Myc is the super controller which is defective in 70% of all cancers whereas the Bcl-2 family regulate cellular survival. How do you decide between drugging Myc and Bcl-2. Why don't we have both!
What happens when you do both will hopefully be answered by Phylogica and its collaborators re: Dual targeting of Myc and apoptosis pathways for improved blood cancer treatment outcomes.
As far as I understand the collaboration builds upon the earlier work by Dr Doug Fairlie's team who observed that the combination therapy improved the cancer killing activity of each drug by up to 600%.
The reason for re-hashing the announcement is to ponder the question why.
I wonder whether the mechanism of action for the combination therapy involves turning down immune suppression from the PD-L1 pathway to facilitate an immune response while simultaneously promoting cancer cell death by inactivating Bcl-2.
In researching the topic I came across the work of Professor Suzanne Cory from the Walter+Eliza Hall Institute. Her laboratory studies leukaemogenesis with a particular focus on Myc and the Bcl-2 family of proteins. Professor Cory is one of the founders of the field of apoptosis and is a member of the Grand Challenge Advisory Panel.
It would appear that Myc and Bcl-2 could be bedfellows in a large number of cancers. Are we on the verge of a major discovery?
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