Authors
Frederick S Varn, Kevin C Johnson, Jan Martinek, Jason T Huse, MacLean P Nasrallah, Pieter Wesseling, Lee AD Cooper, Tathiane M Malta, Taylor E Wade, Thais S Sabedot, Daniel Brat, Peter V Gould, Adelheid Wöehrer, Kenneth Aldape, Azzam Ismail, Santhosh K Sivajothi, Floris P Barthel, Hoon Kim, Emre Kocakavuk, Nazia Ahmed, Kieron White, Indrani Datta, Hyo-Eun Moon, Steven Pollock, Christine Goldfarb, Ga-Hyun Lee, Luciano Garofano, Kevin J Anderson, Djamel Nehar-Belaid, Jill S Barnholtz-Sloan, Spyridon Bakas, Annette T Byrne, Fulvio D’Angelo, Hui K Gan, Mustafa Khasraw, Simona Migliozzi, D Ryan Ormond, Sun Ha Paek, Erwin G Van Meir, Annemiek ME Walenkamp, Colin Watts, Tobias Weiss, Michael Weller, Karolina Palucka, Lucy F Stead, Laila M Poisson, Houtan Noushmehr, Antonio Iavarone, Roel GW Verhaak, Kristin D Alfaro, Samirkumar B Amin, David M Ashley, Christoph Bock, Andrew Brodbelt, Ketan R Bulsara, Ana Valeria Castro, Jennifer M Connelly, Joseph F Costello, John F de Groot, Gaetano Finocchiaro, Pim J French, Anna Golebiewska, Ann C Hau, Chibo Hong, Craig Horbinski, Kasthuri S Kannan, Mathilde CM Kouwenhoven, Anna Lasorella, Peter S LaViolette, Keith L Ligon, Allison K Lowman, Shwetal Mehta, Hrvoje Miletic, Annette M Molinaro, Ho Keung Ng, Simone P Niclou, Johanna M Niers, Joanna J Phillips, Raul Rabadan, Ganesh Rao, Guido Reifenberger, Nader Sanai, Susan C Short, Peter Sillevis Smitt, Andrew E Sloan, Marion Smits, James M Snyder, Hiromichi Suzuki, Ghazaleh Tabatabai, Georgette Tanner, William H Tomaszewski, Michael Wells, Bart A Westerman, Helen Wheeler, Jichun Xie, WK Alfred Yung, Gelareh Zadeh, Junfei Zhao, Roel GW Verhaak
Publication date
2022/6/9
Journal
Cell
Volume
185
Issue
12
Pages
2184-2199. e16
Publisher
Elsevier
Description
The factors driving therapy resistance in diffuse glioma remain poorly understood. To identify treatment-associated cellular and genetic changes, we analyzed RNA and/or DNA sequencing data from the temporally separated tumor pairs of 304 adult patients with isocitrate dehydrogenase (IDH)-wild-type and IDH-mutant glioma. Tumors recurred in distinct manners that were dependent on IDH mutation status and attributable to changes in histological feature composition, somatic alterations, and microenvironment interactions. Hypermutation and acquired CDKN2A deletions were associated with an increase in proliferating neoplastic cells at recurrence in both glioma subtypes, reflecting active tumor growth. IDH-wild-type tumors were more invasive at recurrence, and their neoplastic cells exhibited increased expression of neuronal signaling programs that reflected a possible role for neuronal interactions in …
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Scholar articles
FS Varn, KC Johnson, J Martinek, JT Huse… - Cell, 2022