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Tuesday, July 16, 2019 1:32:38 AM
As I have stated tumors are hetergenous in that they present multiple antigens and always change antigens on the surface to adapt making them harder to kill. Tumors also have a suppressive T-cell microenvironment as well. Being able to get MultiTAA to recruit the dormant immune system to target other antigens is ideal. Makes it harder for the tumor to stop imminent attacks from T-cells and other parts of the immune system.
The problem with CAR-T is that they are engineered in the lab. That means once the engineered CAR-T cells die out, the durable response ends up dying out as well. That's why if you see the Marker presentation you will see that with blood cancer MultiTAA was able to generate a more longer durable response and then you see Kite's CAR-T cells tart to drop off lower on the chart. That's the CAR-T cells dying off. They don't get passed on to other T-cells already in the patient's immune system.
Which is why also with Marker Therapeutics, which the CEO noted, that every patient that has achieved a complete response when given MultiTAA has not relapsed in cancer. That's because once it works as a complete response MultiTAA along with epitope spreading keeps the cancer from growing back.
Good things are coming for Marker, I'm glad I found this biotech after doing some heavy DD on it.
Recent MRKR News
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