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Leukemia ; 32(3): 736-743, 2018 03.
Article in English | MEDLINE | ID: mdl-29064484

ABSTRACT

Cell adhesion in the multiple myeloma (MM) microenvironment has been recognized as a major mechanism of MM cell survival and the development of drug resistance. Here we addressed the hypothesis that the protein junctional adhesion molecule-A (JAM-A) may represent a novel target and a clinical biomarker in MM. We evaluated JAM-A expression in MM cell lines and in 147 MM patient bone marrow aspirates and biopsies at different disease stages. Elevated JAM-A levels in patient-derived plasma cells were correlated with poor prognosis. Moreover, circulating soluble JAM-A (sJAM-A) levels were significantly increased in MM patients as compared with controls. Notably, in vitro JAM-A inhibition impaired MM migration, colony formation, chemotaxis, proliferation and viability. In vivo treatment with an anti-JAM-A monoclonal antibody (αJAM-A moAb) impaired tumor progression in a murine xenograft MM model. These results demonstrate that therapeutic targeting of JAM-A has the potential to prevent MM progression, and lead us to propose JAM-A as a biomarker in MM, and sJAM-A as a serum-based marker for clinical stratification.


Subject(s)
Biomarkers, Tumor , Junctional Adhesion Molecule A/blood , Multiple Myeloma/blood , Multiple Myeloma/mortality , Animals , Antineoplastic Agents/pharmacology , Antineoplastic Agents/therapeutic use , Bone Marrow/pathology , Cell Line, Tumor , Cell Movement/drug effects , Cell Proliferation/drug effects , Female , Gene Expression , Humans , Junctional Adhesion Molecule A/genetics , Male , Mice , Molecular Targeted Therapy , Multiple Myeloma/drug therapy , Multiple Myeloma/pathology , Prognosis
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