Professor & Dattels Family Chair at The Jackson Laboratory @jacksonlab studying hematopoietic stem cell biology, aging & cancer. 🇨🇦🇺🇸 Tweets are my own.

Bar Harbor, Maine
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Eeeeeeee!!!!!!! 🥰
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Peter @vangalenlab and I are very appreciative and grateful for the support of the Waxman Institute @WaxmanCancer to pursue our exciting collaborative studies! #BloodCancerAwarenessMonth #JAXresearch #JAXstemcellsdev
We're proud to fund @TrowbridgeLab & @vangalenlab as they investigate how age-related inflammation may fuel blood cancers—and uncover potential paths to prevention. This is why connecting aging biology & cancer research matters! with @TheMarkFdn #BloodCancerAwarenessMonth
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Very grateful for the support of @TheMarkFdn to pursue our biggest and boldest ideas!! #BloodCancerAwarenessMonth #JAXresearch #JAXstemcellsdev
This #BloodCancerAwarenessMonth, we’re spotlighting 2023 Emerging Leader Award winner Jennifer Trowbridge (@TrowbridgeLab) of @JacksonLab. She’s looking for answers to a big question: why aging blood cells develop into cancer in some individuals but not others.
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The Jackson Laboratory is a wonderful, collaborative place to pursue basic & translational science. On the faculty job market? I strongly encourage you to consider joining us in Bar Harbor, Maine! Apply: go.jax.org/276n55 #JAXresearch #JAXstemcellsdev
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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! 🩷
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You mean squealing pig! But it's closed down 😭
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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 😁
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Thank you to The Waxman Institute @WaxmanCancer for supporting our research!!
We are thrilled to be supporting such amazing researchers, including @TrowbridgeLab and @RossLevineLab. Check out all our funded research teams here: waxmaninstitute.org/our-rese…
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We are grateful for support from The Mark Foundation for Cancer Research @TheMarkFdn!! Particularly for high-risk, high-reward endeavors that are challenging to fund through conventional mechanisms.
New in @Nature: Insights on pre-malignant clones from ELA and Aging & Cancer grantee @TrowbridgeLab, Momentum Fellow Inés Fernández Maestre, and Scientific Advisory Committee chair @RossLevineLab! nature.com/articles/s41556-0…
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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
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Thank you Keisuke! Looking forward to seeing you soon!
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Thank you, Peggy! There's still so much to learn - I love projects like this that have sparked even more new ideas for us to pursue!!
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Huge thanks to lab members including @Dr_YoungBlood, @ColomPatricia_ and Maria Telpoukhovskaia for their work on the project, our funding sources, and our amazing collaborators: the labs of @GoetzeKatharina @DrStass @rosslevinemd! #JAXresearch #JAXstemcellsdev
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This may reach beyond the bone marrow. Clonal expansion happens broadly in tissues including skin, colon, and esophagus. If senescence-driven niche remodeling turns out to be a general feature of pre-malignant clones, it could matter across multiple tissue contexts.
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Bottom line: the bone marrow niche has been reported to change in CH. What was missing was proof that those changes matter functionally. Our depletion experiments provide that: aged/senescent stroma isn't just a marker of CH, it's a driver of it.
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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.
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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.
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