(1/10) How do diverse leukemia mutations converge on the same molecular program? In our new study @CellCellPress,the @RibackLab and @Goodell_Lab show that disparate mutations rewire shared protein networks to form nuclear condensates called coordinating bodies (C-bodies).🫧

Happy to see that another our paper is out @iScience_CP https://t.co/UykWbQKqQB Exciting insights on the chromatin remodeling factor BRD9! It exhibits distinct behaviors in fetal development compared to hematopoiesis.

Incredibly insightful comments/feedback to our Blood paper from Pooranee K. Morgan and Andrew J. Murphy. "Make hematopoiesis great again: countering oxidative stress!" https://t.co/VyrZFPlrKA Truly grateful to all involved in this work. We will keep on deepening our science!

We are excited to share our recent publication in @BloodJournal Selenoprotein-mediated redox regulation shapes the cell fate of HSCs and mature lineages https://t.co/WXpMLHHOpr

Thrilled to announce our recent work, "Selenoprotein-Mediated Redox Regulation Shapes the Cell Fate of HSCs and Mature Lineages" @bloodjournal https://t.co/W5g8I1dWkJ

Droplet Hi-C enables scalable, single-cell profiling of chromatin architecture in heterogeneous tissues https://t.co/wZ3GDaJrTL

Pleased to share our story @NatureComms on the discovery of genes regulating #hPSC pluripotent identity versus cell fitness through genome-scale CRISPR-Cas9 KO screens, as part of the #MorPhiC initiative aiming at establishing the function of human genes. https://t.co/z7RPMZ1U15

Mutant HSCs in human clonal haematopoiesis have an attenuated response to inflammation and ageing, which may give them a selective advantage.   Happy to share our new paper published in @CellStemCell: https://t.co/TehWdhmkVw   A thread below… /1

Out in @CellCellPress today! We describe the first humans with inherited, complete FLT3L deficiency. Despite a lack of most dendritic cells, they reached adulthood. See the thread below for the main highlights of our paper.

The first prime editing clinical trial has been cleared by @US_FDA to begin: prime editing of HSCs to treat chronic granulomatous disease (CGD). Congratulations to @PrimeMedicine on achieving this key milestone only 4.5 years after we published the first prime editing paper.

Looking forward to your presence in Osaka, Japan – an exhilarating city! We’re currently expanding our talented team and invite you to join us in making impactful contributions to cancer research. Your expertise will be invaluable as we work towards our shared goals.

Now thrilled to contribute to @osaka_univ’s esteemed legacy. Our research will continue to push boundaries in understanding cancer pathogenesis and targeting vulnerabilities. Focused on RNA, chromatin, redox, metabolism, and cell death in non-heme malignancies alongside MDS/AML.

Excited to announce my appointment as a full professor of Cancer Pathology at Osaka University, starting April 2024. Gratitude to @MSKCancerCenter, @English_IMSUT, FBRI/Kobe, and all of my mentors like @AbdelWahablab for their support so far.

Wonderful to have our paper 'Deciphering cell states and genealogies of human haematopoiesis' led by @chenweng1991, in a great collaboration with @JswLab, published today in @Nature: https://t.co/7RGJWdFEWu

Excited to share our work on ASXL1 mutations in clonal hematopoiesis and myeloid malignancies, out in Blood Cancer Discovery @BCD_AACR

The extensive work would not be possible without the hard work of Muran Xiao, Shinji Kondo, and Masaki Nomura. I appreciate the help from Dr. Hinohara’s lab, @AbdelWahablab, @StanleyCLee, @TheDoctorIsVin, and other great collaborators. (fin)

These data thereby elucidate a mechanistic basis for BRD9/ncBAF in hematopoiesis, delineating a role for pathologic perturbation in hematologic malignancies with SF3B1 mutations. (8/n)

Interestingly, BRD9 is essential for developing and maintaining acute myeloid leukemia (AML), as its loss remarkably promotes myeloid differentiation with open chromatin at BRD9/CTCF sites. (7/n)

Mechanistically, in HSCs, BRD9 loss increases CTCF-binding and the formation of chromatin loops, thereby inducing differential gene expression with topologically associating domains (TADs) and A/B compartments intact. (6/n)

They undergo myeloid skewing while impairing B cell lineage development and self-renewal capacity. Brd9 KO induced MDS-like disease and significantly hastened the death. (5/n)