisa C., Gupta, Nalin, Weiss, William A., Tirapelli, Daniela, Carlotti, Carlos, Li, Kay K. W., Ryzhova, Marina, Golanov, Andrey, Zheludkova, Olga, Absalyamova, Oksana, Okonechnikov, Konstantin, Stichel, Damian, von Deimling, Andreas, Giannini, Caterina, Raskin, Scott, Van Meir, Erwin G., Chan, Jennifer A., Fults, Daniel, Chambless, Lola B., Kim, Seung-Ki, Vasiljevic, Alexandre, Faure-Conter, Cecile, Vibhakar, Rajeev, Jung, Shin, Leary, Sarah, Mora, Jaume, McLendon, Roger E., Pollack, Ian F., Hauser, Peter, Grajkowska, Wieslawa A., Rubin, Joshua B., van Veelen, Marie-Lise C., French, Pim J., Kros, Johan M., Liau, Linda M., Pfister, Stefan M., Kool, Marcel, Kijima, Noriyuki, Taylor, Michael D., Packer, Roger J., Northcott, Paul A., Korshunov, Andrey, and Ramaswamy, Vijay

Published
2021
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7. Heterogeneity within the PF-EPN-B ependymoma subgroup

Author

Cavalli, Florence MG, Hübner, Jens-Martin, Sharma, Tanvi, Luu, Betty, Sill, Martin, Zapotocky, Michal, Mack, Stephen C, Witt, Hendrik, Lin, Tong, Shih, David JH, Ho, Ben, Santi, Mariarita, Emery, Lyndsey, Hukin, Juliette, Dunham, Christopher, McLendon, Roger E, Lipp, Eric S, Gururangan, Sridharan, Grossbach, Andrew, French, Pim, Kros, Johan M, van Veelen, Marie-Lise C, Rao, Amulya A Nageswara, Giannini, Caterina, Leary, Sarah, Jung, Shin, Faria, Claudia C, Mora, Jaume, Schüller, Ulrich, Alonso, Marta M, Chan, Jennifer A, Klekner, Almos, Chambless, Lola B, Hwang, Eugene I, Massimino, Maura, Eberhart, Charles G, Karajannis, Matthias A, Lu, Benjamin, Liau, Linda M, Zollo, Massimo, Ferrucci, Veronica, Carlotti, Carlos, Tirapelli, Daniela PC, Tabori, Uri, Bouffet, Eric, Ryzhova, Marina, Ellison, David W, Merchant, Thomas E, Gilbert, Mark R, Armstrong, Terri S, Korshunov, Andrey, Pfister, Stefan M, Taylor, Michael D, Aldape, Kenneth, Pajtler, Kristian W, Kool, Marcel, and Ramaswamy, Vijay

Subjects
Genetics, Cancer, Clinical Research, Rare Diseases, Human Genome, Brain Cancer, Brain Disorders, Adolescent, Adult, Age Factors, Child, Cohort Studies, DNA Copy Number Variations, DNA Methylation, Ependymoma, Female, Gene Expression Profiling, Humans, Infratentorial Neoplasms, Kaplan-Meier Estimate, Male, Microarray Analysis, Middle Aged, Young Adult, Posterior fossa, Subgrouping, PFB, PFA, Clustering, Clinical Sciences, Neurosciences, Neurology & Neurosurgery
Abstract

Posterior fossa ependymoma comprise three distinct molecular variants, termed PF-EPN-A (PFA), PF-EPN-B (PFB), and PF-EPN-SE (subependymoma). Clinically, they are very disparate and PFB tumors are currently being considered for a trial of radiation avoidance. However, to move forward, unraveling the heterogeneity within PFB would be highly desirable. To discern the molecular heterogeneity within PFB, we performed an integrated analysis consisting of DNA methylation profiling, copy-number profiling, gene expression profiling, and clinical correlation across a cohort of 212 primary posterior fossa PFB tumors. Unsupervised spectral clustering and t-SNE analysis of genome-wide methylation data revealed five distinct subtypes of PFB tumors, termed PFB1-5, with distinct demographics, copy-number alterations, and gene expression profiles. All PFB subtypes were distinct from PFA and posterior fossa subependymomas. Of the five subtypes, PFB4 and PFB5 are more discrete, consisting of younger and older patients, respectively, with a strong female-gender enrichment in PFB5 (age: p = 0.011, gender: p = 0.04). Broad copy-number aberrations were common; however, many events such as chromosome 2 loss, 5 gain, and 17 loss were enriched in specific subtypes and 1q gain was enriched in PFB1. Late relapses were common across all five subtypes, but deaths were uncommon and present in only two subtypes (PFB1 and PFB3). Unlike the case in PFA ependymoma, 1q gain was not a robust marker of poor progression-free survival; however, chromosome 13q loss may represent a novel marker for risk stratification across the spectrum of PFB subtypes. Similar to PFA ependymoma, there exists a significant intertumoral heterogeneity within PFB, with distinct molecular subtypes identified. Even when accounting for this heterogeneity, extent of resection remains the strongest predictor of poor outcome. However, this biological heterogeneity must be accounted for in future preclinical modeling and personalized therapies.

Published
2018

8. The whole-genome landscape of medulloblastoma subtypes

Author

Northcott, Paul A, Buchhalter, Ivo, Morrissy, A Sorana, Hovestadt, Volker, Weischenfeldt, Joachim, Ehrenberger, Tobias, Gröbner, Susanne, Segura-Wang, Maia, Zichner, Thomas, Rudneva, Vasilisa A, Warnatz, Hans-Jörg, Sidiropoulos, Nikos, Phillips, Aaron H, Schumacher, Steven, Kleinheinz, Kortine, Waszak, Sebastian M, Erkek, Serap, Jones, David TW, Worst, Barbara C, Kool, Marcel, Zapatka, Marc, Jäger, Natalie, Chavez, Lukas, Hutter, Barbara, Bieg, Matthias, Paramasivam, Nagarajan, Heinold, Michael, Gu, Zuguang, Ishaque, Naveed, Jäger-Schmidt, Christina, Imbusch, Charles D, Jugold, Alke, Hübschmann, Daniel, Risch, Thomas, Amstislavskiy, Vyacheslav, Gonzalez, Francisco German Rodriguez, Weber, Ursula D, Wolf, Stephan, Robinson, Giles W, Zhou, Xin, Wu, Gang, Finkelstein, David, Liu, Yanling, Cavalli, Florence MG, Luu, Betty, Ramaswamy, Vijay, Wu, Xiaochong, Koster, Jan, Ryzhova, Marina, Cho, Yoon-Jae, Pomeroy, Scott L, Herold-Mende, Christel, Schuhmann, Martin, Ebinger, Martin, Liau, Linda M, Mora, Jaume, McLendon, Roger E, Jabado, Nada, Kumabe, Toshihiro, Chuah, Eric, Ma, Yussanne, Moore, Richard A, Mungall, Andrew J, Mungall, Karen L, Thiessen, Nina, Tse, Kane, Wong, Tina, Jones, Steven JM, Witt, Olaf, Milde, Till, Von Deimling, Andreas, Capper, David, Korshunov, Andrey, Yaspo, Marie-Laure, Kriwacki, Richard, Gajjar, Amar, Zhang, Jinghui, Beroukhim, Rameen, Fraenkel, Ernest, Korbel, Jan O, Brors, Benedikt, Schlesner, Matthias, Eils, Roland, Marra, Marco A, Pfister, Stefan M, Taylor, Michael D, and Lichter, Peter

Subjects
Cancer, Human Genome, Brain Disorders, Pediatric Cancer, Brain Cancer, Genetics, Biotechnology, Rare Diseases, Neurosciences, Pediatric, Aetiology, 2.1 Biological and endogenous factors, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Good Health and Well Being, Carcinogenesis, Carrier Proteins, Cohort Studies, DNA Methylation, DNA Mutational Analysis, Datasets as Topic, Epistasis, Genetic, Genome, Human, Genomics, Humans, Medulloblastoma, Molecular Targeted Therapy, Muscle Proteins, Mutation, Oncogenes, Transcription Factors, Whole Genome Sequencing, Wnt Proteins, General Science & Technology
Abstract

Current therapies for medulloblastoma, a highly malignant childhood brain tumour, impose debilitating effects on the developing child, and highlight the need for molecularly targeted treatments with reduced toxicity. Previous studies have been unable to identify the full spectrum of driver genes and molecular processes that operate in medulloblastoma subgroups. Here we analyse the somatic landscape across 491 sequenced medulloblastoma samples and the molecular heterogeneity among 1,256 epigenetically analysed cases, and identify subgroup-specific driver alterations that include previously undiscovered actionable targets. Driver mutations were confidently assigned to most patients belonging to Group 3 and Group 4 medulloblastoma subgroups, greatly enhancing previous knowledge. New molecular subtypes were differentially enriched for specific driver events, including hotspot in-frame insertions that target KBTBD4 and 'enhancer hijacking' events that activate PRDM6. Thus, the application of integrative genomics to an extensive cohort of clinical samples derived from a single childhood cancer entity revealed a series of cancer genes and biologically relevant subtype diversity that represent attractive therapeutic targets for the treatment of patients with medulloblastoma.

Published
2017

9. 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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10. 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

11. 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

12. Very low mutation burden is a feature of inflamed recurrent glioblastomas responsive to cancer immunotherapy

Author

Gromeier, Matthias, Brown, Michael C., Zhang, Gao, Lin, Xiang, Chen, Yeqing, Wei, Zhi, Beaubier, Nike, Yan, Hai, He, Yiping, Desjardins, Annick, Herndon, II, James E., Varn, Frederick S., Verhaak, Roel G., Zhao, Junfei, Bolognesi, Dani P., Friedman, Allan H., Friedman, Henry S., McSherry, Frances, Muscat, Andrea M., Lipp, Eric S., Nair, Smita K., Khasraw, Mustafa, Peters, Katherine B., Randazzo, Dina, Sampson, John H., McLendon, Roger E., Bigner, Darell D., and Ashley, David M.

Published
2021
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14. EGFR phosphorylation of DCBLD2 recruits TRAF6 and stimulates AKT-promoted tumorigenesis

Author

Feng, Haizhong, Lopez, Giselle Y, Kim, Chung Kwon, Alvarez, Angel, Duncan, Christopher G, Nishikawa, Ryo, Nagane, Motoo, Su, An-Jey A, Auron, Philip E, Hedberg, Matthew L, Wang, Lin, Raizer, Jeffery J, Kessler, John A, Parsa, Andrew T, Gao, Wei-Qiang, Kim, Sung-Hak, Minata, Mutsuko, Nakano, Ichiro, Grandis, Jennifer R, McLendon, Roger E, Bigner, Darell D, Lin, Hui-Kuan, Furnari, Frank B, Cavenee, Webster K, Hu, Bo, Yan, Hai, and Cheng, Shi-Yuan

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Biological Sciences, Rare Diseases, Cancer, 2.1 Biological and endogenous factors, Aetiology, Brain Neoplasms, Carcinogenesis, Cells, Cultured, ErbB Receptors, Glioma, Head and Neck Neoplasms, Humans, Membrane Proteins, Phosphorylation, Proto-Oncogene Proteins c-akt, Signal Transduction, TNF Receptor-Associated Factor 6, Medical and Health Sciences, Immunology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Aberrant activation of EGFR in human cancers promotes tumorigenesis through stimulation of AKT signaling. Here, we determined that the discoidina neuropilin-like membrane protein DCBLD2 is upregulated in clinical specimens of glioblastomas and head and neck cancers (HNCs) and is required for EGFR-stimulated tumorigenesis. In multiple cancer cell lines, EGFR activated phosphorylation of tyrosine 750 (Y750) of DCBLD2, which is located within a recently identified binding motif for TNF receptor-associated factor 6 (TRAF6). Consequently, phosphorylation of DCBLD2 Y750 recruited TRAF6, leading to increased TRAF6 E3 ubiquitin ligase activity and subsequent activation of AKT, thereby enhancing EGFR-driven tumorigenesis. Moreover, evaluation of patient samples of gliomas and HNCs revealed an association among EGFR activation, DCBLD2 phosphorylation, and poor prognoses. Together, our findings uncover a pathway in which DCBLD2 functions as a signal relay for oncogenic EGFR signaling to promote tumorigenesis and suggest DCBLD2 and TRAF6 as potential therapeutic targets for human cancers that are associated with EGFR activation.

Published
2014

15. Repurposing Clemastine to Target Glioblastoma Cell Stemness

Author

Sun, Michael A., primary, Yang, Rui, additional, Liu, Heng, additional, Wang, Wenzhe, additional, Song, Xiao, additional, Hu, Bo, additional, Reynolds, Nathan, additional, Roso, Kristen, additional, Chen, Lee H., additional, Greer, Paula K., additional, Keir, Stephen T., additional, McLendon, Roger E., additional, Cheng, Shi-Yuan, additional, Bigner, Darell D., additional, Ashley, David M., additional, Pirozzi, Christopher J., additional, and He, Yiping, additional

Published
2023
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19. Subgroup-specific structural variation across 1,000 medulloblastoma genomes.

Author

Northcott, Paul A, Shih, David JH, Peacock, John, Garzia, Livia, Morrissy, A Sorana, Zichner, Thomas, Stütz, Adrian M, Korshunov, Andrey, Reimand, Jüri, Schumacher, Steven E, Beroukhim, Rameen, Ellison, David W, Marshall, Christian R, Lionel, Anath C, Mack, Stephen, Dubuc, Adrian, Yao, Yuan, Ramaswamy, Vijay, Luu, Betty, Rolider, Adi, Cavalli, Florence MG, Wang, Xin, Remke, Marc, Wu, Xiaochong, Chiu, Readman YB, Chu, Andy, Chuah, Eric, Corbett, Richard D, Hoad, Gemma R, Jackman, Shaun D, Li, Yisu, Lo, Allan, Mungall, Karen L, Nip, Ka Ming, Qian, Jenny Q, Raymond, Anthony GJ, Thiessen, Nina T, Varhol, Richard J, Birol, Inanc, Moore, Richard A, Mungall, Andrew J, Holt, Robert, Kawauchi, Daisuke, Roussel, Martine F, Kool, Marcel, Jones, David TW, Witt, Hendrick, Fernandez-L, Africa, Kenney, Anna M, Wechsler-Reya, Robert J, Dirks, Peter, Aviv, Tzvi, Grajkowska, Wieslawa A, Perek-Polnik, Marta, Haberler, Christine C, Delattre, Olivier, Reynaud, Stéphanie S, Doz, François F, Pernet-Fattet, Sarah S, Cho, Byung-Kyu, Kim, Seung-Ki, Wang, Kyu-Chang, Scheurlen, Wolfram, Eberhart, Charles G, Fèvre-Montange, Michelle, Jouvet, Anne, Pollack, Ian F, Fan, Xing, Muraszko, Karin M, Gillespie, G Yancey, Di Rocco, Concezio, Massimi, Luca, Michiels, Erna MC, Kloosterhof, Nanne K, French, Pim J, Kros, Johan M, Olson, James M, Ellenbogen, Richard G, Zitterbart, Karel, Kren, Leos, Thompson, Reid C, Cooper, Michael K, Lach, Boleslaw, McLendon, Roger E, Bigner, Darell D, Fontebasso, Adam, Albrecht, Steffen, Jabado, Nada, Lindsey, Janet C, Bailey, Simon, Gupta, Nalin, Weiss, William A, Bognár, László, Klekner, Almos, Van Meter, Timothy E, Kumabe, Toshihiro, Tominaga, Teiji, Elbabaa, Samer K, Leonard, Jeffrey R, and Rubin, Joshua B

Subjects
Humans, Medulloblastoma, Cerebellar Neoplasms, Translocation, Genetic, Transforming Growth Factor beta, Proteins, Carrier Proteins, NF-kappa B, Oncogene Proteins, Fusion, Nerve Tissue Proteins, Genomics, Signal Transduction, Gene Duplication, Genes, myc, Genome, Human, Child, Hedgehog Proteins, Genomic Structural Variation, DNA Copy Number Variations, RNA, Long Noncoding, Pediatric, Neurosciences, Genetics, Brain Disorders, Pediatric Research Initiative, Brain Cancer, Cancer, Rare Diseases, Pediatric Cancer, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, General Science & Technology
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 Parkinson's 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

21. Supplementary Table 2 from Mutant IDH1 Disrupts the Mouse Subventricular Zone and Alters Brain Tumor Progression

Author

Pirozzi, Christopher J., primary, Carpenter, Austin B., primary, Waitkus, Matthew S., primary, Wang, Catherine Y., primary, Zhu, Huishan, primary, Hansen, Landon J., primary, Chen, Lee H., primary, Greer, Paula K., primary, Feng, Jie, primary, Wang, Yu, primary, Bock, Cheryl B., primary, Fan, Ping, primary, Spasojevic, Ivan, primary, McLendon, Roger E., primary, Bigner, Darell D., primary, He, Yiping, primary, and Yan, Hai, primary

Published
2023
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22. Supplementary Table 3 from Mutant IDH1 Disrupts the Mouse Subventricular Zone and Alters Brain Tumor Progression

Author

Pirozzi, Christopher J., primary, Carpenter, Austin B., primary, Waitkus, Matthew S., primary, Wang, Catherine Y., primary, Zhu, Huishan, primary, Hansen, Landon J., primary, Chen, Lee H., primary, Greer, Paula K., primary, Feng, Jie, primary, Wang, Yu, primary, Bock, Cheryl B., primary, Fan, Ping, primary, Spasojevic, Ivan, primary, McLendon, Roger E., primary, Bigner, Darell D., primary, He, Yiping, primary, and Yan, Hai, primary

Published
2023
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26. Supplementary Figures 1 through 5 from Mutant IDH1 Disrupts the Mouse Subventricular Zone and Alters Brain Tumor Progression

Author

Pirozzi, Christopher J., primary, Carpenter, Austin B., primary, Waitkus, Matthew S., primary, Wang, Catherine Y., primary, Zhu, Huishan, primary, Hansen, Landon J., primary, Chen, Lee H., primary, Greer, Paula K., primary, Feng, Jie, primary, Wang, Yu, primary, Bock, Cheryl B., primary, Fan, Ping, primary, Spasojevic, Ivan, primary, McLendon, Roger E., primary, Bigner, Darell D., primary, He, Yiping, primary, and Yan, Hai, primary

Published
2023
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27. Data from Mutant IDH1 Disrupts the Mouse Subventricular Zone and Alters Brain Tumor Progression

Author

Pirozzi, Christopher J., primary, Carpenter, Austin B., primary, Waitkus, Matthew S., primary, Wang, Catherine Y., primary, Zhu, Huishan, primary, Hansen, Landon J., primary, Chen, Lee H., primary, Greer, Paula K., primary, Feng, Jie, primary, Wang, Yu, primary, Bock, Cheryl B., primary, Fan, Ping, primary, Spasojevic, Ivan, primary, McLendon, Roger E., primary, Bigner, Darell D., primary, He, Yiping, primary, and Yan, Hai, primary

Published
2023
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32. Supplementary Materials and Methods from Mutant IDH1 Disrupts the Mouse Subventricular Zone and Alters Brain Tumor Progression

Author

Pirozzi, Christopher J., primary, Carpenter, Austin B., primary, Waitkus, Matthew S., primary, Wang, Catherine Y., primary, Zhu, Huishan, primary, Hansen, Landon J., primary, Chen, Lee H., primary, Greer, Paula K., primary, Feng, Jie, primary, Wang, Yu, primary, Bock, Cheryl B., primary, Fan, Ping, primary, Spasojevic, Ivan, primary, McLendon, Roger E., primary, Bigner, Darell D., primary, He, Yiping, primary, and Yan, Hai, primary

Published
2023
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36. Supplementary Table 1 from Mutant IDH1 Disrupts the Mouse Subventricular Zone and Alters Brain Tumor Progression

Author

Pirozzi, Christopher J., primary, Carpenter, Austin B., primary, Waitkus, Matthew S., primary, Wang, Catherine Y., primary, Zhu, Huishan, primary, Hansen, Landon J., primary, Chen, Lee H., primary, Greer, Paula K., primary, Feng, Jie, primary, Wang, Yu, primary, Bock, Cheryl B., primary, Fan, Ping, primary, Spasojevic, Ivan, primary, McLendon, Roger E., primary, Bigner, Darell D., primary, He, Yiping, primary, and Yan, Hai, primary

Published
2023
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37. Supplementary Figure Legends from A Modified Nucleoside 6-Thio-2′-Deoxyguanosine Exhibits Antitumor Activity in Gliomas

Author

Yu, Shengnan, primary, Wei, Shiyou, primary, Savani, Milan, primary, Lin, Xiang, primary, Du, Kuang, primary, Mender, Ilgen, primary, Siteni, Silvia, primary, Vasilopoulos, Themistoklis, primary, Reitman, Zachary J., primary, Ku, Yin, primary, Wu, Di, primary, Liu, Hao, primary, Tian, Meng, primary, Chen, Yaohui, primary, Labrie, Marilyne, primary, Charbonneau, Casey M., primary, Sugarman, Eric, primary, Bowie, Michelle, primary, Hariharan, Seethalakshmi, primary, Waitkus, Matthew, primary, Jiang, Wen, primary, McLendon, Roger E., primary, Pan, Edward, primary, Khasraw, Mustafa, primary, Walsh, Kyle M., primary, Lu, Yiling, primary, Herlyn, Meenhard, primary, Mills, Gordon, primary, Herbig, Utz, primary, Wei, Zhi, primary, Keir, Stephen T., primary, Flaherty, Keith, primary, Liu, Lunxu, primary, Wu, Kongming, primary, Shay, Jerry W., primary, Abdullah, Kalil, primary, Zhang, Gao, primary, and Ashley, David M., primary

Published
2023
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38. Supplementary fig 2 from A Modified Nucleoside 6-Thio-2′-Deoxyguanosine Exhibits Antitumor Activity in Gliomas

Author

Yu, Shengnan, primary, Wei, Shiyou, primary, Savani, Milan, primary, Lin, Xiang, primary, Du, Kuang, primary, Mender, Ilgen, primary, Siteni, Silvia, primary, Vasilopoulos, Themistoklis, primary, Reitman, Zachary J., primary, Ku, Yin, primary, Wu, Di, primary, Liu, Hao, primary, Tian, Meng, primary, Chen, Yaohui, primary, Labrie, Marilyne, primary, Charbonneau, Casey M., primary, Sugarman, Eric, primary, Bowie, Michelle, primary, Hariharan, Seethalakshmi, primary, Waitkus, Matthew, primary, Jiang, Wen, primary, McLendon, Roger E., primary, Pan, Edward, primary, Khasraw, Mustafa, primary, Walsh, Kyle M., primary, Lu, Yiling, primary, Herlyn, Meenhard, primary, Mills, Gordon, primary, Herbig, Utz, primary, Wei, Zhi, primary, Keir, Stephen T., primary, Flaherty, Keith, primary, Liu, Lunxu, primary, Wu, Kongming, primary, Shay, Jerry W., primary, Abdullah, Kalil, primary, Zhang, Gao, primary, and Ashley, David M., primary

Published
2023
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39. Supplementary Table S2 from Cic Loss Promotes Gliomagenesis via Aberrant Neural Stem Cell Proliferation and Differentiation

Author

Yang, Rui, primary, Chen, Lee H., primary, Hansen, Landon J., primary, Carpenter, Austin B., primary, Moure, Casey J., primary, Liu, Heng, primary, Pirozzi, Christopher J., primary, Diplas, Bill H., primary, Waitkus, Matthew S., primary, Greer, Paula K., primary, Zhu, Huishan, primary, McLendon, Roger E., primary, Bigner, Darell D., primary, He, Yiping, primary, and Yan, Hai, primary

Published
2023
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40. Supplementary Figure 7 from Differential Immune Microenvironments and Response to Immune Checkpoint Blockade among Molecular Subtypes of Murine Medulloblastoma

Author

Pham, Christina D., primary, Flores, Catherine, primary, Yang, Changlin, primary, Pinheiro, Elaine M., primary, Yearley, Jennifer H., primary, Sayour, Elias J., primary, Pei, Yanxin, primary, Moore, Colin, primary, McLendon, Roger E., primary, Huang, Jianping, primary, Sampson, John H., primary, Wechsler-Reya, Robert, primary, and Mitchell, Duane A., primary

Published
2023
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41. Figure S4 from A Three-Dimensional Organoid Culture System Derived from Human Glioblastomas Recapitulates the Hypoxic Gradients and Cancer Stem Cell Heterogeneity of Tumors Found In Vivo

Author

Hubert, Christopher G., primary, Rivera, Maricruz, primary, Spangler, Lisa C., primary, Wu, Qiulian, primary, Mack, Stephen C., primary, Prager, Briana C., primary, Couce, Marta, primary, McLendon, Roger E., primary, Sloan, Andrew E., primary, and Rich, Jeremy N., primary

Published
2023
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42. Data from Cic Loss Promotes Gliomagenesis via Aberrant Neural Stem Cell Proliferation and Differentiation

Author

Yang, Rui, primary, Chen, Lee H., primary, Hansen, Landon J., primary, Carpenter, Austin B., primary, Moure, Casey J., primary, Liu, Heng, primary, Pirozzi, Christopher J., primary, Diplas, Bill H., primary, Waitkus, Matthew S., primary, Greer, Paula K., primary, Zhu, Huishan, primary, McLendon, Roger E., primary, Bigner, Darell D., primary, He, Yiping, primary, and Yan, Hai, primary

Published
2023
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43. Supplementary Data from Long-term Survival in Glioblastoma with Cytomegalovirus pp65-Targeted Vaccination

Author

Batich, Kristen A., primary, Reap, Elizabeth A., primary, Archer, Gary E., primary, Sanchez-Perez, Luis, primary, Nair, Smita K., primary, Schmittling, Robert J., primary, Norberg, Pam, primary, Xie, Weihua, primary, Herndon, James E., primary, Healy, Patrick, primary, McLendon, Roger E., primary, Friedman, Allan H., primary, Friedman, Henry S., primary, Bigner, Darell, primary, Vlahovic, Gordana, primary, Mitchell, Duane A., primary, and Sampson, John H., primary

Published
2023
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44. Supplementary fig 6 from A Modified Nucleoside 6-Thio-2′-Deoxyguanosine Exhibits Antitumor Activity in Gliomas

Author

Yu, Shengnan, primary, Wei, Shiyou, primary, Savani, Milan, primary, Lin, Xiang, primary, Du, Kuang, primary, Mender, Ilgen, primary, Siteni, Silvia, primary, Vasilopoulos, Themistoklis, primary, Reitman, Zachary J., primary, Ku, Yin, primary, Wu, Di, primary, Liu, Hao, primary, Tian, Meng, primary, Chen, Yaohui, primary, Labrie, Marilyne, primary, Charbonneau, Casey M., primary, Sugarman, Eric, primary, Bowie, Michelle, primary, Hariharan, Seethalakshmi, primary, Waitkus, Matthew, primary, Jiang, Wen, primary, McLendon, Roger E., primary, Pan, Edward, primary, Khasraw, Mustafa, primary, Walsh, Kyle M., primary, Lu, Yiling, primary, Herlyn, Meenhard, primary, Mills, Gordon, primary, Herbig, Utz, primary, Wei, Zhi, primary, Keir, Stephen T., primary, Flaherty, Keith, primary, Liu, Lunxu, primary, Wu, Kongming, primary, Shay, Jerry W., primary, Abdullah, Kalil, primary, Zhang, Gao, primary, and Ashley, David M., primary

Published
2023
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45. Data from Dendritic Cells Enhance Polyfunctionality of Adoptively Transferred T Cells That Target Cytomegalovirus in Glioblastoma

Author

Reap, Elizabeth A., primary, Suryadevara, Carter M., primary, Batich, Kristen A., primary, Sanchez-Perez, Luis, primary, Archer, Gary E., primary, Schmittling, Robert J., primary, Norberg, Pamela K., primary, Herndon, James E., primary, Healy, Patrick, primary, Congdon, Kendra L., primary, Gedeon, Patrick C., primary, Campbell, Olivia C., primary, Swartz, Adam M., primary, Riccione, Katherine A., primary, Yi, John S., primary, Hossain-Ibrahim, Mohammed K., primary, Saraswathula, Anirudh, primary, Nair, Smita K., primary, Dunn-Pirio, Anastasie M., primary, Broome, Taylor M., primary, Weinhold, Kent J., primary, Desjardins, Annick, primary, Vlahovic, Gordana, primary, McLendon, Roger E., primary, Friedman, Allan H., primary, Friedman, Henry S., primary, Bigner, Darell D., primary, Fecci, Peter E., primary, Mitchell, Duane A., primary, and Sampson, John H., primary

Published
2023
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46. Supplementary fig 4 from A Modified Nucleoside 6-Thio-2′-Deoxyguanosine Exhibits Antitumor Activity in Gliomas

Author

Yu, Shengnan, primary, Wei, Shiyou, primary, Savani, Milan, primary, Lin, Xiang, primary, Du, Kuang, primary, Mender, Ilgen, primary, Siteni, Silvia, primary, Vasilopoulos, Themistoklis, primary, Reitman, Zachary J., primary, Ku, Yin, primary, Wu, Di, primary, Liu, Hao, primary, Tian, Meng, primary, Chen, Yaohui, primary, Labrie, Marilyne, primary, Charbonneau, Casey M., primary, Sugarman, Eric, primary, Bowie, Michelle, primary, Hariharan, Seethalakshmi, primary, Waitkus, Matthew, primary, Jiang, Wen, primary, McLendon, Roger E., primary, Pan, Edward, primary, Khasraw, Mustafa, primary, Walsh, Kyle M., primary, Lu, Yiling, primary, Herlyn, Meenhard, primary, Mills, Gordon, primary, Herbig, Utz, primary, Wei, Zhi, primary, Keir, Stephen T., primary, Flaherty, Keith, primary, Liu, Lunxu, primary, Wu, Kongming, primary, Shay, Jerry W., primary, Abdullah, Kalil, primary, Zhang, Gao, primary, and Ashley, David M., primary

Published
2023
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47. Figure S1_S2 from Cic Loss Promotes Gliomagenesis via Aberrant Neural Stem Cell Proliferation and Differentiation

Author

Yang, Rui, primary, Chen, Lee H., primary, Hansen, Landon J., primary, Carpenter, Austin B., primary, Moure, Casey J., primary, Liu, Heng, primary, Pirozzi, Christopher J., primary, Diplas, Bill H., primary, Waitkus, Matthew S., primary, Greer, Paula K., primary, Zhu, Huishan, primary, McLendon, Roger E., primary, Bigner, Darell D., primary, He, Yiping, primary, and Yan, Hai, primary

Published
2023
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48. Supplementary Tables from A Modified Nucleoside 6-Thio-2′-Deoxyguanosine Exhibits Antitumor Activity in Gliomas

Author

Yu, Shengnan, primary, Wei, Shiyou, primary, Savani, Milan, primary, Lin, Xiang, primary, Du, Kuang, primary, Mender, Ilgen, primary, Siteni, Silvia, primary, Vasilopoulos, Themistoklis, primary, Reitman, Zachary J., primary, Ku, Yin, primary, Wu, Di, primary, Liu, Hao, primary, Tian, Meng, primary, Chen, Yaohui, primary, Labrie, Marilyne, primary, Charbonneau, Casey M., primary, Sugarman, Eric, primary, Bowie, Michelle, primary, Hariharan, Seethalakshmi, primary, Waitkus, Matthew, primary, Jiang, Wen, primary, McLendon, Roger E., primary, Pan, Edward, primary, Khasraw, Mustafa, primary, Walsh, Kyle M., primary, Lu, Yiling, primary, Herlyn, Meenhard, primary, Mills, Gordon, primary, Herbig, Utz, primary, Wei, Zhi, primary, Keir, Stephen T., primary, Flaherty, Keith, primary, Liu, Lunxu, primary, Wu, Kongming, primary, Shay, Jerry W., primary, Abdullah, Kalil, primary, Zhang, Gao, primary, and Ashley, David M., primary

Published
2023
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49. Table S2 from A Rationally Designed Fully Human EGFRvIII:CD3-Targeted Bispecific Antibody Redirects Human T Cells to Treat Patient-derived Intracerebral Malignant Glioma

Author

Gedeon, Patrick C., primary, Schaller, Teilo H., primary, Chitneni, Satish K., primary, Choi, Bryan D., primary, Kuan, Chien-Tsun, primary, Suryadevara, Carter M., primary, Snyder, David J., primary, Schmittling, Robert J., primary, Szafranski, Scott E., primary, Cui, Xiuyu, primary, Healy, Patrick N., primary, Herndon, James E., primary, McLendon, Roger E., primary, Keir, Stephen T., primary, Archer, Gary E., primary, Reap, Elizabeth A., primary, Sanchez-Perez, Luis, primary, Bigner, Darell D., primary, and Sampson, John H., primary

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2023
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50. Supplementary fig 3 from A Modified Nucleoside 6-Thio-2′-Deoxyguanosine Exhibits Antitumor Activity in Gliomas

Author

Yu, Shengnan, primary, Wei, Shiyou, primary, Savani, Milan, primary, Lin, Xiang, primary, Du, Kuang, primary, Mender, Ilgen, primary, Siteni, Silvia, primary, Vasilopoulos, Themistoklis, primary, Reitman, Zachary J., primary, Ku, Yin, primary, Wu, Di, primary, Liu, Hao, primary, Tian, Meng, primary, Chen, Yaohui, primary, Labrie, Marilyne, primary, Charbonneau, Casey M., primary, Sugarman, Eric, primary, Bowie, Michelle, primary, Hariharan, Seethalakshmi, primary, Waitkus, Matthew, primary, Jiang, Wen, primary, McLendon, Roger E., primary, Pan, Edward, primary, Khasraw, Mustafa, primary, Walsh, Kyle M., primary, Lu, Yiling, primary, Herlyn, Meenhard, primary, Mills, Gordon, primary, Herbig, Utz, primary, Wei, Zhi, primary, Keir, Stephen T., primary, Flaherty, Keith, primary, Liu, Lunxu, primary, Wu, Kongming, primary, Shay, Jerry W., primary, Abdullah, Kalil, primary, Zhang, Gao, primary, and Ashley, David M., primary

Published
2023
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