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