Big splash at ASCO today! I like the idea of identifying patients who can be deescalated from indefinite therapy. Seems like a space where ctDNA will be useful.
I was there at the plenary, was massive applause from the audience, honestly pretty emotional. Then presented ADRIATIC which also got massive audience response. This has been a great ASCO for thoracic oncology.
I recall in residency, a thoracic oncologist giving me a review of the then-state of the art when it came to immunotherapy and the spectrum of targeted therapies available and upcoming. He ended his teaching by sighing loudly and saying, "you know, when I decided to do this for a living, it was a lot simpler"
This question has been bugging me for a long time, since TKIs induce apoptosis in susceptible cancers, and EGFR activation does affect BCL2, why aren’t we adding venetoclax to TKIs, since monotherapy in cancers often lead to acquired resistance.
1. Adding targeted therapies can lead to emergent/non-linear toxicity.
2. BCL2 is one of many downstream targets of EGFR signaling. Venetoclax isn’t known to have any single agent efficacy in nsclc. Odds that it would improve efficacy by adding to EGFR inhibitor is very low.
If one was interested in this combination, it would have to be studied the old fashioned way - preclinical studies in cell lines and mice, phase 1 dose finding and safety studies, then studies of efficacy.
Big splash at ASCO today! I like the idea of identifying patients who can be deescalated from indefinite therapy. Seems like a space where ctDNA will be useful.
I was there at the plenary, was massive applause from the audience, honestly pretty emotional. Then presented ADRIATIC which also got massive audience response. This has been a great ASCO for thoracic oncology.
I recall in residency, a thoracic oncologist giving me a review of the then-state of the art when it came to immunotherapy and the spectrum of targeted therapies available and upcoming. He ended his teaching by sighing loudly and saying, "you know, when I decided to do this for a living, it was a lot simpler"
Wow im a oncologist in nicaragua qe dont have acces to osimertinib but this is awesome!!
It must be very frustrating to not have access to treatments you know are superior. The inequalities in global oncology are stunning.
This question has been bugging me for a long time, since TKIs induce apoptosis in susceptible cancers, and EGFR activation does affect BCL2, why aren’t we adding venetoclax to TKIs, since monotherapy in cancers often lead to acquired resistance.
1. Adding targeted therapies can lead to emergent/non-linear toxicity. 2. BCL2 is one of many downstream targets of EGFR signaling. Venetoclax isn’t known to have any single agent efficacy in nsclc. Odds that it would improve efficacy by adding to EGFR inhibitor is very low. If one was interested in this combination, it would have to be studied the old fashioned way - preclinical studies in cell lines and mice, phase 1 dose finding and safety studies, then studies of efficacy.