多发性骨髓瘤
医学
癌症研究
体内
生物标志物
骨髓
阿尔坎
单克隆抗体
免疫学
抗体
病理
细胞粘附分子
生物
生物化学
生物技术
作者
Antonio Giovanni Solimando,Andreas Brandl,Katharina Martini,Caroline Graf,Miriam Ritz,Anna Ruckdeschel,Thorsten Stühmer,Zeinab Mokhtari,Martina Rudelius,Julia Dotterweich,Max Bittrich,Vanessa Desantis,Regina Ebert,Paolo Trerotoli,Fei Ma,Andreas Rosenwald,Angelo Vacca,Hermann Einsele,Franz Jakob,Andreas Beilhack
出处
期刊:Leukemia
[Springer Nature]
日期:2017-09-28
卷期号:32 (3): 736-743
被引量:56
摘要
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.
科研通智能强力驱动
Strongly Powered by AbleSci AI