Thanks @GMT2, all things come to those who wait…About IMU’s...

Thanks @GMT2, all things come to those who wait…

About IMU’s participation at the AACR meeting, Leslie Chong quoted -

Further analysis of the T cell repertoire reveals that T cell diversity may serve a predictive biomarker, which can be used to prospectively identified appropriate patients for treatment

I don’t know if this information has been made public before. But it seems important. If anyone with knowledge in this area could comment, it would be good to get their interpretation of Leslie‘s quote.

CF33-HNIS (vaxinia) kills tumours directly, so why would the virus be more effective in the presence of a more diverse T cell environment? Are the more “useful” variants of T cells doing more killing work after the virus has done its initial bit? Is the virus, therefore, not quite as potent on its own, relying on the right kind of T cells? Would this imply that a modified T cell e.g. azer-cell ( with a Chimeric Antigen Receptor) will, in tandem with a modified CF33, kill more tumours than CF33-HNIS alone? If so, might onCARlytics (virus plus CAR Therapy) be Imugene’s main game?

These might be old news type questions. But I also agree that many visitors at AACR meeting would not be up to speed with IMU’s endeavours, therefore it was a very important event to introduce the medical technology to those who matter. Even if us shareholders think we’ve heard it all before.