B16 melanoma secretomes and in vitro invasiveness: syntenin as an invasion modulator

2010 ◽  
Vol 20 (2) ◽  
pp. 77-84 ◽  
Author(s):  
Fabien Rondepierre ◽  
Bernadette Bouchon ◽  
Mathilde Bonnet ◽  
Nicole Moins ◽  
Jean M. Chezal ◽  
...  
1998 ◽  
Vol 274 (5) ◽  
pp. R1454-R1459 ◽  
Author(s):  
J. M. Davis ◽  
M. L. Kohut ◽  
D. A. Jackson ◽  
L. H. Colbert ◽  
E. P. Mayer ◽  
...  

This study examined the effects of moderate and prolonged exercise on 1) lung tumor metastases and 2) alveolar macrophage antitumor response in vitro. C57Bl/6 mice were assigned to either Ex-30 (30-min run), Ex-F (run to fatigue), Ex-F-24 h (run to fatigue 24 h before tumor injection), or Con (rested in lanes above the treadmill). Mice received intravenous injections of syngeneic B16 melanoma cells 30 min postexercise. Lungs were removed 7 or 10 days later, and tumor foci were counted. Ex-F had fewer tumors than either Ex-30 or Con, whereas Ex-F-24 h also showed a strong trend toward fewer tumors. The initial localization of tumor cells in the lungs after injection was not different among groups. For the in vitro experiment, mice were killed immediately after exercise or 8 h later. Alveolar macrophages were removed and cultured in vitro with B16 melanoma cells. The growth of the tumors cultured with macrophages from Ex-F was lower than Con after exercise and, to a lesser extent, 8 h later. In Ex-30, this effect was only found immediately after exercise. The data suggest that prolonged exercise has a protective effect on lung tumor metastases and enhances alveolar macrophage antitumor cytotoxicity.


2011 ◽  
Vol 4 (3) ◽  
pp. 178-188 ◽  
Author(s):  
Aws Alshamsan ◽  
Samar Hamdy ◽  
Azita Haddadi ◽  
John Samuel ◽  
Ayman O.S. El-Kadi ◽  
...  

2021 ◽  
Vol 22 (18) ◽  
pp. 9859
Author(s):  
Anna V. Izosimova ◽  
Diana V. Yuzhakova ◽  
Valeria D. Skatova ◽  
Lilia N. Volchkova ◽  
Elena V. Zagainova ◽  
...  

Recent advances in cancer immunotherapy have great promise for the treatment of solid tumors. One of the key limiting factors that hamper the decoding of physiological responses to these therapies is the inability to distinguish between specific and nonspecific responses. The identification of tumor-specific lymphocytes is also the most challenging step in cancer cell therapies such as adoptive cell transfer and T cell receptor (TCR) cloning. Here, we have elaborated a protocol for the identification of tumor-specific T lymphocytes and the deciphering of their repertoires. B16 melanoma engraftment following anti-PD1 checkpoint therapy provides better antitumor immunity compared to repetitive immunization with heat-shocked tumor cells. We have also revealed that the most error-prone part of dendritic cell (DC) generation, i.e., their maturation step, can be omitted if DCs are cultured at a sufficiently high density. Using this optimized protocol, we have achieved a robust IFNγ response to B16F0 antigens, but only within CD4+ T helper cells. A comparison of the repertoires of IFNγ-positive and -negative cells shows a prominent enrichment of certain clones with putative tumor specificity among the IFNγ+ fraction. In summary, our optimized protocol and the data provided here will aid in the acquisition of broad statistical data and the creation of a meaningful database of B16-specific TCRs.


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