Muir Lab

Very helpful methods and protocol! www.sciexplor.com/articles/fos...

Great work @ginadenicola.bsky.social and team!

Excited to announce that registration is officially open for #METPHYS2026!

All meeting details can be found here:
www.sablesys.com/metphys-the-...

Join us for the 2026 NYAS Cancer Metabolism conference on March 24th at NYU Langone! The poster deadline is rapidly approaching. Speakers include @airdlab.bsky.social @bensahralab.bsky.social Javier Garcia-Bermudez, Marcus Goncalves, @naama-kanarek.bsky.social @bdmanning.bsky.social Erika Pearce,

"What the state attorney general, what the city of Chicago has done in lots of ways has been remarkable in standing up for people" Futterman said. "But one of the ways in which they've fallen short so far, one of the tools they haven't used that they have, is actually the power to arrest people."

Another attorney representing the plaintiffs in the case, Craig Futterman with the UChicago law school, called on state and local officials to do more to hold federal agents legally accountable for their actions.

Tumor-draining Lymph nodes - Online event next week!
follow the link to register

On January 13 from 11:30 – 1:00 pm ET, @thelundlab.bsky.social , Dr. Ivan Maillard, @actonlab.bsky.social , & Dr. Burkhard Ludewig will discuss lymph node remodeling in cancer:

events.cancer.gov/dcb/tdln #TLDNForums

Interested in stable isotope infusions but daunted by jugular catheter surgery? New from postdoc @kimyumi0201.bsky.social: our simple tail vein catheter method enables anesthesia-free infusions in awake, freely moving mice. 🧵

Lymph node environment drives FSP1 targetability in metastasizing melanoma - Nature Targeting FSP1 in lymph nodes has considerable potential for blocking melanoma progression.

Melanoma cells that spread to lymph nodes depend on FSP1 to survive, revealing a new metabolic vulnerability. New study in Nature by @mariopalma.bsky.social @ubellackerlab.bsky.social and colleagues shows that blocking FSP1 triggers ferroptosis and suppresses tumor growth in lymph node metastases.

FSP1-mediated lipid droplet quality control prevents neutral lipid peroxidation and ferroptosis - Nature Cell Biology Lange et al. identify a lipid droplet quality control pathway in which FSP1 safeguards stored neutral lipids from lipid peroxidation, thereby preventing the induction of ferroptosis.

Excited to share our study out in @natcellbio.nature.com! Led by @mikelangelipid.bsky.social, we identify the first #LipidDroplet lipid quality control pathway: LD-localized FSP1 protects stored lipids from oxidative damage and prevents LD-initiated #ferroptosis.
www.nature.com/articles/s41...

Our work detailing the metabolic roles of serum for cancer cell proliferation is now out at JBC, @asbmbjournals.bsky.social!

Congrats to Oliver and Eric and many thanks to the editor and reviewers for a thoughtful and efficient review process.

See here:
www.sciencedirect.com/science/arti...

Repost! Please apply by October 15th for full consideration.

Just out in @science.org: Together with the lab of @wilhelmpalm.bsky.social, we used sequential in-vitro/in-vivo CRISPR screens to decipher metabolic adaptations in tumors. We find that acidosis is a dominant factor that shapes energy metabolism and stress resilience. www.science.org/doi/10.1126/...

A microneedle device for rapid dermal interstitial fluid sampling A device collects enough skin interstitial fluid for omics studies in just five minutes.

A microneedle device for rapid dermal interstitial fluid sampling @stanforduniversity.bsky.social 🇺🇲 www.science.org/doi/10.1126/...

Thanks Natalie! @cssheehan.bsky.social responsible for all monthy python jokes :)

Looking forward to your feedback as we continue to work this problem!

Super great to work with James LaBelle’s lab on this project! And thanks to everyone involved in the study: Kay Macleod, @cjhphd.bsky.social, Alica Beutel,
@leahziolkowski.bsky.social, Mumina Sadullozoda, @patrickjonker.bsky.social, Darby Agovino, Grace Croley, @guillaumecognet.bsky.social.

(3) Fortress model is insufficient to explain drug resistance in pancreatic. Tolerance (tis but a scratch) also critical to drug resistance. Will need effort on overcoming tolerance in addition to improving drug delivery to improve treatment outcomes.

(2) Simple changes to culture models, like growing cells in the right nutrients, keeps cells in in vivo relevant states that we care about, like being drug resistant. Important for getting models that are predictive for things like drug discovery and for precision medicine.

Implications: (1) Using standard culture models to do things like drug screens, will make apoptosis inducers look great, even though they will have limited efficacy in vivo. Could be fruitful to look at other treatment modalities that kill cells non-apoptotically.

How does the TME/TIFM cause drug resistance? Apoptotic priming gets turn wayyyyy down. So, cells just don’t die from chemo or targeted therapies despite on target action. Call this the “tis but a scratch model” of drug resistance.

Interestingly, we recently made a new cell culture model (TIFM) where PDAC cells are grown in the nutrients they would see IRL (elifesciences.org/articles/81289). TIFM-derived PDAC cell lines maintain the therapy resistant state! So, have a tractable model to study this state now.

Why haven’t we seen this before? Well, if you keep the cancer cells in culture, after a few weeks, the cells become drug sensitive again! So, the tumor imprints a drug-resistant state that cell culture can’t maintain. Critical for chemo and targeted therapy resistance.

So, how else do tumors become drug resistant? @cssheehan.bsky.social cial found even if you take pancreatic cancer cells out of the tumor and look at drug response ex vivo, the cells are drug resistant. Clearly, something else going on beyond the fortress model.

But fortress model can't explain recent findings that tumors are still resistant even if you work to get the drugs in there (pubmed.ncbi.nlm.nih.gov/32030361/) and new mass spec imaging data (pubmed.ncbi.nlm.nih.gov/35005896/) that shows drugs getting into tumors.

Know that pancreatic cancer cells are not inherently drug resistant but that tumors are. What about tumors makes them drug resistant? Longstanding hypothesis is that fibrosis limits drug delivery to tumors making them resistant. We call this the “fortress model”.

Tumor nutrient stress gives rise to a drug tolerant cell state in pancreatic cancer Cytotoxic chemotherapy remains the standard-of-care treatment for patients with pancreatic ductal adenocarcinoma (PDAC). However, chemotherapy only has modest effects at improving patient survival due...

Super excited to share our new preprint from @cssheehan.bsky.social on how the tumor microenvironment causes drug resistance in pancreatic cancer: www.biorxiv.org/content/10.1...

An alternative route for β-hydroxybutyrate metabolism supports cytosolic acetyl-CoA synthesis in cancer cells - Nature Metabolism Kaluba, Rogers et al. show that in cancer cells that can metabolize ketones, they may reroute them to produce cytosolic acetyl-CoA and support tumour growth.

An alternative route for β-hydroxybutyrate metabolism supports cytosolic acetyl-CoA synthesis in cancer cells www.nature.com/articles/s42...

I am thrilled to share that I have received an ERC Starting Grant for our project SpaceMet!
I am grateful for the ERC’s commitment to ambitious early-stage research and to KU Leuven for their support!
Stay tuned, new postdoc positions coming soon!I @erc.europa.eu @kuleuvenuniversity.bsky.social

Hot off the presses! Was an honor to team up with Scott Dixon @stanforduniversity.bsky.social on this Nature Cancer review. We reflect on hurdles that have slowed translation of ferroptosis-directed therapies and share ideas on what it will take to bring these therapies to the clinic. rdcu.be/eBbqV

Super cool and excited to read!