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At ASH 2016 in San Diego, CA, I had the honor of once again interviewing Dr. Adrian Wiestner from the NIH (National Institute of Health) about the prototype BTK inhibitor, ibrutinib and how and why it works so well in chronic lymphocytic leukemia (CLL).
We have known for a while that for its survival and well-being, our cancer is dependent on BCR (B cell receptor) signaling. Blocking BTK (Bruton’s Tyrosine Kinase), blocks that BCR signaling and that blocking usually leads to our cancer’s retreat.
This is a well-understood critical tenet of why ibrutinib works as well as it does, but it is hardly the whole story as we are learning over time.
At the NIH, Dr. Wiestner and his team not only did some of the earliest clinical research on ibrutinib, but also has been doing the bench science on how it works.
Take Away Points
- When we start taking ibrutinib, it immediately begins to stops the cancer cells from growing.
- CLL cells have the ability to shape their microenvironment to favor their survival.
- Over time, ibrutinib’s effect on the cancer’s microenvironment grows stronger.
- It is the broad activity of ibrutinib not only on the cancer, but also on its microenvironment that may explain its durable activity.
- Responses can grow deeper over time with more patients reaching complete remissions.
- While we don’t know for certain, there is growing evidence from multiple sources that it is the BTK inhibition that is the critical action in controlling the CLL.
Please enjoy this interview that gets under the hood, and explains how ibrutinib and likely other similar drugs works
Brian Koffman, MD 2/7/17