Congrats! Impressed and proud !

Grateful to our incredible team—scientists, artists, and collaborators—who built this story with us. We hope the science and imagery inspire new ways of seeing how leukemias take shape. @gandhardatar.bsky.social , @sciencyelmira.bsky.social , @drawimpacts.bsky.social , and others!

Even more exciting, we find that other AML drivers—like NUP98 and KMT2A fusions—coerce their own “majestic creatures” into the same C-body nightmare, revealing a shared structural logic behind clinically similar leukemias. See the original thread ⬇️ for more insights.

Disparate leukemia mutations converge on nuclear phase-separated condensates Mutant NPM1 and various leukemia oncofusions form biophysically indistingishable nuclear condensates, termed C-bodies, which orchestrate leukemogenic gene expression. These findings consolidate divers...

And here’s the twist we uncover in the new work ⬇️: the gremlin’s power was never in the cytoplasm at all. NPM1c must act *in the nucleus* through phase separation, bringing together multiple proteins on chromatin to drive AML... Overturning years of assumptions.

Now: NPM1c becomes a nestling contemplating potential destinies—(1) majesty of wild-type NPM1’s eagle-like order (2) a menacing hawk that shatters the nucleus as it sparks C-body formation and unleashes HOX programs - subverting life-giving differentiation to life-taking self-perpetuation

Mutant NPM1 Maintains the Leukemic State through HOX Expression Brunetti et al. show that specific loss of NPM1c from the cytoplasm leads to downregulation of HOX genes and differentiation in NPM1 mutant AML. Blocking NPM1c nuclear export by XPO1 inhibition reduce...

Original work here ⬇️, led by the inimitable Lorenzo Brunetti and Michael Gundry. This work became foundational in the field.

NPM1c comes from a tiny frameshift that creates a nuclear export signal in what is normally a nucleolar protein. In earlier work, we portrayed its HOX-activating force as a mischievous gremlin straining to escape the nucleus—an image that captured how disruptive this mutant is.

Today's the print release of a #RibackLab and #GoodellLab collaboration— we’re excited to share the visual story behind the science, including the dramatic artwork that inspired how we thought about aberrant function of NPM1c - which occurs in about 1 in 3 adult acute myeloid leukemias (#AML).

Hallmarks of stem cell aging Aging disrupts core functions of somatic stem cells throughout the body, leading to impaired tissue maintenance and repair. We identify five key features of aged stem cells, highlighting how their dys...

Happy to share our review at Cell Stem Cell as part of their Hallmarks series. As always, a pleasure to work with friends and colleagues Anne Brunet (@brunetlab.bsky.social) and Peggy Goodell(@goodell-lab.bsky.social).

Hallmarks of stem cell aging: Cell Stem Cell www.cell.com/cell-stem-ce...

It was great to work with the inimitable @brunetlab.bsky.social and Tom Rando on this review of stem cell #aging!

Hallmarks of stem cell aging As organisms age, somatic stem cells progressively lose their ability to sustain tissue homeostasis and support regeneration. Although stem cells are …

Excited to share our review on Hallmark of Stem Cell Aging! With Tom Rando and Peggy Goodell @goodell-lab.bsky.social!!

www.sciencedirect.com/science/arti...

Thank you so much, Dan! It’s such a huge honor. When I started my lab more than 25 years ago, I never imagined this would be possible. I give enormous credit to being in a fantastic supportive environment and many amazing trainees who did all the hard work.

Age-related blood condition counteracted with a common diabetes drug Metformin could reduce people’s risk of certain age-associated blood cancers, but more work is needed to identify who is likely to benefit.

New paper from my lab! Elevated mitochondrial membrane potential is a therapeutic vulnerability in Dnmt3a-mutant clonal hematopoiesis: rdcu.be/eh1Nb Complementary to new work from Steven Chan & @georgevassiliou.bsky.social as described by @goodell-lab.bsky.social: www.nature.com/articles/d41...

Excited to share the @goodell-lab.bsky.social News&Views on 3 exciting studies by Vassiliou Lab, Chan Lab, and @trowbridgelab.bsky.social in @nature.com and @natcomms.nature.com, showing that #DNMT3A mutant (major driver of Clonal Hematopoiesis) blood cells depend on mitochondrial respiration.

Thrilled to share our new work on #aging in the murine hematopoietic system! There is a lot here- stem cell numbers, self-renewal rates, mutation rates, mutation signatures, clonal fitness, environmental effects...