J
Jan A. Burger
Researcher at University of Texas MD Anderson Cancer Center
Publications - 543
Citations - 33028
Jan A. Burger is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Chronic lymphocytic leukemia & Ibrutinib. The author has an hindex of 83, co-authored 511 publications receiving 28306 citations. Previous affiliations of Jan A. Burger include University of Texas Health Science Center at Houston & University of Freiburg.
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Journal ArticleDOI
Clinical and molecular characteristics of XPO1 mutations in patients with chronic lymphocytic leukemia.
Preetesh Jain,Rashmi Kanagal-Shamanna,William G. Wierda,Michael J. Keating,Nawid Sarwari,Uri Rozovski,Philip A. Thompson,Jan A. Burger,Hagop M. Kantarjian,Keyur P. Patel,L. Jeffrey Medeiros,Rajyalakshmi Luthra,Zeev Estrov +12 more
TL;DR: The clinical significance of XPO1 mutations in patients with chronic lymphocytic leukemia is investigated and NGS-based mutation analysis with a panel of CLL-related genes including NOTCH1, SF3B1, POT1, BTK, and BIRC3 is performed.
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Ofatumumab and Lenalidomide for Patients with Relapsed or Refractory Chronic Lymphocytic Leukemia: Correlation between Responses and Immune Characteristics
Candida Vitale,Lorenzo Falchi,Elisa Ten Hacken,Hui Gao,Hila Shaim,Katrien Van Roosbroeck,George A. Calin,Susan O'Brien,Stefan Faderl,Xuemei Wang,William G. Wierda,Katayoun Rezvani,James M. Reuben,Jan A. Burger,Michael J. Keating,Alessandra Ferrajoli +15 more
TL;DR: The combination of ofatumumab and lenalidomide is a well-tolerated regimen that induces durable responses in the majority of patients with relapsed/refractory CLL, suggesting a role of competent immune system in supporting the efficacy of this treatment.
Journal ArticleDOI
Resistance Mutations to BTK Inhibitors Originate From the NF-κB but Not From the PI3K-RAS-MAPK Arm of the B Cell Receptor Signaling Pathway.
C. I. Edvard Smith,Jan A. Burger +1 more
TL;DR: In this paper, the authors compared the primary and acquired mutation spectrum in BTKi-sensitive malignancies with the phenotype of the corresponding germline alterations, and found that certain observations do not readily fit with the existing models of BCR signaling.
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Efficacy of a Type I FLT3 Inhibitor, Crenolanib, with Idarubicin and High-Dose Ara-C in Multiply Relapsed/Refractory FLT3+ AML
Maro Ohanian,Hagop M. Kantarjian,Gautam Borthakur,Tapan M. Kadia,Marina Konopleva,Guillermo Garcia-Manero,Zeev Estrov,Alessandra Ferrajoli,Koichi Takahashi,Elias Jabbour,Naval Daver,Steven M. Kornblau,William G. Wierda,Jan A. Burger,Kiran Naqvi,Christopher B. Benton,Prithviraj Bose,John R. Eckardt,Farhad Ravandi,Jorge E. Cortes +19 more
TL;DR: The first 13 pts with R/R FLT3+ AML treated with salvage idarubicin (Ida) and high-dose ara-C (HiDAC) followed by crenolanib achieved a CR/CRi response and no dose-limiting toxicities were observed at any of the dose levels explored and there were no dose reductions required.
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Plasmids encoding granulocyte-macrophage colony-stimulating factor and CD154 enhance the immune response to genetic vaccines.
TL;DR: It is concluded that plasmids encoding GM-CSF and CD154 are particularly effective genetic adjuvants when used together to enhance the humoral and cellular immune response to a plasmid-encoded antigen.