Grants submitted, paper submitted, experiments on pause. taking a break and getting out into our backyard National park! E-bikes for the win 🙌

RT @Fusion_Conf: Day 2 of #MyeloidMalignancies25 is underway. We have more exciting talks after lunch & the poster session later this eve….

A fantastic meeting in the beautiful location of Crete!!.

It is the best feeling when a former trainee surprises you by being in the audience for your talk. and THEN you take that opportunity to shout out the foundational contributions that they have made to your lab and to the field!! @LobergMatthew was and is an absolute rockstar!.

Looking forward to speaking at this symposium and hearing about fantastic new work by @SignerLab Stephnie Xie & James DeGregori! #AACR25.

RT @FASEBorg: For 30 years, #HEMSRC has brought together researchers of hematologic malignancies to share their work at the leading edge of….

RT @jacksonlab: Now published in @NatureComms, JAX scientist Jennifer Trowbridge and team (@TrowbridgeLab) uncovered that supercharged mito….

Congrats to Kira Young who spearheaded this work & all contributing authors. This was a fun (and long!) collaboration with Marc Mansour, Grant Challen, Eric Pietras, Kelsey Fisher-Wellman, @The_Ito_Lab & Steven Chan. Supported by @NIH, EvansMDS & @LLSusa .

To me, one of the coolest things about these papers is that three different labs in three different countries (US, Canada, UK) INDEPENDENTLY observed the same foundational phenotype of increased mitochondrial OXPHOS in Dnmt3a-mutant hematopoietic stem & progenitor cells 🇨🇦🇬🇧🇺🇸.

Together, we report that mitochondrial activity is a targetable mechanism by which clonal hematopoiesis-mutant HSCs gain a selective advantage over wild-type HSCs.

We find that MitoQ also targets elevated mitochondrial respiration and the selective advantage of human DNMT3A-mutant HSCs, supporting species conservation.

Exploiting elevated mitochondrial membrane potential, we used long-chain alkyl-TPP molecules (ex. MitoQ) that selectively accumulate in the mitochondria. These caused reduced mitochondrial respiration, apoptosis, and ablated the competitive advantage of Dnmt3a-mutant HSCs.

Dnmt3a-mutant HSCs have DNA hypomethylation and increased expression of oxidative phosphorylation gene signatures, increased functional OXPHOS capacity, high.mitochondrial membrane potential & greater dependence on mitochondrial respiration versus wild-type HSCs.

Using a mouse model of Dnmt3a-mutant CH that our lab previously developed, we found that mutant HSCs sustain elevated mitochondrial respiration which is associated with their resistance to aging-induced changes in the bone marrow microenvironment.

Drivers of clonal hematopoiesis include aging and inflammation. How HSCs with somatic mutations gain a selective advantage in these contexts is an unresolved question that we set out to tackle.

New paper from my lab! Elevated mitochondrial membrane potential is a therapeutic vulnerability in Dnmt3a-mutant clonal hematopoiesis: Complementary to new work from Steven Chan & George Vassiliou as described by @Goodell_Lab:

I am honored to have been selected by my colleagues to serve a 4-year term as vice president & president of the International Society of Experimental Hematology. Now, as ever, uniting, empowering and inspiring our collective scientific community to press on is essential.

RT @MilsomMick: Amazing collection of reviews on developmental hematopoiesis from leaders in the field. Just out in @ISEHSociety journal, E….

It is an honor to be considered alongside the fantastic @scienceadvocacy for the role of Vice President of ISEH. To all @ISEHSociety members: please make an important contribution to the society by voting. It's easy! Good luck to all of the nominees; we are in great hands!!.

RT @AACR: Kirsten Grønbaek, Jennifer Trowbridge, Alexander G. Bick, Katherine King, and Ieva Budriunait discussed "Clonal Hematopoiesis" in….