Tremendously proud to share my fellowship work, online today in @NatureMedicine. We tried to understand why CAR T therapy for AML doesn't work as well as we hoped it would, and how we can solve that. 👇🧵1/10.@PennMedicine @CHOP_Research @GillSaar

Unbelievably honored to have received a career award from @BWFUND. Hard to express how meaningful this support is in times like today. Also hard to express enough gratitude to my family, to my mentors, and to the patients we do this for.

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In clinical practice, we are always learning from our patients. I most of all want to thank the patients who participated in this study. I also want to thank all the co-authors, mentors, and especially my family, who supported this work in so many ways. -10-.

Why didn't we see this coming? Well these cytokines don't seem to help B-ALL, for example. They're myeloid-supporting cytokines, so this makes sense. Could other cytokines in CRS support B-ALL and contribute to CART19 treatment failures? Why not? 9/

It's worth noting that CART cells are still functional and still eliminate AML if numbers work in their favor. The first wave seems to kill AML blasts, but then the resulting cytokines make the remainder resistant. Poor responses or faster relapses result. 8/

Of course it remains to be seen whether this will work in people 🤞, but I'm excited to see how this combination therapy fares as we re-open this trial. We think this axis of resistance will apply generally to AML immunotherapies, so we need compelling approaches to block it. 7/.

Luckily we can block JAK/STAT signaling with ruxolitinib. To our delight, this indeed can reverse cytokine-mediated resistance and restore CART123 killing of primary AML. We can block BCL2 and restore killing that way, too. CART doesn't care about venetoclax–more to come. 6/