Returning home from the Karolinska StratRegen retreat as a keynote speaker. I heard inspiring science spanning bioengineering, aging, stem cell & organoid models, immunology, regeneration, & more. Fantastic to catch up with my postdoc labmate Sidinh Luc after nearly 10 years!

Bittersweet to say goodbye to our lab manager @griffin_nye after 5 years. He's kept the lab running & brought endless enthusiasm along the way. So grateful for all he's given. I'll miss him, but I'm excited to see him follow his dream of becoming a teacher! 🩷

I had the privilege and joy of returning yesterday to the @DanaFarber and @BostonChildrens where I did my postdoctoral training, this time as an invited speaker. Grateful to Zuzana Tothova for hosting me! It was a full circle moment and can't wait for the next time 😁

With mixed emotions, we said farewell to our summer student Eva Rios. She was a JOY to have in the lab - thoughtful, engaged, creative, a dot-connector and with a great sense of humor and desire to learn and be challenged 🤩 #SSP26 #JAXGenomicEducation #JAXstemcellsdev

Clearing senescent MSCs at the CH stage delayed progression to AML and extended survival. Targeting the niche, not just the mutant cells themselves, slowed malignant evolution.

Correlation isn't causation, so we tested it 3 independent ways: genetic depletion of p16-hi cells (p16-3MR mice), the BCL2/BCLxL-targeted ABT-263, and senolytics dasatinib + quercetin. All three depleted senescent MSCs and shrank Dnmt3a-mutant chimerism in vivo.

Mechanism: Dnmt3a-mutant HSPCs secrete TNFα and IL-6 that selectively activate Stat3 and ROS in MSCs, driving p53/p21-dependent senescence. Blocking TNFα, IL-6, or Stat3 each prevented it.

Buried in Fig. 2 but important: transplant conditioning (irradiation/busulfan) can be a confound. Using non-conditioned transplants, we show mutant clones still gain a fitness edge with natural aging, the first demonstration that Dnmt3a-mutant clones can do this.

MSCs from Dnmt3a-mutant mice show upregulated p53 targets, ROS, SASP, and senescence signatures, and the same signal shows up in human bone marrow MSCs from CHIP carriers across 4 different driver mutations (DNMT3A, TET2, ASXL1, CCAR1).

We ran scRNA-seq across non-hematopoietic bone marrow populations (MSCs, osteoblasts, endothelial cells) in mice with Dnmt3a-mutant vs. control hematopoiesis. One population stood out: mesenchymal stromal cells (MSCs) had the most changes, dominated by a senescence signature.

A huge congratulations to the newest graduate of the Trowbridge lab, Dr. Shawn David!! Shawn did a fantastic job defending his thesis today. So proud! 🎉 👏 🎊 #JAXGenomicEducation #UMaineGSBSE #JAXresearch #JAXstemcellsdev

#ISSCR2026 is a wrap - so what's next? 🔬 The JAX-NYSCF Conference Sept 23–24 | The Rockefeller University, NYC Fabulous program and registration is open! See you there!! conference.nyscf.org/ #JAXresearch #JAXstemcellsdev