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5. Correction to: The CXCL12gamma chemokine immobilized by heparan sulfate on stromal niche cells controls adhesion and mediates drug resistance in multiple myeloma (Journal of Hematology & Oncology, (2021), 14, 1, (11), 10.1186/s13045-021-01031-3)

Author

Ren, Zemin, Lantermans, Hildo, Kuil, Annemieke, Kraan, Willem, Arenzana-Seisdedos, Fernando, Kersten, Marie José, Spaargaren, Marcel, Pals, Steven T., Pathology, AII - Cancer immunology, CCA - Cancer biology and immunology, Clinical Haematology, and 09 Laboratory specialisms

Abstract

The original article [1] contained an error in the order of the citations in the manuscript which was mistakenly introduced by the production team of the journal and not by the authors of this article. The article has since been corrected to ensure that all citations correspond to their appropriate references.

Published
2021

7. Additional file 1 of The CXCL12gamma chemokine immobilized by heparan sulfate on stromal niche cells controls adhesion and mediates drug resistance in multiple myeloma

Author

Zemin Ren, Lantermans, Hildo, Kuil, Annemieke, Kraan, Willem, Arenzana-Seisdedos, Fernando, Kersten, Marie José, Spaargaren, Marcel, and Pals, Steven T.

Abstract

Additional file 1. The CXCL12γ chemokine immobilized by heparan sulfate on stromal niche cells controls adhesion and mediates drug resistance in multiple myeloma.

Published
2021
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10. Cell lines generated from a chronic lymphocytic leukemia mouse model exhibit constitutive Btk and Akt signaling

Author

Singh, Simar Pal, primary, Pillai, Saravanan Y., additional, de Bruijn, Marjolein J.W., additional, Stadhouders, Ralph, additional, Corneth, Odilia B.J., additional, van den Ham, Henk Jan, additional, Muggen, Alice, additional, van IJcken, Wilfred, additional, Slinger, Erik, additional, Kuil, Annemieke, additional, Spaargaren, Marcel, additional, Kater, Arnon P., additional, Langerak, Anton W., additional, and Hendriks, Rudi W., additional

Published
2017
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16. Egress of CD19+CD5+cells into peripheral blood following treatment with the Bruton tyrosine kinase inhibitor ibrutinib in mantle cell lymphoma patients

Author

Chang, Betty Y., Francesco, Michelle, De Rooij, Martin F.M., Magadala, Padmaja, Steggerda, Susanne M., Huang, Min Mei, Kuil, Annemieke, Herman, Sarah E.M., Chang, Stella, Pals, Steven T., Wilson, Wyndham, Wiestner, Adrian, Spaargaren, Marcel, Buggy, Joseph J., and Elias, Laurence

Abstract

Ibrutinib (PCI-32765) is a highly potent oral Bruton tyrosine kinase (BTK) inhibitor in clinical development for treating B-cell lymphoproliferative diseases. Patients with chronic lymphocytic leukemia (CLL) often show marked, transient increases of circulating CLL cells following ibrutinib treatments, as seen with other inhibitors of the B-cell receptor (BCR) pathway. In a phase 1 study of ibrutinib, we noted similar effects in patients with mantle cell lymphoma (MCL). Here, we characterize the patterns and phenotypes of cells mobilized among patients with MCL and further investigate the mechanism of this effect. Peripheral blood CD19+CD5+cells from MCL patients were found to have significant reduction in the expression of CXCR4, CD38, and Ki67 after 7 days of treatment. In addition, plasma chemokines such as CCL22, CCL4, and CXCL13 were reduced 40% to 60% after treatment. Mechanistically, ibrutinib inhibited BCR- and chemokine-mediated adhesion and chemotaxis of MCL cell lines and dose-dependently inhibited BCR, stromal cell, and CXCL12/CXCL13 stimulations of pBTK, pPLCγ2, pERK, or pAKT. Importantly, ibrutinib inhibited migration of MCL cells beneath stromal cells in coculture. We propose that BTK is essential for the homing of MCL cells into lymphoid tissues, and its inhibition results in an egress of malignant cells into peripheral blood. This trial was registered at www.clinicaltrials.govas #NCT00114738.

Published
2013
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17. Egress of CD19+CD5+ cells into peripheral blood following treatment with the Bruton tyrosine kinase inhibitor ibrutinib in mantle cell lymphoma patients.

Author

Chang, Betty Y., Francesco, Michelle, De Rooij, Martin F. M., Magadala, Padmaja, Steggerda, Susanne M., Min Mei Huang, Kuil, Annemieke, Herman, Sarah E. M., Chang, Stella, Pals, Steven T., Wilson, Wyndham, Wiestner, Adrian, Spaargaren, Marcel, Buggy, Joseph J., and Elias, Laurence

Subjects
*PROTEIN-tyrosine kinases, *LYMPHOCYTIC leukemia, *LYMPHOPROLIFERATIVE disorders, *GENOTYPE-environment interaction, *CYTOKINES
Abstract

Ibrutinib (PCI-32765) is a highly potent oral Bruton tyrosine kinase (BTK) inhibitor in clinical development for treating B-cell lymphoproliferative diseases. Patients with chronic lymphocytic leukemia (CLL) often show marked, transient increases of circulating CLL cells following ibrutinib treatments, as seen with other inhibitors of the B-cell receptor (BCR) pathway. In a phase 1 study of ibrutinib, we noted similar effects in patients with mantle cell lymphoma (MCL). Here, we characterize the patterns and phenotypes of cells mobilized among patients with MCL and further investigate the mechanism of this effect. Peripheral blood CD19+ CD5+ cells from MCL patients were found to have significant reduction in the expression of CXCR4, CD38, and Ki67 after 7 days of treatment. In addition, plasma chemokines such as CCL22, CCL4, and CXCL13 were reduced 40% to 60% after treatment. Mechanistically, ibrutinib inhibited BCR- and chemokine-mediated adhesion and chemo-taxis of MCL cell lines and dose-dependently inhibited BCR, stromal cell, and CXCL12/ CXCL13 stimulations of pBTK, PPLCγ2, pERK, or pAKT. Importantly, ibrutinib inhibited migration of MCL cells beneath stromal cells in coculture. We propose that BTK is essential for the homing of MCL cells into lymphoid tissues, and its inhibition results in an egress of malignant cells into peripheral blood. [ABSTRACT FROM AUTHOR]

Published
2013
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18. Ibrutinib and idelalisib target B cell receptor- but not CXCL12/CXCR4-controlled integrin-mediated adhesion in Waldenström macroglobulinemia.

Author

de Rooij MF, Kuil A, Kraan W, Kersten MJ, Treon SP, Pals ST, and Spaargaren M

Subjects
Adenine analogs & derivatives, Agammaglobulinaemia Tyrosine Kinase, Cell Adhesion drug effects, Cell Line, Tumor, Cell Proliferation drug effects, Cell Survival drug effects, Chemokine CXCL12 genetics, Chemokine CXCL12 immunology, Humans, Integrin alpha4beta1 genetics, Integrin alpha4beta1 immunology, Molecular Targeted Therapy, Myeloid Differentiation Factor 88 genetics, Myeloid Differentiation Factor 88 immunology, Piperidines, Plasma Cells immunology, Plasma Cells pathology, Protein-Tyrosine Kinases genetics, Protein-Tyrosine Kinases immunology, Receptors, Antigen, B-Cell antagonists & inhibitors, Receptors, Antigen, B-Cell immunology, Receptors, CXCR4 genetics, Receptors, CXCR4 immunology, Signal Transduction, Vascular Cell Adhesion Molecule-1 genetics, Vascular Cell Adhesion Molecule-1 immunology, Waldenstrom Macroglobulinemia genetics, Waldenstrom Macroglobulinemia immunology, Waldenstrom Macroglobulinemia pathology, Antineoplastic Agents pharmacology, Gene Expression Regulation, Neoplastic, Plasma Cells drug effects, Purines pharmacology, Pyrazoles pharmacology, Pyrimidines pharmacology, Quinazolinones pharmacology, Receptors, Antigen, B-Cell genetics
Published
2016
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