Cited by 1,128Chronic Lymphocytic Leukemia ResearchLymphoma Diagnosis and TreatmentCutaneous lymphoproliferative disorders research

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Bruton Tyrosine Kinase Inhibitor Ibrutinib (PCI-32765) Has Significant Activity in Patients With Relapsed/Refractory B-Cell Malignancies

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Advani, Ranjana H., Buggy, Joseph J., Sharman, Jeff P., Smith, Sonali M., Boyd, Thomas E., Grant, Barbara, Kolibaba, Kathryn S., Furman, Richard R., Rodriguez, Sara, Chang, Betty Y., Sukbuntherng, Juthamas, Izumi, Raquel, Hamdy, Ahmed, Hedrick, Eric, Fowler, Nathan H.·2013·Journal of Clinical Oncology

DOI 10.1200/jco.2012.42.7906PMC PMC5505166

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Abstract

Purpose: Survival and progression of mature B-cell malignancies depend on signals from the B-cell antigen receptor, and Bruton tyrosine kinase (BTK) is a critical signaling kinase in this pathway. We evaluated ibrutinib (PCI-32765), a small-molecule irreversible inhibitor of BTK, in patients with B-cell malignancies. Patients and Methods: Patients with relapsed or refractory B-cell lymphoma and chronic lymphocytic leukemia received escalating oral doses of ibrutinib. Two schedules were evaluated: one, 28 days on, 7 days off; and two, once-daily continuous dosing. Occupancy of BTK by ibrutinib in peripheral blood was monitored using a fluorescent affinity probe. Dose escalation proceeded until either the maximum-tolerated dose (MTD) was achieved or, in the absence of MTD, until three dose levels above full BTK occupancy by ibrutinib. Response was evaluated every two cycles. Results: Fifty-six patients with a variety of B-cell malignancies were treated over seven cohorts. Most adverse events were grade 1 and 2 in severity and self-limited. Dose-limiting events were not observed, even with prolonged dosing. Full occupancy of the BTK active site occurred at 2.5 mg/kg per day, and dose escalation continued to 12.5 mg/kg per day without reaching MTD. Pharmacokinetic data indicated rapid absorption and elimination, yet BTK occupancy was maintained for at least 24 hours, consistent with the irreversible mechanism. Objective response rate in 50 evaluable patients was 60%, including complete response of 16%. Median progression-free survival in all patients was 13.6 months. Conclusion: Ibrutinib, a novel BTK-targeting inhibitor, is well tolerated, with substantial activity across B-cell histologies.

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Background
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BackgroundInfluential
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Background
TLR signaling is activated in lymph-node resident CLL cells and is only partially inhibited by ibrutinib
Dadashian, E. L., McAuley, E., Liu, D.-L., Shaffer, A., Young, R. M., Iyer, J. R., Kruhlak, M., Staudt, L., Wiestner, A., & Herman, S. E. M. (2018) · Cancer Research · doi:10.1158/0008-5472.can-18-0781 · Cited by 50
“The persistence of CLL cells despite virtually complete inhibition of BTK and tumor proliferation suggest that BTK-independent pathways canmaintain tumor viability (15, 46).”
Background
Ibrutinib, but not zanubrutinib, induces platelet receptor shedding of GPIb-IX-V complex and integrin αIIbβ3 in mice and humans
Dobie, G., Kuriri, F. A., Omar, M. M. A., Alanazi, F. G., Gazwani, A. M., Tang, C. P. S., Sze, D., Handunnetti, S. M., Tam, C. S. L., & Jackson, D. E. (2019) · Blood Advances · doi:10.1182/bloodadvances.2019000640 · Cited by 61
“Ibrutinib is also improved for marginal zone lymphoma and graft-versus-host disease in the United States.(3-8) Although ibrutinib is generally well tolerated, clinical studies have reported grade$3 bleeding events, including hematomas, hematuria, and gastrointestinal bleeding in 5% to 6% of patients.”
BackgroundMethodInfluential
How will B-cell-receptor–targeted therapies change future CLL therapy?
Jones, J. A., & Byrd, J. C. (2014) · Blood · doi:10.1182/blood-2013-09-453092 · Cited by 58
“A phase 1 study of ibrutinib in B-cell malignancies was initiated in which durable clinical activity was noted in non-Hodgkin lymphoma and 9 of 16CLL/ small lymphocytic lymphoma patients.(26) No dose-limiting toxicity was identified, and toxicity, includingmyelosuppression, wasmodest.”
Background
Microenvironment dependency in Chronic Lymphocytic Leukemia: The basis for new targeted therapies
ten Hacken, E., & Burger, J. A. (2014) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2014.07.003 · Cited by 64
Development of BTK inhibitors for the treatment of B-cell malignancies
Kim, H.-O. (2019) · Archives of Pharmacal Research · doi:10.1007/s12272-019-01124-1 · Cited by 60
Non-Covalent BTK Inhibitors—The New BTKids on the Block for B-Cell Malignancies
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“Preclinical efficacy in B-cell malignancies was first reported in 2010 [14] and results from a phase 1 clinical trial using ibrutinib to treat patients with B-cell malignancies was published in 2012 [15].”
Bruton’s Tyrosine Kinase Mediates the Synergistic Signalling between TLR9 and the B Cell Receptor by Regulating Calcium and Calmodulin
Kenny, E. F., Quinn, S. R., Doyle, S., Vink, P. M., van Eenennaam, H., & O'Neill, L. A. J. (2013) · PLoS ONE · doi:10.1371/journal.pone.0074103 · Cited by 57
“As abnormal BCR activation is linked to chronic lymphocytic leukaemia (CLL) the BTK inhibitor has also been examined as a tool to kill CLL cells.”
BackgroundInfluential
Targeting B-cell receptor signaling: changing the paradigm
Fowler, N. H., & Davis, R. E. (2013) · Hematology · doi:10.1182/asheducation-2013.1.553 · Cited by 56
Self-citation
Optimized Near-IR Fluorescent Agents for in Vivo Imaging of Btk Expression
Kim, E., Yang, K. S., Köhler, R. H., Dubach, J. M., Mikula, H., & Weissleder, R. (2015) · Bioconjugate Chemistry · doi:10.1021/acs.bioconjchem.5b00152 · Cited by 57
The impact of dose modification and temporary interruption of ibrutinib on outcomes of chronic lymphocytic leukemia patients in routine clinical practice
Parikh, S. A., Achenbach, S. J., Call, T. G., Rabe, K. G., Ding, W., Leis, J. F., Kenderian, S. S., Chanan-Khan, A. A., Koehler, A. B., Schwager, S. M., et al. (2020) · Cancer Medicine · doi:10.1002/cam4.2998 · Cited by 58
From identification of the BTK kinase to effective management of leukemia
Smith, C. I. E. (2016) · Oncogene · doi:10.1038/onc.2016.343 · Cited by 57
Ibrutinib, a Bruton’s tyrosine kinase inhibitor used for treatment of lymphoproliferative disorders, eliminates both aeroallergen skin test and basophil activation test reactivity
Regan, J. A., Cao, Y., Dispenza, M. C., Ma, S., Gordon, L. I., Petrich, A. M., & Bochner, B. S. (2017) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2017.03.013 · Cited by 57
Novel Indications for Bruton’s Tyrosine Kinase Inhibitors, beyond Hematological Malignancies
Campbell, R., Chong, G., & Hawkes, E. A. (2018) · Journal of Clinical Medicine · doi:10.3390/jcm7040062 · Cited by 56
“Ibrutinib efficacy is currently being explored in most B-cell malignancies including diffuse large B-cell lymphoma [11], follicular lymphoma [12], lymphoplasmacytic lymphoma [13], multiple myeloma [14], and primary CNS lymphoma [15].”
Background
Oral Bruton tyrosine kinase inhibitors block activation of the platelet Fc receptor CD32a (FcγRIIA): a new option in HIT?
Goldmann, L., Duan, R., Kragh, T., Wittmann, G., Weber, C., Lorenz, R. L., von Hundelshausen, P., Spannagl, M., & Siess, W. (2019) · Blood Advances · doi:10.1182/bloodadvances.2019000617 · Cited by 56
“78 mM, respectively) that are required to fully inhibit BTK in peripheral blood mononuclear cells.(40,41) Third, fenebrutinib, which belongs to the class of reversible BTKi’s that do not inhibit Tec in kinase assays,(20) completely suppressed platelet FcgRIIA activation in blood with a very low IC50 value (11 nM).”
Background
Targeting BCL-2 in Hematologic Malignancies
Khan, N., & Kahl, B. S. (2018) · Targeted Oncology · doi:10.1007/s11523-018-0560-7 · Cited by 59
“and parallel the high responses seen with the first-in-class BTK inhibitor, ibrutinib, in MCL [34].”
ResultInfluential
Waldenstrom macroglobulinemia: prognosis and management
Oza, A. M., & Rajkumar, S. V. (2015) · Blood Cancer Journal · doi:10.1038/bcj.2015.28 · Cited by 58
Targeting glycogen synthase kinase 3 for therapeutic benefit in lymphoma
Wu, X., Stenson, M. J., Abeykoon, J. P., Nowakowski, K. E., Zhang, L., Lawson, J., Wellik, L. E., Li, Y., Krull, J. E., Wenzl, K., et al. (2019) · Blood · doi:10.1182/blood.2018874560 · Cited by 55
Overcoming resistance to targeted therapies in chronic lymphocytic leukemia
Skånland, S. S., & Mato, A. R. (2021) · Blood Advances · doi:10.1182/bloodadvances.2020003423 · Cited by 55
“5 mg/kg per day).(43) Furthermore, treatment with ibrutinib decreases the level of BTK transcripts and protein in a time-dependent manner, which may suggest that ibrutinib can be administered at lower doses for long-term maintenance.”
Background
Acalabrutinib: A Selective Bruton Tyrosine Kinase Inhibitor for the Treatment of B-Cell Malignancies
Abbas, H. A., & Wierda, W. G. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.668162 · Cited by 54
“Completed N/A Active, not recruiting (64) Active, not recruiting N/A Active, not recruiting (54)”
Background
Targeting Protein Kinases Degradation by PROTACs
Yu, F., Cai, M., Shao, L., & Zhang, J. (2021) · Frontiers in Chemistry · doi:10.3389/fchem.2021.679120 · Cited by 55
“Research on BTKs is advancing considerably, with the BTK inhibitors ibrutinib (Advani et al., 2013), acalabrutinib (Byrd et al.”
Background
BTK inhibition limits microglia-perpetuated CNS inflammation and promotes myelin repair
Geladaris, A., Torke, S., Saberi, D., Alankus, Y. B., Streit, F., Zechel, S., Stadelmann, C., Fischer, A., Boschert, U., Häusler, D., et al. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02730-0 · Cited by 54
“…in peripheral blood mononuclear cells has been used as a surrogate marker for inhibition of BTK activity by first line BTK inhibitors in cancer [2] and clinical data generated during the Phase 2 evobrutinib development program in participants with relapsing MS demonstrated a dose-dependent…”
Background
Synergistic induction of apoptosis by combination of BTK and dual mTORC1/2 inhibitors in diffuse large B cell lymphoma
Ezell, S. A., Mayo, M., Bihani, T., Tepsuporn, S., Wang, S., Passino, M. A., Grosskurth, S. E., Collins, M., Parmentier, J. M., Reimer, C., et al. (2014) · Oncotarget · doi:10.18632/oncotarget.2071 · Cited by 54
Discovery of a Selective Irreversible BMX Inhibitor for Prostate Cancer
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Ibrutinib and venetoclax target distinct subpopulations of CLL cells: implication for residual disease eradication
Lu, P., Wang, S., Franzen, C. A., Venkataraman, G., McClure, R. F., Li, L., Wu, W., Niu, N., SUKHANOVA, M. J., Pei, J., et al. (2021) · Blood Cancer Journal · doi:10.1038/s41408-021-00429-z · Cited by 53
Long-term follow-up of patients with CLL treated with the selective Bruton’s tyrosine kinase inhibitor ONO/GS-4059
Walter, H. S., Jayne, S., Rule, S. A., Cartron, G., Morschhauser, F., Macip, S., Karlin, L., Jones, C. H., Herbaux, C., Quittet, P., et al. (2017) · Blood · doi:10.1182/blood-2017-02-765115 · Cited by 53
“Nevertheless, the kinome of ibrutinib is broad, resulting in toxicities including bleeding, arthralgia, diarrhea, hypertension, and atrial fibrillation.(3-6) Up to 20% of patients discontinue ibrutinib due to toxicity.”
Background
Ibrutinib inhibits BTK-driven NF-κB p65 activity to overcome bortezomib-resistance in multiple myeloma
Murray, M. Y., Zaitseva, L., Auger, M. J., Craig, J. I. O., MacEwan, D. J., Rushworth, S. A., & Bowles, K. M. (2015) · Cell Cycle · doi:10.1080/15384101.2014.998067 · Cited by 55
The orally available Btk inhibitor ibrutinib (PCI-32765) protects against osteoclast-mediated bone loss
Shinohara, M., Chang, B. Y., Buggy, J. J., Nagai, Y., Kodama, T., Asahara, H., & Takayanagi, H. (2013) · Bone · doi:10.1016/j.bone.2013.11.025 · Cited by 54
“In contrast, ibrutinib treatment did not affect serum levels of a variety of components determined by blood chemistry tests in a various mouse model [14], and there was no effect of ibrutinib on liver and renal functions even in humans [32–34], suggesting that ibrutinib has no severe side effects.”
BackgroundSelf-citation
Dual SYK/JAK inhibition overcomes ibrutinib resistance in chronic lymphocytic leukemia: Cerdulatinib, but not ibrutinib, induces apoptosis of tumor cells protected by the microenvironment
Guo, A., Lu, P., Coffey, G., Conley, P., Pandey, A., & Wang, Y. L. (2017) · Oncotarget · doi:10.18632/oncotarget.14588 · Cited by 52
“Our previous studies showed that ibrutinib, at a clinically achievable concentration of 500 nM (in human Cmax is 408 nM [1]), had little effect on cell survival with stromal co-culture [9, 14].”
Background
Heightened BTK-dependent cell proliferation in unmutated chronic lymphocytic leukemia confers increased sensitivity to ibrutinib
Guo, A., Lu, P., Galanina, N., Nabhan, C., Smith, S. M., Coleman, M., & Wang, Y. L. (2015) · Oncotarget · doi:10.18632/oncotarget.6727 · Cited by 51
“The maximal plasma concentration achievable in patients is 408 nM according to a previous pharmacokinetics study [38, 39].”
Self-citation
Inhibitors of BCR signalling interrupt the survival signal mediated by the micro‐environment in mantle cell lymphoma
Bernard, S., Danglade, D., Gardano, L., Laguillier, C., Lazarian, G., Roger, C., Thiéblemont, C., Marzec, J., Gribben, J. G., Cymbalista, F., et al. (2014) · International Journal of Cancer · doi:10.1002/ijc.29326 · Cited by 52
Overview on the management of non-gastric MALT lymphomas
Defrancesco, I., & Arcaini, L. (2017) · Best Practice & Research Clinical Haematology · doi:10.1016/j.beha.2017.11.001 · Cited by 52
A drug–drug interaction study of ibrutinib with moderate/strong CYP3A inhibitors in patients with B-cell malignancies
de Jong, J., Hellemans, P., Wilde, S. D., Patricia, D., Masterson, T. J., Manikhas, G., Myasnikov, A., Шевкетович, О. Д., Córdoba, R., Panizo, C., et al. (2018) · Leukemia & lymphoma/Leukemia and lymphoma · doi:10.1080/10428194.2018.1460474 · Cited by 54
Self-citation
Lenalidomide plus rituximab (R2) in previously untreated marginal zone lymphoma: subgroup analysis and long‐term follow‐up of an open‐label phase 2 trial
Becnel, M., Nastoupil, L. J., Samaniego, F., Davis, R. E., You, M. J., Green, M., Hagemeister, F. B., Fanale, M. A., Fayad, L., Westin, J. R., et al. (2019) · British Journal of Haematology · doi:10.1111/bjh.15843 · Cited by 52
Self-citation
Overcoming Ibrutinib Resistance in Chronic Lymphocytic Leukemia
Puła, B., Gołoś, A., Górniak, P., & Jamroziak, K. (2019) · Cancers · doi:10.3390/cancers11121834 · Cited by 52
“In the phase I study (#NCT00849654), ibrutinib monotherapy showed a 69% overall response rate (ORR) with 16% patients achieving complete response (CR) [49].”
Background
Regulation of B-Cell Receptor Signaling and Its Therapeutic Relevance in Aggressive B-Cell Lymphomas
Profitós-Pelejà, N., Santos, J. C., Marín‐Niebla, A., Roué, G., & Ribeiro, M. L. (2022) · Cancers · doi:10.3390/cancers14040860 · Cited by 53
Improving the Solubility, Dissolution, and Bioavailability of Ibrutinib by Preparing It in a Coamorphous State With Saccharin
Shi, X., Song, S., Ding, Z., Fan, B., Huang, W. Z., & Xu, T. (2019) · Journal of Pharmaceutical Sciences · doi:10.1016/j.xphs.2019.04.031 · Cited by 52
Ibrutinib: A Review of Its Use in Patients with Mantle Cell Lymphoma or Chronic Lymphocytic Leukaemia
Kim, E., & Dhillon, S. (2015) · Drugs · doi:10.1007/s40265-015-0380-3 · Cited by 51
“This lymphocytosis is thought to reflect a redistribution of malignant lymphocytes between different anatomical compartments, probably because of a disruption of BCR-mediated stromal chemotaxis and adhesion [27, 29].”
Influential
Hair and Nail Changes During Long-term Therapy With Ibrutinib for Chronic Lymphocytic Leukemia
Bitar, C., Farooqui, M. Z. H., Valdez, J., Saba, N. S., Soto, S., Bray, A., Marti, G. E., Wiestner, A. U., & Cowen, E. W. (2016) · JAMA Dermatology · doi:10.1001/jamadermatol.2016.0225 · Cited by 50
The potential of venetoclax (ABT-199) in chronic lymphocytic leukemia
Itchaki, G., & Brown, J. R. (2016) · Therapeutic Advances in Hematology · doi:10.1177/2040620716655350 · Cited by 51
Pharmacokinetic and pharmacodynamic evaluation of ibrutinib for the treatment of chronic lymphocytic leukemia: rationale for lower doses
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“5 mg/kg/day of ibrutinib in the phase I study in relapsed/refractory B-cell malignancies [48].”
BackgroundMethodInfluential
XPO1 Inhibitor Selinexor Overcomes Intrinsic Ibrutinib Resistance in Mantle Cell Lymphoma via Nuclear Retention of IκB
Ming, M., Wu, W., Xie, B., SUKHANOVA, M. J., Wang, W., Kadri, S., Sharma, S., Lee, J., Shacham, S., Landesman, Y., et al. (2018) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-17-0789-atr · Cited by 50
Addition of BTK inhibitor orelabrutinib to rituximab improved anti-tumor effects in B cell lymphoma
Yu, H., Wang, X., Li, J., Ye, Y., Wang, D., Fang, W., Mi, L., Ding, N., Wang, X., Song, Y., et al. (2021) · Molecular Therapy — Oncolytics · doi:10.1016/j.omto.2021.03.015 · Cited by 49
Next Generation BTK Inhibitors in CLL: Evolving Challenges and New Opportunities
Frustaci, A. M., Deodato, M., Zamprogna, G., Cairoli, R., Montillo, M., & Tedeschi, A. (2023) · Cancers · doi:10.3390/cancers15051504 · Cited by 50
“It is important to highlight that at this dosage, when adjusted for plasma protein binding, zanubrutinib exposure is approximately eight-fold higher than that observed with ibrutinib 560 mg daily [37,38].”
Background
Liquid chromatography–tandem mass spectrometric assay for the simultaneous determination of the irreversible BTK inhibitor ibrutinib and its dihydrodiol-metabolite in plasma and its application in mouse pharmacokinetic studies
Rood, J. J. M., van Hoppe, S., Schinkel, A. H., Schellens, J. H. M., Beijnen, J. H., & Sparidans, R. W. (2015) · Journal of Pharmaceutical and Biomedical Analysis · doi:10.1016/j.jpba.2015.10.033 · Cited by 49
Binding Sites of Anticancer Drugs on Human Serum Albumin (HSA): A Review
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Dose Optimization in Oncology Drug Development: The Emerging Role of Pharmacogenomics, Pharmacokinetics, and Pharmacodynamics
Papachristos, A., Patel, J. N., Vasileiou, M., & Patrinos, G. P. (2023) · Cancers · doi:10.3390/cancers15123233 · Cited by 48
“5 mg/kg (more than half the fixed-dose in an average adult weighing 70–80 kg) resulted in 95% BTK receptor occupancy, which did not increase with further dose escalation [47].”
Background
Final results of EFC6663: A multicenter, international, phase 2 study of alvocidib for patients with fludarabine-refractory chronic lymphocytic leukemia
Lanasa, M. C., Andritsos, L. A., Brown, J. R., Gabrilove, J. L., Caligaris‐Cappio, F., Ghia, P., Larson, R. A., Kipps, T. J., Leblond, V., Milligan, D. W., et al. (2015) · Leukemia Research · doi:10.1016/j.leukres.2015.02.001 · Cited by 48
Single cell imaging of Bruton's Tyrosine Kinase using an irreversible inhibitor
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BCR Signaling in Chronic Lymphocytic Leukemia and Related Inhibitors Currently in Clinical Studies
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“%) patients with CLL/SLL. Median progression free survival (PFS) in all patients was 13.6 months.”
MethodInfluential
B-Cell Receptor Signaling in Lymphoid Malignancies and Autoimmunity
Avalos, A. M., Meyer‐Wentrup, F. A. G., & Ploegh, H. L. (2014) · Advances in immunology · doi:10.1016/b978-0-12-800266-7.00004-2 · Cited by 47
“In a phase I study of adult patients with relapsed and refractory B-NHL and CLL, a complete or partial response was observed in 40% of participants (Advani et al., 2013).”
Background
Development of the Bruton's tyrosine kinase inhibitor ibrutinib for B cell malignancies
Gayko, U., Fung, M., Clow, F., Sun, S. H., Faust, E. A., Price, S., James, D. F., Doyle, M., Bari, S., & Zhuang, S. H. (2015) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.12878 · Cited by 52

Authors: Advani, R. H., Buggy, J. J., Sharman, J. P., Smith, S. M., Boyd, T. E., Grant, B., Kolibaba, K. S., Furman, R. R., Rodriguez, S., Chang, B. Y., Sukbuntherng, J., Izumi, R., Hamdy, A., Hedrick, E., & Fowler, N. H.
Affiliations: University of Vermont (US)
Corresponding author: Advani, Ranjana H.
ORCID: Advani, Ranjana H.
Sharman, Jeff P.
Smith, Sonali M.
Kolibaba, Kathryn S.
Furman, Richard R.
Chang, Betty Y.
Izumi, Raquel
Hamdy, Ahmed
Fowler, Nathan H.
Venue: Journal of Clinical Oncology
Publisher: American Society of Clinical Oncology (ASCO)
Published: 2013-01-01
Volume: 31
Issue: 1
Pages: 88-94
ISSN: 0732-183X (ISSN-L)
1527-7755
DOI: 10.1200/jco.2012.42.7906
PMC: PMC5505166
OpenAlex: W2171771895
Cited by: 1,128
References: 32
Citations by year: 2026: 17 · 2025: 38 · 2024: 47 · 2023: 44 · 2022: 46 · 2021: 90 · 2020: 79 · 2019: 92 · 2018: 73 · 2017: 117 · 2016: 94 · 2015: 135 · 2014: 134 · 2013: 110
FWCI: 58.95
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Oncology (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Abbott Laboratories
GlaxoSmithKline
Gilead Sciences
Celgene
Genentech
Takeda Oncology
Pharmacyclics
National Cancer Institute (P30CA016672)
Topics: Health Sciences › Medicine › Hematology › Chronic Lymphocytic Leukemia Research
Health Sciences › Medicine › Pathology and Forensic Medicine › Lymphoma Diagnosis and Treatment
Health Sciences › Medicine › Dermatology › Cutaneous lymphoproliferative disorders research
Keywords: ibrutinib, BTK inhibitors, relapsed/refractory B-cell malignancies, B-cell lymphoma, chronic lymphocytic leukemia, B cell receptor signaling, irreversible kinase inhibitors, BTK occupancy, dose-limiting toxicity, pharmacokinetics, progression-free survival
MeSH terms: Agammaglobulinaemia Tyrosine Kinase, Adenine, Administration, Oral, Adult, Aged, Aged, 80 and over, Female, Follow-Up Studies, Humans, Male, Middle Aged, Neoplasm Recurrence, Local, Neoplasm Staging, Piperidines, Prognosis, Protein-Tyrosine Kinases, Pyrazoles, Pyrimidines, Leukemia, Lymphocytic, Chronic, B-Cell, Lymphoma, B-Cell, Salvage Therapy, Drug Resistance, Neoplasm, Maximum Tolerated Dose, Protein Kinase Inhibitors

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Bruton Tyrosine Kinase Inhibitor Ibrutinib (PCI-32765) Has Significant Activity in Patients With Relapsed/Refractory B-Cell Malignancies

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