7 results on '"Northcott, Paul A"'
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2. UTX-mediated enhancer and chromatin remodeling suppresses myeloid leukemogenesis through noncatalytic inverse regulation of ETS and GATA programs
- Author
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Gozdecka, Malgorzata, Meduri, Eshwar, Mazan, Milena, Tzelepis, Konstantinos, Dudek, Monika, Knights, Andrew J., Pardo, Mercedes, Yu, Lu, Choudhary, Jyoti S., Metzakopian, Emmanouil, Iyer, Vivek, Yun, Haiyang, Park, Naomi, Varela, Ignacio, Bautista, Ruben, Collord, Grace, Dovey, Oliver, Garyfallos, Dimitrios A., De Braekeleer, Etienne, Kondo, Saki, Cooper, Jonathan, Göttgens, Berthold, Bullinger, Lars, Northcott, Paul A., Adams, David, Vassiliou, George S., and Huntly, Brian J. P.
- Published
- 2018
- Full Text
- View/download PDF
3. Spatial heterogeneity in medulloblastoma
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Morrissy, A Sorana, primary, Cavalli, Florence M G, additional, Remke, Marc, additional, Ramaswamy, Vijay, additional, Shih, David J H, additional, Holgado, Borja L, additional, Farooq, Hamza, additional, Donovan, Laura K, additional, Garzia, Livia, additional, Agnihotri, Sameer, additional, Kiehna, Erin N, additional, Mercier, Eloi, additional, Mayoh, Chelsea, additional, Papillon-Cavanagh, Simon, additional, Nikbakht, Hamid, additional, Gayden, Tenzin, additional, Torchia, Jonathon, additional, Picard, Daniel, additional, Merino, Diana M, additional, Vladoiu, Maria, additional, Luu, Betty, additional, Wu, Xiaochong, additional, Daniels, Craig, additional, Horswell, Stuart, additional, Thompson, Yuan Yao, additional, Hovestadt, Volker, additional, Northcott, Paul A, additional, Jones, David T W, additional, Peacock, John, additional, Wang, Xin, additional, Mack, Stephen C, additional, Reimand, Jüri, additional, Albrecht, Steffen, additional, Fontebasso, Adam M, additional, Thiessen, Nina, additional, Li, Yisu, additional, Schein, Jacqueline E, additional, Lee, Darlene, additional, Carlsen, Rebecca, additional, Mayo, Michael, additional, Tse, Kane, additional, Tam, Angela, additional, Dhalla, Noreen, additional, Ally, Adrian, additional, Chuah, Eric, additional, Cheng, Young, additional, Plettner, Patrick, additional, Li, Haiyan I, additional, Corbett, Richard D, additional, Wong, Tina, additional, Long, William, additional, Loukides, James, additional, Buczkowicz, Pawel, additional, Hawkins, Cynthia E, additional, Tabori, Uri, additional, Rood, Brian R, additional, Myseros, John S, additional, Packer, Roger J, additional, Korshunov, Andrey, additional, Lichter, Peter, additional, Kool, Marcel, additional, Pfister, Stefan M, additional, Schüller, Ulrich, additional, Dirks, Peter, additional, Huang, Annie, additional, Bouffet, Eric, additional, Rutka, James T, additional, Bader, Gary D, additional, Swanton, Charles, additional, Ma, Yusanne, additional, Moore, Richard A, additional, Mungall, Andrew J, additional, Majewski, Jacek, additional, Jones, Steven J M, additional, Das, Sunit, additional, Malkin, David, additional, Jabado, Nada, additional, Marra, Marco A, additional, and Taylor, Michael D, additional
- Published
- 2017
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4. Pan-cancer analysis of somatic copy-number alterations implicates IRS4 and IGF2 in enhancer hijacking
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Weischenfeldt, Joachim, primary, Dubash, Taronish, additional, Drainas, Alexandros P, additional, Mardin, Balca R, additional, Chen, Yuanyuan, additional, Stütz, Adrian M, additional, Waszak, Sebastian M, additional, Bosco, Graziella, additional, Halvorsen, Ann Rita, additional, Raeder, Benjamin, additional, Efthymiopoulos, Theocharis, additional, Erkek, Serap, additional, Siegl, Christine, additional, Brenner, Hermann, additional, Brustugun, Odd Terje, additional, Dieter, Sebastian M, additional, Northcott, Paul A, additional, Petersen, Iver, additional, Pfister, Stefan M, additional, Schneider, Martin, additional, Solberg, Steinar K, additional, Thunissen, Erik, additional, Weichert, Wilko, additional, Zichner, Thomas, additional, Thomas, Roman, additional, Peifer, Martin, additional, Helland, Aslaug, additional, Ball, Claudia R, additional, Jechlinger, Martin, additional, Sotillo, Rocio, additional, Glimm, Hanno, additional, and Korbel, Jan O, additional
- Published
- 2016
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5. Pan-cancer analysis of somatic copy-number alterations implicates IRS4 and IGF2 in enhancer hijacking
- Author
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Weischenfeldt, Joachim, Dubash, Taronish, Drainas, Alexandros P, Mardin, Balca R, Chen, Yuanyuan, Stütz, Adrian M, Waszak, Sebastian M, Bosco, Graziella, Halvorsen, Ann Rita, Raeder, Benjamin, Efthymiopoulos, Theocharis, Erkek, Serap, Siegl, Christine, Brenner, Hermann, Brustugun, Odd Terje, Dieter, Sebastian M, Northcott, Paul A, Petersen, Iver, Pfister, Stefan M, Schneider, Martin, Solberg, Steinar K, Thunissen, Erik, Weichert, Wilko, Zichner, Thomas, Thomas, Roman, Peifer, Martin, Helland, Aslaug, Ball, Claudia R, Jechlinger, Martin, Sotillo, Rocio, Glimm, Hanno, and Korbel, Jan O
- Abstract
Extensive prior research focused on somatic copy-number alterations (SCNAs) affecting cancer genes, yet the extent to which recurrent SCNAs exert their influence through rearrangement of cis-regulatory elements (CREs) remains unclear. Here we present a framework for inferring cancer-related gene overexpression resulting from CRE reorganization (e.g., enhancer hijacking) by integrating SCNAs, gene expression data and information on topologically associating domains (TADs). Analysis of 7,416 cancer genomes uncovered several pan-cancer candidate genes, including IRS4, SMARCA1 and TERT. We demonstrate that IRS4 overexpression in lung cancer is associated with recurrent deletions in cis, and we present evidence supporting a tumor-promoting role. We additionally pursued cancer-type-specific analyses and uncovered IGF2 as a target for enhancer hijacking in colorectal cancer. Recurrent tandem duplications intersecting with a TAD boundary mediate de novo formation of a 3D contact domain comprising IGF2 and a lineage-specific super-enhancer, resulting in high-level gene activation. Our framework enables systematic inference of CRE rearrangements mediating dysregulation in cancer.
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- 2017
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6. Multiple recurrent genetic events converge on control of histone lysine methylation in medulloblastoma
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Northcott, Paul A, primary, Nakahara, Yukiko, additional, Wu, Xiaochong, additional, Feuk, Lars, additional, Ellison, David W, additional, Croul, Sid, additional, Mack, Stephen, additional, Kongkham, Paul N, additional, Peacock, John, additional, Dubuc, Adrian, additional, Ra, Young-Shin, additional, Zilberberg, Karen, additional, Mcleod, Jessica, additional, Scherer, Stephen W, additional, Sunil Rao, J, additional, Eberhart, Charles G, additional, Grajkowska, Wiesia, additional, Gillespie, Yancey, additional, Lach, Boleslaw, additional, Grundy, Richard, additional, Pollack, Ian F, additional, Hamilton, Ronald L, additional, Van Meter, Timothy, additional, Carlotti, Carlos G, additional, Boop, Frederick, additional, Bigner, Darrell, additional, Gilbertson, Richard J, additional, Rutka, James T, additional, and Taylor, Michael D, additional
- Published
- 2009
- Full Text
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7. Recurrent somatic alterations of FGFR1 and NTRK2 in pilocytic astrocytoma.
- Author
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Jones DT, Hutter B, Jäger N, Korshunov A, Kool M, Warnatz HJ, Zichner T, Lambert SR, Ryzhova M, Quang DA, Fontebasso AM, Stütz AM, Hutter S, Zuckermann M, Sturm D, Gronych J, Lasitschka B, Schmidt S, Seker-Cin H, Witt H, Sultan M, Ralser M, Northcott PA, Hovestadt V, Bender S, Pfaff E, Stark S, Faury D, Schwartzentruber J, Majewski J, Weber UD, Zapatka M, Raeder B, Schlesner M, Worth CL, Bartholomae CC, von Kalle C, Imbusch CD, Radomski S, Lawerenz C, van Sluis P, Koster J, Volckmann R, Versteeg R, Lehrach H, Monoranu C, Winkler B, Unterberg A, Herold-Mende C, Milde T, Kulozik AE, Ebinger M, Schuhmann MU, Cho YJ, Pomeroy SL, von Deimling A, Witt O, Taylor MD, Wolf S, Karajannis MA, Eberhart CG, Scheurlen W, Hasselblatt M, Ligon KL, Kieran MW, Korbel JO, Yaspo ML, Brors B, Felsberg J, Reifenberger G, Collins VP, Jabado N, Eils R, Lichter P, and Pfister SM
- Subjects
- Animals, Astrocytoma metabolism, Base Sequence, Brain Neoplasms metabolism, Cell Line, Cell Transformation, Neoplastic genetics, Cell Transformation, Neoplastic metabolism, Chromosome Breakpoints, Chromosomes, Human, Pair 6, Chromosomes, Human, Pair 9, Fibroblast Growth Factors metabolism, Humans, MAP Kinase Signaling System, Mice, Models, Molecular, Oncogene Proteins, Fusion chemistry, Oncogene Proteins, Fusion genetics, Protein Conformation, Proto-Oncogene Proteins B-raf chemistry, Proto-Oncogene Proteins B-raf genetics, Receptor, Fibroblast Growth Factor, Type 1 metabolism, Receptor, trkB metabolism, Astrocytoma genetics, Brain Neoplasms genetics, Mutation, Receptor, Fibroblast Growth Factor, Type 1 genetics, Receptor, trkB genetics
- Abstract
Pilocytic astrocytoma, the most common childhood brain tumor, is typically associated with mitogen-activated protein kinase (MAPK) pathway alterations. Surgically inaccessible midline tumors are therapeutically challenging, showing sustained tendency for progression and often becoming a chronic disease with substantial morbidities. Here we describe whole-genome sequencing of 96 pilocytic astrocytomas, with matched RNA sequencing (n = 73), conducted by the International Cancer Genome Consortium (ICGC) PedBrain Tumor Project. We identified recurrent activating mutations in FGFR1 and PTPN11 and new NTRK2 fusion genes in non-cerebellar tumors. New BRAF-activating changes were also observed. MAPK pathway alterations affected all tumors analyzed, with no other significant mutations identified, indicating that pilocytic astrocytoma is predominantly a single-pathway disease. Notably, we identified the same FGFR1 mutations in a subset of H3F3A-mutated pediatric glioblastoma with additional alterations in the NF1 gene. Our findings thus identify new potential therapeutic targets in distinct subsets of pilocytic astrocytoma and childhood glioblastoma.
- Published
- 2013
- Full Text
- View/download PDF
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