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Molecular Oncology, Markers, Clinical Correlates |
1 Laboratory of Oncology, G. Gaslini Institute, Genova; 2 Laboratory of Phagocyte Physiopathology and Inflammation, Department of Internal Medicine, University of Genova, Genova; 3 Laboratory of Pathology, S. Andrea Hospital, La Spezia; 4 Division of Internal Medicine, Department of Medical Sciences, Amedeo Avogadro, University of Eastern Piedmont, Novara; and 5 Academic Department of Clinical and Experimental Medicine, Clinical Immunology Branch, Padua University School of Medicine, Padova, Italy
Purpose: Few data are available in the literature on chemokine receptor expression and migratory capability of mantle cell lymphoma (MCL) B cells. Information on these issues may allow us to identify novel mechanisms of chemokine-driven tumor cell migration.
Experimental Design: The research was designed to investigate: (a) expression of CCR1 to CCR7 and CXCR1 to CXCR5 chemokine receptors; and (b) chemotaxis to the respective ligands in MCL B cells and in their normal counterparts, i.e., CD5+ B cells.
Results: Malignant B cells from MCL patients and normal counterparts displayed similar chemokine receptor profiles. MCL B cells were induced to migrate by CXCL12 and CCL19, whereas normal CD5+ B cells migrated to the former, but not the latter chemokine. Overnight culture of MCL B cells and their normal counterparts with CXCL12 cross-sensitized other chemokine receptors to their ligands in some tumor samples but not in CD5+ B cells.
Conclusions: CCR7 and CXCR4 ligands may play a key role in tumor cell migration and spreading in vivo. CXCL12 may additionally contribute by sensitizing MCL B cells to respond to the ligands of other chemokine receptors.
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