Sensitivity to PI3K and AKT inhibitors is mediated by divergent molecular mechanisms in subtypes of DLBCL-Reference-Cited by-同舟云学术

Sensitivity to PI3K and AKT inhibitors is mediated by divergent molecular mechanisms in subtypes of DLBCL

Published:2017-07-20 Issue:3 Volume:130 Page:310-322
ISSN:0006-4971
Container-title:Blood
language:en
Short-container-title:

Author:

Erdmann Tabea¹²³,Klener Pavel⁴⁵,Lynch James T.⁶,Grau Michael¹²,Vočková Petra⁴⁵,Molinsky Jan⁴⁵,Tuskova Diana⁴⁵,Hudson Kevin⁶,Polanska Urszula M.⁶,Grondine Michael⁷,Mayo Michele⁷,Dai Beiying¹²,Pfeifer Matthias⁸,Erdmann Kristian¹²,Schwammbach Daniela¹²,Zapukhlyak Myroslav¹²,Staiger Annette M.⁹¹⁰,Ott German⁹,Berdel Wolfgang E.²¹¹,Davies Barry R.⁶,Cruzalegui Francisco⁶,Trneny Marek⁴⁵,Lenz Peter¹²,Barry Simon T.⁶,Lenz Georg¹²¹¹

Affiliation:

1. Translational Oncology, University Hospital Münster, Münster, Germany;

2. Cluster of Excellence EXC 1003, Cells in Motion, Münster, Germany;

3. Fachbereich Chemie und Pharmazie, University of Münster, Münster, Germany;

4. Institute of Pathological Physiology, First Faculty of Medicine, Charles University Prague, Prague, Czech Republic;

5. First Medical Department, Department of Hematology, Charles University General Hospital Prague, Prague, Czech Republic;

6. Innovative Medicines and Early Development (IMED) Oncology AstraZeneca, Li Ka Shing Centre, Cambridge, United Kingdom;

7. IMED Oncology AstraZeneca, Gatehouse Park, Boston, MA;

8. Division of Cancer, Department of Surgery & Cancer, Imperial College, London, United Kingdom;

9. Department of Clinical Pathology, Robert-Bosch-Hospital, Stuttgart, Germany;

10. Dr. Margarete Fischer-Bosch-Institute of Clinical Pharmacology, Stuttgart, Germany;

11. Department of Medicine A, Hematology, Oncology, and Pneumology, University Hospital Münster, Münster, Germany; and

12. Department of Physics, Philipps University, Marburg, Germany

Abstract

Key Points PI3Kα/δ inhibition induces cytotoxicity in ABC DLBCLs through downregulation of NF-κB signaling. Inhibition of AKT induces cytotoxicity by downregulation of MYC in PTEN-deficient DLBCL models in vivo and in vitro.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Link

http://ashpublications.org/blood/article-pdf/130/3/310/1404776/blood758599.pdf

Reference45 articles.

1. A clinical evaluation of the International Lymphoma Study Group classification of non-Hodgkin’s lymphoma. The Non-Hodgkin’s Lymphoma Classification Project;Blood,1997

2. Pathogenesis of non-Hodgkin’s lymphoma;Nogai;J Clin Oncol,2011

3. Distinct types of diffuse large B-cell lymphoma identified by gene expression profiling;Alizadeh;Nature,2000

4. Targeting B cell receptor signaling with ibrutinib in diffuse large B cell lymphoma;Wilson;Nat Med,2015

5. Salvage regimens with autologous transplantation for relapsed large B-cell lymphoma in the rituximab era;Gisselbrecht;J Clin Oncol,2010

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