Functional and clinical relevance of VLA-4 (CD49d/CD29) in ibrutinib-treated chronic lymphocytic leukemia
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The Bruton’s tyrosine kinase (BTK) inhibitor ibrutinib, which antagonizes B cell receptor (BCR) signals, demonstrates remarkable clinical activity in chronic lymphocytic leukemia (CLL). The lymphocytosis experienced by most patients under ibrutinib has previously been attributed to inhibition of BTK-dependent integrin and chemokine cues operating to retain the tumor cells in nodal compartments. Here, we show that the VLA-4 integrin, as expressed by CD49d-positive CLL, can be inside-out activated upon BCR triggering, thus reinforcing the adhesive capacities of CLL cells. In vitro and in vivo ibrutinib treatment, although reducing the constitutive VLA-4 activation and cell adhesion, can be overcome by exogenous BCR triggering in a BTK-independent manner involving PI3K. Clinically, in three independent ibrutinib-treated CLL cohorts, CD49d expression identifies cases with reduced lymphocytosis and inferior nodal response and behaves as independent predictor of shorter progression-free survival, suggesting the retention of CD49d-expressing CLL cells in tissue sites via activated VLA-4. Evaluation of CD49d expression should be incorporated in the characterization of CLL undergoing therapy with BCR inhibitors.
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In ibrutinib-treated patients, high CD49d expression (≥30% CD49+ cells) was correlated with reduced treatment-induced lymphocytosis and inferior nodal responses.
“Inibrutinib-treated patients, high CD49d expression (≥30% CD49+ cells) was correlated with reduced treatment-induced lymphocytosis and inferior nodal responses(53).”
From Resistance Mechanisms and Approach to Chronic Lymphocytic Leukemia after BTK Inhibitor Therapy (2025) · cites this paper as [53]
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Integrin Signaling Shaping BTK-Inhibitor Resistance
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Self-citationResistance Mechanisms and Approach to Chronic Lymphocytic Leukemia after BTK Inhibitor Therapy
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“…for cD49d [48,51]. in ibrutinib-treated patients, high cD49d expression (≥30% cD49+ cells) was correlated with reduced treatment-induced lymphocytosis and inferior nodal responses [52]. interestingly, BTK and/or PLCG2 mutations are detected in most of these patients at time of progression [48].”
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- Authors
- Tissino, E., Benedetti, D., Herman, S. E. M., ten Hacken, E., Ahn, I. E., Chaffee, K. G., Rossi, F. M., Dal Bo, M., Bulian, P., Bomben, R., Bayer, E., Härzschel, A., Gutjahr, J. C., Postorino, M., Santinelli, E., Ayed, A., Zaja, F., Chiarenza, A., Pozzato, G., Chigaev, A., Sklar, L. A., Burger, J. A., Ferrajoli, A., Shanafelt, T. D., Wiestner, A., Del Poeta, G., Hartmann, T. N., Gattei, V., & Zucchetto, A.
- Affiliations
- Centro di Riferimento Oncologico (IT)
- National Institutes of Health (US)
- Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX 3
- Mayo Clinic College of Medicine, Rochester, MN 4
- Clinical and Experimental Onco-Hematology Unit, CRO Aviano National Cancer Institute, Aviano, Italy 1
- Paracelsus Medical University (AT)
- University of Rome Tor Vergata (IT)
- Mayo Clinic (US)
- Ospedale Santa Maria della Misericordia di Udine (IT)
- Ferrarotto Hospital (IT)
- University of Trieste (IT)
- University of New Mexico (US)
- The University of Texas MD Anderson Cancer Center (US)
- Division of Hematology, S. Eugenio Hospital and University of Tor Vergata, Rome, Italy 7
- Corresponding author
- Zucchetto, Antonella
- ORCID
- Tissino, Erika
- Benedetti, Dania
- Herman, Sarah E.M.
- Ahn, Inhye E.
- Chaffee, Kari G.
- Rossi, Francesca Maria
- Bulian, Pietro
- Bomben, Riccardo
- Gutjahr, Julia Christine
- Postorino, Massimiliano
- Santinelli, Enrico
- Ayed, Ayed
- Zaja, Francesco
- Chiarenza, Annalisa
- Pozzato, Gabriele
- Chigaev, Alexandre
- Sklar, Larry A.
- Burger, Jan A.
- Ferrajoli, Alessandra
- Shanafelt, Tait D.
- Wiestner, Adrian
- Hartmann, Tanja Nicole
- Gattei, Valter
- Zucchetto, Antonella
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2018-01-04
- Volume
- 215
- Issue
- 2
- Pages
- 681-697
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC5789417
- OpenAlex
- W2781624645
- Cited by
- 92
- References
- 57
- Citations by year
- 2026: 5 · 2025: 8 · 2024: 10 · 2023: 15 · 2022: 10 · 2021: 17 · 2020: 15 · 2019: 9 · 2018: 3
- FWCI
- 6.24
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- The Journal of Experimental Medicine (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- ArTS Archivio della ricerca di Trieste (University of Trieste https://www.units.it/) (submittedVersion, cc-by)
- KOPS (University of Konstanz) (submittedVersion, cc-by)
- Queen Mary Research Online (Queen Mary University of London) (submittedVersion, cc-by)
- Institutional Research Information System (University of Udine) (submittedVersion)
- Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
- Funders
- Associazione Italiana Ricerca Cancro (IG-17622)
- Progetto Giovani Ricercatori (GR-2011-02347441, GR-2011-02346826, GR-2011-02351370)
- Ministero della Salute
- Ricerca clinica, traslazionale, di base, epidemiologica e organizzativa, Regione Friuli Venezia Giulia
- Associazione Italiana contro le Leucemie, Linfomi e Mielomi
- Fondazione per la Vita di Pordenone
- 5x1000 Intramural Program
- National, Heart, Lung, and Blood Institute
- Topics
- Health Sciences › Medicine › Genetics › Chronic Lymphocytic Leukemia Research
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Health Sciences › Medicine › Pathology and Forensic Medicine › Lymphoma Diagnosis and Treatment
- Keywords
- VLA-4, ibrutinib, chronic lymphocytic leukemia, BTK inhibitors, B cell receptor signaling, cell adhesion, PI3K signaling, lymphocytosis, progression-free survival, prognostic factors
- MeSH terms
- Agammaglobulinaemia Tyrosine Kinase, Progression-Free Survival, Phosphoinositide-3 Kinase Inhibitors, Adenine, Cell Adhesion, Humans, Immunoglobulin M, Lymph Nodes, Lymphocytosis, Piperidines, Pyrazoles, Pyrimidines, Receptors, Antigen, B-Cell, Leukemia, Lymphocytic, Chronic, B-Cell, Multivariate Analysis, Proportional Hazards Models, Phosphatidylinositol 3-Kinases, Integrin alpha4beta1, Protein Kinase Inhibitors, Kaplan-Meier Estimate
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