Leukemia study restores silenced gene in mice. Could it point to new treatments for humans? Researchers created a CRISPR-based tool to pinpoint genes the cancer turns off

A key cancer-fighting gene in leukemia is switched off—not broken—and, in a study published in @science.org #ScienceTranslationalMedicine, scientists from JAX have found a way to switch it back on. 🧬🧪

https://go.jax.org/AMLswitch

We are deeply saddened by the passing of our beloved cofounder Marica Vilcek (1936–2026). Known widely in the New York City community and beyond as an insightful art historian and tireless philanthropist, Marica died peacefully at her home in New York at the age of 89. Learn more: vilcek.co/4d0ppWx

Excited about the 2026 Prague Metabolism & Signaling Symposium in Prague, Czechia, bringing together leading scientists to explore cutting-edge research in metabolism, signaling, aging, cancer, immune responses & more! 🧬🔬
📅 June 24–27, 2026

More details at 👉 praguemetabolismsymposium.com

Overall, we conclude that in vitro culture conditions substantially contribute to an overestimation of our ability to induce ferroptosis in tumors. Be careful out there! More details and perspectives in the manuscript!

Our model is that the function of exogenous cystine in cell culture media is principally to enable selenium import and selenoprotein function, particularly that of GPX4, and that this function can be substituted by beta-mercaptoethanol.

We confirm that cystine deprivation causes loss of GPX4 and other selenoproteins. This effect is reversed by beta-mercaptoethanol, despite robust GSH loss. Moreover, expression of a selenium-independent GPX4 mutant enables cells to survive cystine-free media.

Also surprising is that the small molecule thiol beta-mercaptoethanol enables the exponential growth not only of SLC7A11 null cells, but also of cells in cystine-free media… over weeks!

Surprisingly, the non-ferroptotic cell death induced by inhibition of TXNDR1 and BSO treatment could be regulated… by removing cystine from the media… which rescues! Are these cells bad at buffering thiols?

Knockout of TXNRD1 in models previously resistant to BSO, sensitize them to BSO through the same non-ferroptotic cell death AND now result in tumor regressions.

…Except one! SK-MES-1 lung squamous carcinoma cells and tumors are very sensitive to BSO. The BSO does work! SK-MES-1 is the only cell line with dual inactivating mutations in TXNDR1, consistent with prior work describing this synthetic interaction.

Among these, we identified two classes of cell lines that are very sensitive to GCLC inhibitor BSO, triggering either ferroptotic or non-ferroptotic cell death. However, established tumors from these cell lines still failed to respond to BSO…

We therefore expanded our analysis to 100 cell lines and identified heterogeneous responses to canonical ferroptosis induces and suppressors which could be organized into biologically distinct response classes.

Using a suite of robust genetic and pharmacological methods, we failed to impact the growth of established tumors upon inhibition of GPX4, GCLC, or SLC7A11, despite robust activation of ferroptosis in these models in vitro.

I’m excited to share new work out of the lab at @NYULangone led by @kenjifujihara.bsky.social ! We took a first principles approach to evaluating @ferroptosis induction for cancer therapy via targeting the SLC7A11-glutathione-GPX4 axis. www.biorxiv.org/cgi/content/...

Josh Rabinowitz, and Santosha Vardhana!

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,

NY medical schools press Gov. Hochul to put up billions for scientific research The request comes amid continuing uncertainty over federal funding, with research and thousands of jobs on the line.

NYers helps us call on @governor.ny.gov to invest in the Empire Biomedical Research Institute. A robust, stable research ecosystem protects jobs, fuels innovation, and builds community health. NY must invest in our global leadership in science. nycures.org @gothamist.com: tinyurl.com/5fab5k7u

Mutations in mitochondrial ferredoxin FDX2 suppress frataxin deficiency - Nature A forward genetic screen in Caenorhabditis elegans reveals that decreased levels of the ferredoxin FDX2 suppress the loss of frataxin in worms and in mice by relief of FDX2 inhibition of fra...

www.nature.com/articles/s41...

Functionally dominant hotspot mutations of mitochondrial ribosomal RNA genes in cancer Nature Genetics - Analysis of 14,106 tumor genomes highlights recurrent mutations in mitochondrial ribosomal RNA encoded within the mitochondrial genome. Mutations occur at hotspot positions and...

Excited to share our latest work in collaboration with the @edreznik.bsky.social lab @mskcancercenter.bsky.social, where we describe functionally dominant mitochondrial DNA mutations in patient tumors. So, what is functional dominance in mitochondrial genetics, I hear you ask?

rdcu.be/eN1jm

Machine-learning-guided discovery of SLC25A45 as a mediator of mitochondrial methylated amino acid import and carnitine synthesis Khan et al. apply machine learning to identify substrates of UNC93A, SLC45A4, and SLC25A45. Biochemical assays and in vivo metabolite tracing establish SLC25A45 as a key mediator of mitochondrial impo...

Excited to share our work on discovery of SLC25A45 as a mediator of mitochondrial methylated amino acid import and carnitine biosynthesis. @cp-cellmetabolism.bsky.social www.cell.com/cell-metabol...

GCN1 couples GCN2 to ribosomal state to initiate amino acid response pathway signaling During nutrient deprivation, activation of the protein kinase GCN2 regulates cell survival and metabolic homeostasis. In addition to amino acid stress, GCN2 is activated by a variety of cellular stres...

Beautiful reconstitution of amino acid stress-dependent ISR activation by my @harvardcellbio.bsky.social colleagues presenting a unifying mechanism for GCN2 activation, which requires ribosome collisions and is enhanced by cognate uncharged tRNA in the A site! www.science.org/doi/10.1126/...

Basal cell of origin resolves neuroendocrine–tuft lineage plasticity in cancer Nature - Basal cells, rather than neuroendocrine cells, have been identified as the probable origin of small cell lung cancer and other neuroendocrine–tuft cancers, explaining...

Super pleased to announce our latest suggesting the cell of origin for #SCLC is most likely the basal cell @nature.com, not the accepted neuroendocrine cell. Implications for the earliest events in cancer, & providing new models of tuft-like cancer.
rdcu.be/eGUtj

Rewiring of cortical glucose metabolism fuels human brain cancer growth - Nature The cortex fuels essential physiological processes with glucose-derived carbon, while gliomas fuel their aggressiveness by rerouting glucose carbon pathways and scavenging alternative carbon sources s...

New discovery from our team defining how human brain cancers rewire the metabolism of the normal brain published this week @nature.com and led by stellar postdoc Drew Scott (comentored by @lyssiotislab.bsky.social and currently on job market with a K99/R00). www.nature.com/articles/s41...

PEX39 facilitates the peroxisomal import of PTS2-containing proteins - Nature Cell Biology Chen et al. show that PEX39 cooperates with PEX7 in the peroxisomal import of proteins containing a PTS2 site and uncover an (R/K)PWE motif in PEX39 and PEX13 that binds to PEX7 and facilitates the im...

Our work on new paradigm in peroxisome biogenesis and PEX39 (1st human peroxisomal biogenesis protein (peroxin/PEX) found in > 20 yr) is out in @natcellbio.nature.com! Equal collab w/Tony Rodrigues (Jorge Azevedo lab), @dwendscheck.bsky.social (Bettina Warscheid lab)

www.nature.com/articles/s41...

Transient APC/C inactivation by mTOR boosts glycolysis during cell cycle entry - Nature APC/C activity is transiently inhibited to generate a pulse of glycolysis that is required for mammalian cell cycle entry.

www.nature.com/articles/s41...

Transient APC/C inactivation by mTOR boosts glycolysis during cell cycle entry

Conservation and divergence of metabolic phenotypes between patient tumours and matched xenografts - Nature Metabolism Rao and Cai et al. perform a detailed metabolic comparison between primary tumours from patients and their matching xenografts, which identify conserved as well as divergent metabolic patterns.

1/Patient-derived xenografts (PDXs) are used in preclinical testing of cancer therapies, including metabolic therapies. We determined which metabolic properties are retained, and which are lost, when melanomas from patients are implanted and passaged as PDXs in mice.
www.nature.com/articles/s42...

Director Vought: We write to ask you to fully implement the Fiscal Year (FY) 2025 Full-Year Continuing Appropriations and Extensions Act, including funds appropriated for the National Institutes of Health (NIH). The continuing resolution supp011s NIH initiatives across a range of critical research areas­cancer, cardiovascular disease, rare pediatric disorders, and more. These vital efforts are not only necessary to Make America Healthy Again, but also have a direct impact on American families, biomedical innovation, our economy, and competing with Communist China. We are concerned by the slow disbursement rate of FY25 NIH funds, as it risks undermining critical research and the thousands of American jobs it supports. Suspension of these appropriated funds - whether formally withheld or functionally delayed - could threaten Americans' ability to access better treatments and limit our nation's leadership in biomedical science. It also risks inadve11ently severing ongoing NIH-funded research prior to actionable results. We share your commitment to ensuring NIH funds are used responsibly and not diverted to ideological or unaccountable programs. We are confident Secretary Kennedy and Director Bhattacharya are well positioned to uphold gold standard research by ensuring that NIH awards are grounded in transparency, scientific merit, and a clear alignment with national interests. Our shared goal is to restore public trust in the NIH precisely because its work is focused on results, accountability, and real-world impact. Withholding or suspending these funds would jeopardize that trust and hinder progress on critical health challenges facing our nation. Ultimately, this is about finding cures and seeing them through to fruition. We respectfully request that you ensure the timely release of all FY25 NIH appropriations in accordance with congressional intent. Doing so will ensure continued momentum in curing disease, supp011ing American innovation, and delivering result…

Sincerely, Katie Boyd Britt John Boozman Shelly Moore Capito Bill Cassidy Susan Collins Lindsey O. Graham David H. McCormick Mitch McConnel Jerry Moran Lisa Murkowski Thom Tillis Todd Young Dan Sullivan Tim Scott

From @aaas.org check-in with Sudip Parikh: a letter by 14 Republican senators urge the Office of Management and Budget to release NIH funding. If this includes your state (AL, ME, WV, SC, KY, KS, AR, PA, NC, IN, AK), Sudip recommends contacting & thanking them for being American science leaders.

Bill Rutter passed away at age 97 yesterday. He chaired our Department through the 1970s and was instrumental in the development of UCSF basic science. He hired Christine Guthrie, Keith Yamamoto, Bruce Alberts, Marc Kirschner, Pat O’Farrell, Peter Walter, Ira Herskowitz among others.

In 2019, scientists discovered Jo Cameron, a Scottish woman with a rare genetic mutation that prevents her from feeling pain, anxiety, or fear and allows her to heal without scarring. | Science Acumen In 2019, scientists discovered Jo Cameron, a Scottish woman with a rare genetic mutation that prevents her from feeling pain, anxiety, or fear and allows her to heal without scarring. This condition...

Fascinating

www.linkedin.com/posts/scienc...

Child walks again after receiving experimental treatment for rare genetic condition NYU Langone researchers have helped an 8-year-old boy regain mobility using an experimental treatment.

Child walks again after receiving experimental treatment for rare genetic condition www.statnews.com/2025/07/09/n... via @statnews.com