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  • 1. Berger, Ashton C
    et al.
    Korkut, Anil
    Kanchi, Rupa S
    Hegde, Apurva M
    Lenoir, Walter
    Liu, Wenbin
    Liu, Yuexin
    Fan, Huihui
    Shen, Hui
    Ravikumar, Visweswaran
    Rao, Arvind
    Schultz, Andre
    Li, Xubin
    Sumazin, Pavel
    Williams, Cecilia
    KTH, School of Biotechnology (BIO), Proteomics and Nanobiotechnology. KTH, School of Engineering Sciences in Chemistry, Biotechnology and Health (CBH), Protein Science, Cellular and Clinical Proteomics.
    Mestdagh, Pieter
    Gunaratne, Preethi H
    Yau, Christina
    Bowlby, Reanne
    Robertson, A Gordon
    Tiezzi, Daniel G
    Wang, Chen
    Cherniack, Andrew D
    Godwin, Andrew K
    Kuderer, Nicole M
    Rader, Janet S
    Zuna, Rosemary E
    Sood, Anil K
    Lazar, Alexander J
    Ojesina, Akinyemi I
    Adebamowo, Clement
    Adebamowo, Sally N
    Baggerly, Keith A
    Chen, Ting-Wen
    Chiu, Hua-Sheng
    Lefever, Steve
    Liu, Liang
    MacKenzie, Karen
    Orsulic, Sandra
    Roszik, Jason
    Shelley, Carl Simon
    Song, Qianqian
    Vellano, Christopher P
    Wentzensen, Nicolas
    Weinstein, John N
    Mills, Gordon B
    Levine, Douglas A
    Akbani, Rehan
    A Comprehensive Pan-Cancer Molecular Study of Gynecologic and Breast Cancers.2018In: Cancer Cell, ISSN 1535-6108, E-ISSN 1878-3686, Vol. 33, no 4, p. 690-705.e9, article id S1535-6108(18)30119-3Article in journal (Refereed)
    Abstract [en]

    We analyzed molecular data on 2,579 tumors from The Cancer Genome Atlas (TCGA) of four gynecological types plus breast. Our aims were to identify shared and unique molecular features, clinically significant subtypes, and potential therapeutic targets. We found 61 somatic copy-number alterations (SCNAs) and 46 significantly mutated genes (SMGs). Eleven SCNAs and 11 SMGs had not been identified in previous TCGA studies of the individual tumor types. We found functionally significant estrogen receptor-regulated long non-coding RNAs (lncRNAs) and gene/lncRNA interaction networks. Pathway analysis identified subtypes with high leukocyte infiltration, raising potential implications for immunotherapy. Using 16 key molecular features, we identified five prognostic subtypes and developed a decision tree that classified patients into the subtypes based on just six features that are assessable in clinical laboratories.

  • 2.
    Binder, Zev A.
    et al.
    Univ Penn, Perelman Sch Med, Dept Neurosurg, Philadelphia, PA 19104 USA.;Univ Penn, Perelman Sch Med, Ctr Biomed Image Comp & Analyt, Philadelphia, PA 19104 USA..
    Thorne, Amy Haseley
    Ludwig Inst Canc Res, San Diego, CA 92093 USA..
    Bakas, Spyridon
    Univ Penn, Perelman Sch Med, Ctr Biomed Image Comp & Analyt, Philadelphia, PA 19104 USA.;Univ Penn, Perelman Sch Med, Dept Radiol, Philadelphia, PA 19104 USA..
    Wileyto, E. Paul
    Univ Penn, Perelman Sch Med, Dept Biostat Epidemiol & Informat, Philadelphia, PA 19104 USA..
    Bilello, Michel
    Univ Penn, Perelman Sch Med, Ctr Biomed Image Comp & Analyt, Philadelphia, PA 19104 USA.;Univ Penn, Perelman Sch Med, Dept Radiol, Philadelphia, PA 19104 USA..
    Akbari, Hamed
    Univ Penn, Perelman Sch Med, Ctr Biomed Image Comp & Analyt, Philadelphia, PA 19104 USA.;Univ Penn, Perelman Sch Med, Dept Radiol, Philadelphia, PA 19104 USA..
    Rathore, Saima
    Univ Penn, Perelman Sch Med, Ctr Biomed Image Comp & Analyt, Philadelphia, PA 19104 USA.;Univ Penn, Perelman Sch Med, Dept Radiol, Philadelphia, PA 19104 USA..
    Ha, Sung Min
    Univ Penn, Perelman Sch Med, Ctr Biomed Image Comp & Analyt, Philadelphia, PA 19104 USA.;Univ Penn, Perelman Sch Med, Dept Radiol, Philadelphia, PA 19104 USA..
    Zhang, Logan
    Univ Penn, Perelman Sch Med, Dept Neurosurg, Philadelphia, PA 19104 USA..
    Ferguson, Cole J.
    Washington Univ, Div Neuropathol, Dept Pathol & Immunol, Sch Med, St Louis, MO 63108 USA..
    Dahiya, Sonika
    Washington Univ, Div Neuropathol, Dept Pathol & Immunol, Sch Med, St Louis, MO 63108 USA..
    Bi, Wenya Linda
    Brigham & Womans Hosp, Harvard Med Ctr, Dept Neurosurg, Ctr Skull Base & Pituitary Surg, Boston, MA 02115 USA..
    Reardon, David A.
    Dana Farber Canc Inst, Ctr Neurooncol, Boston, MA 02215 USA..
    Idbaih, Ahmed
    Sorbonne Univ, Hop Univ Pitie Salpetriere Charles Foix, AP HP, Serv Neurol Mazarin 2, Inserm,CNRS,UMR S 1127, F-75013 Paris, France..
    Felsberg, Joerg
    Heinrich Heine Univ, Inst Neuropathol, Med Fac, Moorenstr 5, D-40225 Dusseldorf, Germany..
    Hentschel, Bettina
    Univ Leipzig, Med Fac, Inst Med Informat Stat & Epidemiol, Hartelstr 16, D-04107 Leipzig, Germany..
    Weller, Michael
    Univ Hosp, Dept Neurol, CH-8091 Zurich, Switzerland.;Univ Zurich, CH-8091 Zurich, Switzerland..
    Bagley, Stephen J.
    Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA..
    Morrissette, Jennifer J. D.
    Univ Penn, Dept Pathol & Lab Med, Perelman Sch Med, Philadelphia, PA 19104 USA..
    Nasrallah, MacLean P.
    Univ Penn, Perelman Sch Med, Dept Pathol & Lab Med, Div Neuropathol, Philadelphia, PA 19104 USA..
    Ma, Jianhui
    Zanca, Ciro
    Scott, Andrew M.
    La Trobe Univ, Olivia Newton John Canc Res Inst, Melbourne, Vic, Australia..
    Orellana, Laura
    KTH, Centres, Science for Life Laboratory, SciLifeLab. Department of Biochemistry and Biophysics, Stockholm University, Stockholm, Sweden.
    Davatzikos, Christos
    Furnari, Frank B.
    Ludwig Inst Canc Res, San Diego, CA 92093 USA..
    O'Rourke, Donald M.
    Univ Penn, Perelman Sch Med, Dept Neurosurg, Philadelphia, PA 19104 USA.;Univ Penn, Perelman Sch Med, Ctr Biomed Image Comp & Analyt, Philadelphia, PA 19104 USA.;Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA..
    Epidermal Growth Factor Receptor Extracellular Domain Mutations in Glioblastoma Present Opportunities for Clinical Imaging and Therapeutic Development2018In: Cancer Cell, ISSN 1535-6108, E-ISSN 1878-3686, Vol. 34, no 1, p. 163--177.e7Article in journal (Refereed)
    Abstract [en]

    We explored the clinical and pathological impact of epidermal growth factor receptor (EGFR) extracellular domain missense mutations. Retrospective assessment of 260 de novo glioblastoma patients revealed a significant reduction in overall survival of patients having tumors with EGFR mutations at alanine 289 (EGFR(A289D/T/V)). Quantitative multi-parametric magnetic resonance imaging analyses indicated increased tumor invasion for EGFR(A289D/T/V) mutants, corroborated in mice bearing intracranial tumors expressing EGFR(A289V) and dependent on ERK-mediated expression of matrix metalloproteinase-1. EGFR(A289V) tumor growth was attenuated with an antibody against a cryptic epitope, based on in silico simulation. The findings of this study indicate a highly invasive phenotype associated with the EGFR(A289V) mutation in glioblastoma, postulating EGFR(A289V) as a molecular marker for responsiveness to therapy with EGFR-targeting antibodies.

  • 3.
    Ma, Jianhui
    et al.
    Univ Calif San Diego, Ludwig Inst Canc Res, San Diego Branch, 9500 Gilman Dr, La Jolla, CA 92093 USA. i, Jie; Cavenee, Webster K.; Kolodner, Richard D.; Chen, Clark C.; Furnari, Frank B..
    Benite, Jorge A.
    Miki, Shunichiro
    Albuquerqu, Claudio Ponte
    Galatro, Thais
    Orellana, Laura
    KTH, School of Engineering Sciences (SCI), Theoretical Physics, Theoretical & Computational Biophysics. KTH, Centres, Science for Life Laboratory, SciLifeLab.
    Zanca, Ciro
    Reed, Rachel
    Boyer, Antonia
    Koga, Tomoyuki
    Varki, Nissi M.
    Fenton, Tim R.
    Marie, Suely Kazue Nagahashi
    Lindahl, Erik
    KTH, School of Engineering Sciences (SCI), Theoretical Physics, Theoretical & Computational Biophysics. KTH, Centres, Science for Life Laboratory, SciLifeLab.
    Gahman, Timothy C.
    Shiau, Andrew K.
    Zhou, Huilin
    DeGroot, John
    Sulman, Erik P.
    Cavenee, Webster K.
    Kolodner, Richard D.
    Chen, Clark C.
    Furnari, Frank B.
    Inhibition of Nuclear PTEN Tyrosine Phosphorylation Enhances Glioma diation Sensitivity through Attenuated DNA Repair2019In: Cancer Cell, ISSN 1535-6108, E-ISSN 1878-3686, Vol. 35, no 3, p. 504-518.e7Article in journal (Refereed)
    Abstract [en]

    Ionizing radiation (IR) and chemotherapy are standard-of-care treatments for glioblastoma (GBM) patients and both result in DNA damage, however, the clinical efficacy is limited due to therapeutic resistance. We identified a mechanism of such resistance mediated by phosphorylation of PTEN on tyrosine 240 (pY240-PTEN) by FGFR2. pY240-PTEN is rapidly elevated and bound to chromatin through interaction with Ki-67 in response to IR treatment and facilitates the recruitment of RAD51 to promote DNA repair. Blocking Y240 phosphorylation confers radiation sensitivity to tumors and extends survival in GBM preclinical models. Y240F-Pten knockin mice showed radiation sensitivity. These results suggest that FGFR-mediated pY240-PTEN is a key mechanism of radiation resistance and is an actionable target for improving radiotherapy efficacy.

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