Antitumor Activity of Interleukin-18 on Mouse Glioma Cells

2000 ◽  
Vol 23 (2) ◽  
pp. 184-189 ◽  
Author(s):  
Tetsuro Kikuchi ◽  
Yasuharu Akasaki ◽  
Tatsuhiro Joki ◽  
Toshiaki Abe ◽  
Masashi Kurimoto ◽  
...  
1999 ◽  
Vol 22 (3) ◽  
pp. 245-250 ◽  
Author(s):  
Tetsuro Kikuchi ◽  
Tatsuhiro Joki ◽  
Toshiaki Abe ◽  
Tsuneya Ohno

2017 ◽  
Vol 238 (1) ◽  
Author(s):  
A. Cabral–Prieto ◽  
R. López-Callejas ◽  
B. G. Rodríguez-Méndez ◽  
C. L. Santos-Cuevas ◽  
J. Celis-Almazán ◽  
...  
Keyword(s):  
E Coli ◽  

1978 ◽  
Vol 17 (3) ◽  
pp. 453-471 ◽  
Author(s):  
Kyoko Miura ◽  
Keiko Suzuki ◽  
Nobumasa Imura
Keyword(s):  

2021 ◽  
Author(s):  
Luiz Henrique Geraldo ◽  
Yunling Xu ◽  
Laurent Jacob ◽  
Laurence Pibouin Fragner ◽  
Rohit Rao ◽  
...  

AbstractSLIT2 is a secreted polypeptide that guides migration of cells expressing ROBO1&2 receptors. Herein, we investigated SLIT2/ROBO signaling effects in gliomas. In patients with glioblastoma (GBM), SLIT2 expression increased with malignant progression and correlated with poor survival and immunosuppression. Knockdown of SLIT2 in mouse glioma cells and patient derived GBM xenografts reduced tumor growth and synergized with immunotherapy to prolong survival. Tumor cell SLIT2 knockdown inhibited macrophage invasion and promoted a cytotoxic gene expression profile, which improved tumor vessel function and enhanced efficacy of chemotherapy and immunotherapy. Mechanistically, SLIT2 promoted microglia/macrophage chemotaxis and tumor-supportive polarization via ROBO1&2-mediated PI3Kγ activation. Macrophage Robo1&2 deletion and systemic SLIT2 trap delivery mimicked SLIT2 knockdown effects on tumor growth and the tumor microenvironment (TME), revealing SLIT2 signaling through macrophage ROBOs as a novel regulator of the GBM microenvironment and a potential immunotherapeutic target for brain tumors.


2020 ◽  
Vol 163 ◽  
pp. 36-43 ◽  
Author(s):  
Anbazhagan Sathiyaseelan ◽  
Kandasamy Saravanakumar ◽  
Jothi Jayalakshmi ◽  
Margabandhu Gopi ◽  
Azeez Shajahan ◽  
...  

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