tbuckley/cabot-search huggingface dataset:
A Relay Pathway between Arginine and Tryptophan Metabolism Confers Immunosuppressive Properties on Dendritic Cells
Authors: Giada Mondanelli, Roberta Bianchi, Maria Teresa Pallotta, Ciriana Orabona, Elisa Albini, Alberta Iacono, Maria Laura Belladonna, Carmine Vacca, Francesca Fallarino, Antonio Macchiarulo, Stefano Ugel, Vincenzo Bronte, Federica Gevi, Lello Zolla, Auke Verhaar, Maikel Peppelenbosch, Emilia Maria Cristina Mazza, Silvio Bicciato, Yasmina Laouar, Laura Santambrogio, Paolo Puccetti, Claudia Volpi, Ursula Grohmann
Journal: Immunity (2017)

Highlights•Dendritic cells (DCs) can co-express Arg1 and IDO1 immunosuppressive enzymes•Arg1 activity is required for IDO1 induction by TGF-β in DCs•Spermidine, a downstream Arg1 product, but not arginine starvation, induces IDO1 in DCs•Arg1+ myeloid derived suppressor cells (MDSCs) can render DCs immunosuppressive via IDO1SummaryArginase 1 (Arg1) and indoleamine 2,3-dioxygenase 1 (IDO1) are immunoregulatory enzymes catalyzing the degradation of l-arginine and l-tryptophan, respectively, resulting in local amino acid deprivation. In addition, unlike Arg1, IDO1 is also endowed with non-enzymatic signaling activity in dendritic cells (DCs). Despite considerable knowledge of their individual biology, no integrated functions of Arg1 and IDO1 have been reported yet. We found that IDO1 phosphorylation and consequent activation of IDO1 signaling in DCs was strictly dependent on prior expression of Arg1 and Arg1-dependent production of polyamines. Polyamines, either produced by DCs or released by bystander Arg1+ myeloid-derived suppressor cells, conditioned DCs toward an IDO1-dependent, immunosuppressive phenotype via activation of the Src kinase, which has IDO1-phosphorylating activity. Thus our data indicate that Arg1 and IDO1 are linked by an entwined pathway in immunometabolism and that their joint modulation could represent an important target for effective immunotherapy in several disease settings.
Defining the antibody cross-reactome directed against the influenza virus surface glycoproteins
Authors: Raffael Nachbagauer, Angela Choi, Ariana Hirsh, Irina Margine, Sayaka Iida, Aldo Barrera, Marcela Ferres, Randy A Albrecht, Adolfo García-Sastre, Nicole M Bouvier, Kimihito Ito, Rafael A Medina, Peter Palese, Florian Krammer
Journal: Nature Immunology (2017)
EXTH-11. HISTONE DEACETYLASE 6 (HDAC6) INHIBITORS RETARD CELL PROLIFERATION AND INDUCE ROBUST CELL DEATH IN GLIOBLASTOMA (GBM) CELLS AND GBM SPHEROIDS CONTAINING STEM CELLS
Authors: Mohammad Saadatzadeh
Journal: Neuro-Oncology (2016)

Glioblastoma (GBM) comprises the most common and very aggressive form of primary brain tumor with a dismal prognosis and very poor response to the current therapies. HDAC inhibitors (HDACi) induce growth arrest and apoptosis in tumor cells. HDAC6 is a unique enzyme having two deacetylase domains, and an ubiquitin-binding domain. HDAC6 interacts with a number of proteins in the cytoplasm and is involved in tumorigenesis, cell motility, and metastasis. In this study, we evaluated HDAC6 as a relevant target for GBM treatment by using potent HDAC6 inhibitors, CAY 10603, ACY-1215, and Tubastatin A. The ACY-1215 and Tubastatin A inhibitors were selected due to favorable blood-brain-barrier permeability characteristics. Our data indicate that HDAC6 inhibitors target the established GBM cell line U87MG, the early passage GBM10 and M-HBT-161 cultures, and CD133- and SOX2-positive stem cell-like spheroids. These inhibitors at 1-8 μM triggered significant inhibition of cell survival and induced apoptotic cell death in GBM cells and GBM spheroids. CAY 10603, Tubastatin A, and ACY-1215 reduced cell survival in U87MG cells by 50% (IC50) at 1.07, 5.83, and 6.27 μM treatment for 96 h, respectively. Moreover, CAY 10603-triggered cell death in U87MG cells as well as CD133/SOX2-expressing spheroids was associated with activation of caspases-3, -6, and -9 and the general caspase-inhibitor, zVAD-fmk significantly inhibited CAY 10603-triggered cell death at 10 µM treatment for 48 h. Overall, our results show that these HDAC6 inhibitors robustly inhibit the growth of GBM cells, and are effective in eliminating spheroids that contain GBM cancer stem cells which play a major role in drug resistance and disease recurrence. These results suggest that using HDAC6 inhibitors alone or in combination with other agents may potentially improve the survival of brain tumor patients.
Gene Expression Profiling Classifies Splenic Marginal Zone Lymphoma and Hairy Cell Leukemia-Variant as Related Diseases That Are Distinct From Typical Hairy Cell Leukemia.
Authors: Sarah L Hockley, Alison Morilla, Andrew Wotherspoon, Brian A Walker, Nicholas J Dickens, Daniel Catovsky, Gareth J Morgan, Estella Matutes, David Gonzalez
Journal: Blood (2009)
Clonal evolution and drug resistance in the blood of patients with metastatic solid tumors responding to targeted therapies - THE CORNUCOPIA STUDY
Authors: A. Bardelli, F. Montemurro, G. Siravegna, B. Mussolin, A. Milani, F. Leone, D. Marino, M. Spione, S. Corso, F. De Braud, P. Racca, F. Pietrantonio, A. Ponzetti, C. Cristiano, G. Tonini, V. Zagonel, A. Ardizzoni, G. Curigliano, S. Siena, S. Marsoni
Journal: Annals of Oncology (2016)
BMET-02. METASTASES AFFECTING THE MOTOR ELOQUENT CORTEX SHOULD BE RESECTED WITH PREOPERATIVE MOTOR MAPPING DATA BY nTMS
Authors: Sandro M. Krieg, Sebastian Ille, Thomas Picht, Nico Sollmann, Ina Bährend, Florian Ringel, Srikanatan Nagarajan, Peter Vajkoczy, Mitchell S. Berger, Bernhard Meyer, Phiroz E. Tarapore
Journal: Neuro-Oncology (2016)

Improvement in outcome for supratentorial lesions located in motor eloquent areas, especially gliomas, was already shown repeatedly if preoperative mapping of motor areas was performed by navigated transcranial magnetic stimulation (nTMS). Yet, data on motor eloquently located metastases is still lacking. Thus, this multicentric study aimed to compare the surgical outcome of patients with motor eloquently located supratentorial metastases investigated with or without preoperative nTMS. Prospectively enrolled cohorts of our international study group were divided into patients undergoing preoperative nTMS (2010-2015; 120 patients) and patients who were operated on without nTMS data (2006-2015; 60 patients). Tumor location, size, and preoperative deficits were comparable. The nTMS group showed a lower rate of residual tumor on postoperative MRI (OR 0.2278; 95% CI 0.0.0925 – 0.0.5610). On long-term follow-up, surgery-related paresis was superior in the nTMS group (nTMS vs. non-nTMS; improved: 30.8% vs. 13.3%, unchanged: 65.8% vs. 73.3%, worse: 3.3% vs. 13.3% of patients; p=0.0.0036). Moreover, the nTMS group showed smaller craniotomies (nTMS: 16.7 ± 8.6 cm2 vs. non-nTMS: 20.0 ± 10.1 cm2; p=0.0.0395). Surgical time differed significantly between both groups (nTMS: 128.8 ± 49.4 min vs. non-nTMS: 160.1 ± 71.3 min; p=0.0.0013). This work increases the level of evidence for preoperative motor mapping by nTMS for metastases affecting the motor cortex in a group comparison study. We therefore strongly advocate nTMS to become increasingly used for these lesions. However, a randomized trial on the comparison with the gold standard of intraoperative mapping seems mandatory.
MicroRNAs 17-5p/20a/106a Function as a Master Gene Complex Controlling Monocytopoiesis through AML1 Targeting.
Authors: Laura Fontana, Elvira Pelosi, Paolo Greco, Ugo Testa, Francesca Liuzzi, Carlo Maria Croce, Ercole Brunetti, Cesare Peschle
Journal: Blood (2006)
Sustained Complete Metabolic Remission After Allogeneic Hematopoietic Stem Cell Transplantation in Patients with Mitochondrial Neurogastrointestinal Encephalomyopathy (MNGIE).
Authors: Joerg Halter, WM Michael Schuepbach, Carlo Casali, Ronit Elhasid, Keith Fay, Simon Hammans, Isabel Illa, Liliane Kappeler, Stephan Kraehenbuehl, Thomas Lehmann, Hanna Mandel, Ramon Marti, Heinrich Mattle, Kim H. Orchard, David Savage, Carolyn Sue, David Valcárcel, Alois Gratwohl, Michio Hirano
Journal: Blood (2009)
P07.12 Multimodal imaging of the invasive microenvironment predicts survival in glioblastomas
Authors: S. J. Price, N. R. Boonzaier, J. Yan, M. A. McLean
Journal: Neuro-Oncology (2016)

require any further treatments and was on observation with imaging only for 14 months until another area of progression was seen.CONCLUSION: After treatment of a neoplasm, if unexpected clinical or imaging evidence of recurrence is present, it may be a foreign body reaction to hemostatic material used during the initial surgery.The implications of this case lie in recognizing this entity to avoid unnecessary procedures.Given the technical variability of advanced MRI techniques, there are limits to the sensitivity and specificity of such.The standardization of advanced MRI is well recognized as a pressing clinical and research need. P07.
Bortezomib in Combination with High-Dose Dexamethasone (HD dex) and Erythropoietin (EPO) Does Not Result in an Increased Risk of Thromboembolic Complications.
Authors: Jean-Luc Harousseau, Sundar Jagannath, Paul G. Richardson, Pieter Sonneveld, Michael W. Schuster, Dixie-Lee Esseltine, Kenneth C. Anderson
Journal: Blood (2006)
Treatment efficacy and prognostic factors in patients (pts) with malignant ovarian germ cell tumors (MOGCT): Single-center experience
Authors: D. Chekini, A. Tryakin, M. Fedyanin, A. Bulanov, M. Ahmedova, I. Pokataev, T. Zakharova, S. Tjulandin
Journal: Annals of Oncology (2016)
Numbers of Lymphoma Associated Macrophages (LAMS) and Regulatory T-Cells (Tregs) in Follicular Lymphoma (FL) Patients (pts) Treated with and without Monoclonal Antibody (MoAb)-Containing Therapy Do Not Correlate with Overall Survival (OS): A Study from the Southwest Oncology Group (SWOG).
Authors: John William Sweetenham, Eric Hsi, Bryan Goldman, Michael LeBlanc, Raymond R. Tubbs, James R. Cook, Oliver W. Press, Richard I. Fisher, Lisa M. Rimsza
Journal: Blood (2007)
Impact of Prophylactic CD8-Depleted Donor-Lymphocyte Infusions After Allogeneic Hematopoietic Stem Cell Transplantation and Alemtuzumab Mediated T-Cell Depletion,
Authors: Eva M Wagner, Daniela Wehler, Karin Kolbe, Matthias Theobald, Wolfgang Herr, Ralf G Meyer
Journal: Blood (2011)
Safety of necitumumab and pembrolizumab combination therapy in patients with stage IV non-small cell lung cancer (NSCLC): a phase 1b expansion cohort study
Authors: B. Besse, P. Garrido, J. Bennouna, L. Mezquita, A. Gazzah, J. Remon, D. Planchard, M. EOlmedo Garcia, J. Raimbourg, G.Y. Chao, M. Gil
Journal: Annals of Oncology (2016)
Bendamustine for Mantle Cell Lymphoma: Retrospective Analysis of the Spanish Experience
Authors: Ana García-Noblejas, Belén Navarro Matilla, Carolina Da Silva Rodriguez, Raquel De Oña Navarrete, María José Ramirez Sánchez, Concepción Nicolás, Ricardo Pérez Fernández, Blanca Sanchez Gonzalez, Eva Domingo-Domènech, Jose Javier Sanchez Blanco, Jimena Cannata-Ortiz, Tomás José González-López, Reyes Arranz Sáez
Journal: Blood (2011)
Evaluation for surgical treatment options in metastatic colorectal cancer (mCRC) – a retrospective, central evaluation of FIRE-3
Authors: U. Neumann, T. Denecke, J. Pratschke, H. Lang, M. Bemelmans, T. Becker, M. Rentsch, D. Seehofer, C.J. Bruns, B. Gebauer, G. Folprecht, S. Stintzing, S. Held, V. Heinemann, D.P. Modest
Journal: Annals of Oncology (2016)
Targeting IKK Inhibits Multiple Myeloma (MM) Cell Growth in the Bone Marrow Microenvironment.
Authors: Teru Hideshima, Pierfrancesco Tassone, Dharminder Chauhan, Kenji Ishitsuka, Constantine Mitsiades, Noopur Raje, Shaji Kumar, Makoto Hamasaki, Hiromasa Hideshima, Nikhil C. Munshi, Paul G. Richardson, David Schenkein, Kenneth C. Anderson
Journal: Blood (2004)
Impact of genomic heterogeneity and mutation patterns on the outcome of patients with epithelial ovarian cancer (EOC)
Authors: V. Kotoula, S. Lakis, E. Giannoulatou, G. Kouvatseas, G. Lazaridis, I. Tikas, I. Efstratiou, S. Chrisafi, E. Charalambous, A. Papanikolaou, F. Fostira, B. Tarlatzis, G. Fountzilas
Journal: Annals of Oncology (2016)
Chemosensitivity Is Differentially Regulated by SDF-1/CXCR4 and SDF-1/CXCR7 Axes in Acute Lymphoblastic Leukemia.
Authors: Norie Ando, Yoshiyuki Furuichi, Shin Kasai, Keiko Kagami, Kumiko Goi, Takeshi Inukai, Kanji Sugita
Journal: Blood (2012)
Effect of the addition of bevacizumab to first-line FOLFOX on efficacy, including response rate, progression-free survival, and overall survival, in patients with metastatic colorectal cancer.
Authors: M. Suenaga, N. Mizunuma, S. Matsusaka, E. Shinozaki, M. Ogura, Y. Kuboki, T. Watanabe, M. Ozaka, K. Chin, K. Hatake
Journal: Journal of Clinical Oncology (2011)

588 Background: Bevacizumab (BV) is a recombinant, humanized monoclonal antibody against vascular endothelial growth factor. Used in combination with chemotherapy, BV has been shown to improve survival in both first- and second-line treatment for metastatic colorectal cancer (mCRC). However, it was reported that addition of BV to FOLFOX conferred only little survival benefit (Saltz et al. JCO2008). The aim of this study was to assess the efficacy of addition of BV to FOLFOX in first-line treatment for patients with mCRC. Methods: Bevacizumab was approved for mCRC in July 2007 in Japan. This study was conducted at a single institution and comprised 217 consecutive patients receiving first-line treatment for mCRC between 2005 and 2009. The primary objective was to compare survival benefit in patients treated with FOLFOX4 (FF) between 2005 and 2007 with that in patients receiving FOLFOX4+BV 5 mg/kg (FF+BV) between 2007 and 2009. Results: Total number of patients in the FF and FF+BV groups was 132 and 85, respectively. Characteristics of patients were as follows (FF vs. FF+B): median age, 62 yrs (range 28-76 yrs) vs. 60 yrs (range16-74 yrs); ECOG PS0, 98.8% vs. 81.8%; and median follow-up time, 20.8 months vs. 24.4 months. Median progression-free survival (PFS) in the FF and FF+BV groups was 10 months (95% CI, 8.7-11.3) and 17 months (95% CI, 10.2-14.1), while median overall survival (OS) was 21 months (95% CI, 17.9-24.1) and not reached, respectively. Response rate was 46% (95% CI, 37- 54) in FF, and 62% (95% CI, 51-73) in FF+BV. Addition of BV to FOLFOX4 significantly improved PFS (p=0.002) and OS (p&lt;0.001). Conclusions: The additive effect of BV for first-line FOLFOX was reconfirmed. These data indicate potential survival benefits from the addition of BV to FOLFOX in first-line treatment of mCRC. In addition, PFS may be a sensitive indicator of outcome prior to post-treatment. No significant financial relationships to disclose.
Final overall survival (OS) results of the feasibility study of adjuvant chemotherapy with docetaxel (DOC) plus cisplatin (CDDP) followed by maintenance chemotherapy of S-1 in completely resected non-small cell lung cancer (NSCLC): Thoracic Oncology Research Group (TORG) 0809
Authors: S. Niho, N. Ikeda, H. Michimae, K. Suzuki, H. Sakai, T. Kaburagi, K. Yoshiya, K. Minato, T. Kato, H. Okamoto, T. Seto, Y. Hosomi, K. Shimizu, H. Saito, M. Tsuchida, H. Kunitoh, M. Tsuboi, M. Takeuchi, K. Watanabe
Journal: Annals of Oncology (2016)
Safety, clinical activity and biomarkers of atezolizumab (atezo) in advanced ovarian cancer (OC)
Authors: J.R. Infante, F. Braiteh, L.A. Emens, A.S. Balmanoukian, A. Oaknin, Y. Wang, B. Liu, L. Molinero, M. Fasso, C. O'Hear, M. Gordon
Journal: Annals of Oncology (2016)
A novel way to visualise tumour related angiogenesis and detect breast tumours in women: A combined clinical and optical method for breast cancer screening of well-women in Ghana
Authors: F.N. Ghartey, D.J. Watmough, A. Anyanful, S. Debrah, M. Morna, S. Eliason, M. Adamu, L. Derkyi-Kwarteng
Journal: Annals of Oncology (2016)
Treatment for Acute Myelogenous Leukemia by Low Dose Irradiation Based Conditioning and Hematopoietic Cell Transplantation from Related and Unrelated Donors.
Authors: Dietger W. Niederwieser, Ute Hegenbart, Brenda M. Sandmaier, Michael B. Maris, Monic Stuart, Hildegard Greinix, Catherine Cordonnier, Bernard Rio, Alois Gratwohl, Thoralf Lange, Wolfram Pönisch, Leante Grommisch, Barry Storer, David Maloney, Peter McSweeney, Thomas Chauncey, Ed Agura, Karl Blume, Rainer Storb
Journal: Blood (2004)
MBRS-38. MOLECULAR CLASSIFICATION AND CLINICAL CHARACTERISTICS OF 236 MEDULLOBLASTOMAS IN JAPAN
Authors: Yonehiro Kanemura, Tomoko Shofuda, Ema Yoshioka, Daisuke Kanematsu, Koichi Ichimura, Atsushi Sasaki, Takeshi Inoue, Junko Hirato, Yoshinori Kodama, Masayuki Mano, Soichiro Shibui, Hajime Arai, Hiroaki Sakamoto, Isao Date, Ryo Nishikawa
Journal: Neuro-Oncology (2020)

Abstract Recent intensive genomic and molecular biological analyses have made a consensus that medulloblastomas (MBs) are at least classified into four core subgroups, and the new 2016 WHO brain tumor classification has introduced the classification of MBs genetically defined in addition to classical histopathological diagnosis. To establish a nationwide network of a molecular diagnosis system for pediatric brain tumors, the JPMNG co-organized by the Japan Society for Neuro-Oncology and the Japanese Society for Pediatric Neurosurgery have started the clinical researches in 2012, and we have summarized results of molecular analysis of Japanese MBs. Total 236 primary MBs have been subclassified by gene expression profile using the NanoString nCounter system or DNA methylation array, and their single nucleotide mutations and copy number aberrations have been also examined. Mean follow up time was 68.9 months. Proportion of four core subgroups were WNT (16.9%), SHH (25.4%), Group 3 (17.4%) and Group 4 (40.3%), respectively. In cases of less than 3 years old, no WNT have been found and 63.2% cases were SHH. In cases between 3 to 17 years old, Group 4 is the most (47%), and these trends is almost consistent with published references. TP53 mutations were identified in 23.3% of SHH, and they were significantly poor prognosis. Metastatic or MYC gain Group 3 MBs were poor prognosis, while Group 4 MBs with loss of chromosome 11 or whole chromosomal aberration were good prognosis. These findings reveal molecular properties of Japanese MBs and will contribute to develop new therapeutic strategies.
OS4.7 CXCL13 in cerebrospinal fluid (CSF) as a biomarker for primary central nervous system cell lymphoma (PCNSL)
Authors: T. Sasayama, K. Tanaka, M. Nishihara, H. Nagashima, J. Sakata, T. Mizowaki, K. Mizukawa, E. Kohmura
Journal: Neuro-Oncology (2016)

BACKGROUND AND AIM: Differential diagnosis between radionecrotic (RN) and progressive (PD) brain metastases after radiosurgery (SRS) is a diagnostic challenge.In a former exploratory study, we showed that 6-[18F]-fluoro-L-3,4-dihydroxyphenylalanine (F-DOPA) PET/CT is able to discriminate between RN and PD metastases with excellent diagnostic accuracy, outperforming MRI including perfusion-weighted imaging.Borderline uptake values often represent the coexistence of necrotic and viable neoplastic cells.The aim of the present report was to analyze the long term followup of predominantly radionecrotic metastases by means of serial F-DOPA PET/CT scans.MATERIALS AND METHODS: Eighty-one patients with suspected radiological progression at the site of previously irradiated brain metastases referred for F-DOPA PET at our institution between May 2010 and March 2016 were screened.All metastases had previously been treated with single fraction or multifraction SRS.To be included in the final analysis, patients were required to have i) a mildly positive F-DOPA defined by visual analysis and borderline lesion-to-background uptake ratio (rSUV) values defined according to a previously published method ii) a diagnosis of radionecrosis after initial PET/CT evaluation, defined histologically as the presence of <20% neoplastic features within the surgical specimen or radiologically as a stable or shrinking lesion over an observational period of 6 months and ii) a minimum of 12 month follow up.Standard patient monitoring in this setting includes repeated magnetic resonance imaging (MRI) every 3-6 months and repeated F-DOPA every 6-12 months.RESULTS: A total of 68 F-DOPA scans from 19 patients (11 F, 8 M) were evaluated.Median follow-up was 30.5 months (range:14-51).At the time of writing, 4 (21%) patients have died because of intracranial (n=3) or extracranial (n=1) PD.Ten (52%) metastases remained in histologically confirmed (n=4) or unconfirmed RN, while 9 (48%) showed a slow PD (n=3 histological confirmations).All progressive metastases showed a steady rSUV increase over time; however, PET/CT was false positive in one case of histologically confirmed RN.In two cases of confirmed RN (one histologically, one radiologically), there was an increase of rSUV followed by a subsequent slight decrease.PET/CT and MRI were concordant in 12 (63%) and discordant in 7 (37%) cases.MRI was false positive in 4/10 (40%) cases of RN and false negative in 2/9 (22%) cases of PD.CONCLUSION: Amino acid PET with F-DOPA is a reliable tool to assess the evolution over time of metastatic brain lesions after SRS, and performs better than MRI.Different patterns of F-DOPA uptake over time can discriminate with excellent diagnostic accuracy between PD and RN in the context of mixed viable and radionecrotic neoplastic cells.OS4.
GENT-04. ACT LOCALLY: THE 3q26 genes SOX2, PIK3CA, MFN1 AND OPA1 CO-REGULATE GBM CELL INVASION
Authors: Archana Ramadoss, Severina Leu, Marie-Françoise Ritz, Thorsten Schaefer, Lionel Tintignac, Cristóbal Tostado, Stephan Frank, Luigi Mariani, Jean-Louis Boulay
Journal: Neuro-Oncology (2016)

3q26, a major target for genetic alterations in GBM, contains the genes encoding transcription factor SOX2, growth-factor-AKT signaling activator PIK3CA, and two effectors of mitochondria fusion MFN1 and OPA1. Since mitochondria fission has been linked to cell motility, we aimed at determining the roles of these four genes in GBM cell invasion. Parental LN319 GBM cells and those knocked-down for 3q26 genes were tested for invasion, migration and proliferation parameters, mitochondria morphology, AKT pathway activation status, SOX2 subcellular location and 3q26 gene promoter activation. All four knock-downs consistently enhanced cell invasion and motility, reduced proliferation, and shortened mitochondria. This common phenotype may suggest that the four 3q26 genes act on the same pathway. Chromatin immuno-precipitation and luciferase reporter gene assays show that SOX2 activates PIK3CA, MFN1 and OPA1 transcription. PIK3CA or downstream AKT pharmacological inactivation impairs SOX2 nuclear localization and aggravates SOX2 turnover, indicative of a positive regulation loop where AKT signaling activates SOX2 function, which in turn activates PIK3CA as well as MFN1 and OPA1 transcription. 3q26 copy number variations, analyzed in 100 glioma biopsies show frequent SOX2 gain (29%) and OPA1 loss (32%). Whereas SOX2 amplification is consistent with the transcriptional activation of known oncogenic targets, including PIK3CA, OPA1 loss may be related to increased invasion and mitochondrial fragmentation. Thus, SOX2 activates oncogenic and tumor suppressor target genes. While the oncogenic ones (PIK3CA) are kept ‘on’, OPA1 may need to be turned ‘off’. Copy number variations of 3q26 genes are currently being tested for impact on patient survival and tumor invasion status. We provide evidence that a regional interplay between 3q26 genes promotes glioma invasion. Copy number variations of individual genes suggest optimization of oncogenic activities.