TY  - JOUR
A1  - Solimando, A G
A1  - Brandl, A
A1  - Mattenheimer, K
A1  - Graf, C
A1  - Ritz, M
A1  - Ruckdeschel, A
A1  - Stühmer, T
A1  - Mokhtari, Z
A1  - Rudelius, M
A1  - Dotterweich, J
A1  - Bittrich, M
A1  - Desantis, V
A1  - Ebert, R
A1  - Trerotoli, P
A1  - Frassanito, M A
A1  - Rosenwald, A
A1  - Vacca, A
A1  - Einsele, H
A1  - Jakob, F
A1  - Beilhack, A
T1  - JAM-A as a prognostic factor and new therapeutic target in multiple myeloma
T2  - Leukemia
N2  - 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.
KW  - haematological cancer
KW  - myeloma
Y1  - 2018
UR  - https://opus.bibliothek.uni-wuerzburg.de/frontdoor/index/index/docId/23906
UR  - https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-239069
VL  - 32
ER  -