I'd be curious to know if/how the Itaconate Shunt model fits into this? It sounds very similar what with the idea that it's a chronic "deny pathogens any access to energy" response.
Star--I do think it is similar. As I mentioned at the start, there will not be one single answer, one magic bullet. Our biochemistry--thanks to millions of years of evolution--is, on one hand, mind bogglingly complex (at least to me!!) but on the other hand, that biochemistry is filled with patterns characterized especially by redundancy, back doors, shunts. Almost every key process--and again I emphasize I am not even close to being a biochemist--has alternative pathways evolved to survive dysfunction and/or 'attack'.
I have heard Rob Phair and Chris Armstrong speak at length about he shunt at the same meetings where Paul Hwang presented.
To me the big question is how these different survival pathways interact, how they lead to a 'frozen' CDR, and why. As we tease this apart, I am confident we will come up with interventions and that's why I am so excited about the WASF3 pathway and what I will discuss next, the molecule SMPDL3B. Stay tuned. And pls keep the questions coming.
This was such a great article. I would love to participate in a trial if that opportunity ever arrived. Thank you for sharing all this information in a way non-medical brains like myself can still grasp. 😀
Thanks. I'm glad you enjoyed it and found it informative. Unfortunately, it will take a while to get any trial launched since the NIH moves very slowly even in the best of times...which this isn't. But will be writing more about this and other emerging info.
Oh, I definitely realize the snail’s pace of these things. ☺️ But it sounds like a great area of potential hopefully will get the funding it deserves.?
I'd be curious to know if/how the Itaconate Shunt model fits into this? It sounds very similar what with the idea that it's a chronic "deny pathogens any access to energy" response.
Star--I do think it is similar. As I mentioned at the start, there will not be one single answer, one magic bullet. Our biochemistry--thanks to millions of years of evolution--is, on one hand, mind bogglingly complex (at least to me!!) but on the other hand, that biochemistry is filled with patterns characterized especially by redundancy, back doors, shunts. Almost every key process--and again I emphasize I am not even close to being a biochemist--has alternative pathways evolved to survive dysfunction and/or 'attack'.
I have heard Rob Phair and Chris Armstrong speak at length about he shunt at the same meetings where Paul Hwang presented.
To me the big question is how these different survival pathways interact, how they lead to a 'frozen' CDR, and why. As we tease this apart, I am confident we will come up with interventions and that's why I am so excited about the WASF3 pathway and what I will discuss next, the molecule SMPDL3B. Stay tuned. And pls keep the questions coming.
We are in this together and learning together.
Thanks for reading.
This was such a great article. I would love to participate in a trial if that opportunity ever arrived. Thank you for sharing all this information in a way non-medical brains like myself can still grasp. 😀
Thanks. I'm glad you enjoyed it and found it informative. Unfortunately, it will take a while to get any trial launched since the NIH moves very slowly even in the best of times...which this isn't. But will be writing more about this and other emerging info.
Oh, I definitely realize the snail’s pace of these things. ☺️ But it sounds like a great area of potential hopefully will get the funding it deserves.?
Hopefully. But since the drug is FDA approved any doctor can use it off label .
Oh - well in that case I am going to raise this with my own doctor.
Good! I'm happy to share with your doc more info the treatment with PB.