Search our Database of Scientific Publications and Authors

I’m looking for a
    Ibrutinib in PCNSL: The Curious Cases of Clinical Responses and Aspergillosis.
    • Authors:
    • Christian Grommes
      Case Western Reserve University
      United States
      Anas Younes
      The University of Texas MD Anderson Cancer Center
      United States
    Cancer Cell 2017 06 25;31(6):731-733. Epub 2017 May 25.
    Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Electronic address:
    In this issue of Cancer Cell, Lionakis et al. demonstrate that the combination of temozolomide, etoposide, doxorubicin, dexamethasone, rituximab, and the Bruton tyrosine kinase (BTK) inhibitor ibrutinib induced frequent responses in patients with primary central nervous system lymphoma but was associated with significant toxicity, including pulmonary and cerebral aspergillosis infections.

    Similar Publications

    Inhibition of B Cell Receptor Signaling by Ibrutinib in Primary CNS Lymphoma.
    Cancer Cell 2017 Jun 25;31(6):833-843.e5. Epub 2017 May 25.
    Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address:
    Primary CNS lymphoma (PCNSL) harbors mutations that reinforce B cell receptor (BCR) signaling. Ibrutinib, a Bruton's tyrosine kinase (BTK) inhibitor, targets BCR signaling and is particularly active in lymphomas with mutations altering the BCR subunit CD79B and MYD88. We performed a proof-of-concept phase Ib study of ibrutinib monotherapy followed by ibrutinib plus chemotherapy (DA-TEDDi-R). Read More
    Combination of ibrutinib with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) for treatment-naive patients with CD20-positive B-cell non-Hodgkin lymphoma: a non-randomised, phase 1b study.
    Lancet Oncol 2014 Aug 17;15(9):1019-26. Epub 2014 Jul 17.
    The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
    Background: Present first-line therapy for diffuse large B-cell lymphoma, a subtype of non-Hodgkin lymphoma, is rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP). Ibrutinib, a novel oral Bruton's tyrosine kinase inhibitor, has shown single-drug activity in relapsed or refractory B-cell malignancies. We investigated the safety and efficacy of ibrutinib in combination with R-CHOP for patients with previously untreated CD20-positive B-cell non-Hodgkin lymphoma. Read More
    Bruton tyrosine kinase inhibitors: a promising novel targeted treatment for B cell lymphomas.
    Br J Haematol 2013 Nov 24;163(4):436-43. Epub 2013 Sep 24.
    Stanford University Medical Center, Stanford, CA, USA.
    Constitutive or aberrant signalling of the B cell receptor signalling cascade has been implicated in the propagation and maintenance of a variety of B cell malignancies. Small molecule inhibitors of Bruton tyrosine kinase (BTK), a protein early in this cascade and specifically expressed in B cells, have emerged as a new class of targeted agents. There are several BTK inhibitors, including ONO-WG-307, LFM-A13, dasatinib, CC-292, and PCI-32765 (ibrutinib), in preclinical and/or clinical development of which ibrutinib is currently in phase III trials. Read More
    Cell-cycle reprogramming for PI3K inhibition overrides a relapse-specific C481S BTK mutation revealed by longitudinal functional genomics in mantle cell lymphoma.
    Cancer Discov 2014 Sep 31;4(9):1022-35. Epub 2014 Jul 31.
    Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, New York. Graduate Program in Immunology and Microbial Pathogenesis, Weill Cornell Medical College, New York, New York.
    Unlabelled: Despite the unprecedented clinical activity of the Bruton tyrosine kinase (BTK) inhibitor ibrutinib in mantle cell lymphoma (MCL), acquired resistance is common. By longitudinal integrative whole-exome and whole-transcriptome sequencing and targeted sequencing, we identified the first relapse-specific C481S mutation at the ibrutinib binding site of BTK in MCL cells at progression following a durable response. This mutation enhanced BTK and AKT activation and tissue-specific proliferation of resistant MCL cells driven by CDK4 activation. Read More