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Effect of ibrutinib on CCR7 expression and functionality in chronic lymphocytic leukemia and its implication for the activity of CAP-100, a novel therapeutic anti-CCR7 antibody.
Mateu-Albero, Tamara; Juárez-Sánchez, Raquel; Loscertales, Javier; Mol, Wim; Terrón, Fernando; Muñoz-Calleja, Cecilia; Cuesta-Mateos, Carlos.
Afiliación
  • Mateu-Albero T; Immunology Department, Hospital Universitario de La Princesa, IIS-IP, Diego de León 62, 28006, Madrid, Spain.
  • Juárez-Sánchez R; Immunology Department, Hospital Universitario de La Princesa, IIS-IP, Diego de León 62, 28006, Madrid, Spain.
  • Loscertales J; IMMED S.L., Immunological and Medicinal Products, C/ Velázquez 57, 6º derecha, 28001, Madrid, Spain.
  • Mol W; Hematology Department, Hospital Universitario de La Princesa, IIS-IP, Diego de León 62, 28006, Madrid, Spain.
  • Terrón F; Catapult Therapeutics, Lelystad, The Netherlands.
  • Muñoz-Calleja C; IMMED S.L., Immunological and Medicinal Products, C/ Velázquez 57, 6º derecha, 28001, Madrid, Spain.
  • Cuesta-Mateos C; Catapult Therapeutics, Lelystad, The Netherlands.
Cancer Immunol Immunother ; 71(3): 627-636, 2022 Mar.
Article en En | MEDLINE | ID: mdl-34297159
CAP-100 is a novel therapeutic antibody directed against the ligand binding site of human CCR7. This chemokine receptor is overexpressed in chronic lymphocytic leukemia (CLL) and orchestrates the homing of CLL cells into the lymph node. Previous studies, on a very limited number of samples, hypothesized that the Bruton's tyrosine kinase inhibitor (BTKi) ibrutinib might induce loss of surface CCR7 levels in CLL cells. CAP-100 will be evaluated in clinical trials as a therapy for relapse/refractory CLL patients, who have received at least two systemic therapies (NCT04704323). As nowadays many relapse/refractory CLL patients will have received ibrutinib as a prior therapy, we aimed to investigate in a large cohort of CLL patients the impact of this BTKi on CCR7 expression and functionality as well as on the therapeutic activity of CAP-100. Our data confirm that ibrutinib moderately down-regulates the very high expression of CCR7 in CLL cells but has no apparent effect on CCR7-induced chemotaxis. Moreover, CLL cells are perfectly targetable by CAP-100 which led to a complete inhibition of CCR7-mediated migration and induced strong target cell killing through antibody-dependent cell-mediated cytotoxicity, irrespective of previous or contemporary ibrutinib administration. Together, these results validate the therapeutic utility of CAP-100 as a next-line single-agent therapy for CLL patients who failed to ibrutinib and confirm that CAP-100 and ibrutinib have complementary non-overlapping mechanisms of action, potentially allowing for combination therapy.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Piperidinas / Adenina / Regulación Neoplásica de la Expresión Génica / Inhibidores de Proteínas Quinasas / Receptores CCR7 / Antineoplásicos Inmunológicos Límite: Humans Idioma: En Revista: Cancer Immunol Immunother Asunto de la revista: ALERGIA E IMUNOLOGIA / NEOPLASIAS / TERAPEUTICA Año: 2022 Tipo del documento: Article País de afiliación: España Pais de publicación: Alemania

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Piperidinas / Adenina / Regulación Neoplásica de la Expresión Génica / Inhibidores de Proteínas Quinasas / Receptores CCR7 / Antineoplásicos Inmunológicos Límite: Humans Idioma: En Revista: Cancer Immunol Immunother Asunto de la revista: ALERGIA E IMUNOLOGIA / NEOPLASIAS / TERAPEUTICA Año: 2022 Tipo del documento: Article País de afiliación: España Pais de publicación: Alemania