Rich Possemato

@richpossemato.bsky.social

Associate Professor studying cellular metabolism, iron, cancer research. 🏳️‍🌈Father of two possematolab.org

After a bit of a rough patch my lab's funding situation has taken a significant upturn, so if you're looking for a Postdoc position please keep us in mind...Pseudomonas aeruginosa genetics, regulation, and physiology - with a focus on the cell envelope. Please repost. andrewdarwinlab.org

Microbiology | Andrew Darwin Lab | United States

Andrew Darwin Laboratory website. Academic Microbiology research laboratory at NYU School of Medicine. New York, NY, USA.

andrewdarwinlab.org

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/...

Systematic Evaluation Defines the Limits of Ferroptosis in Cancer Therapy

Ferroptosis is a cell death mechanism characterized by the accumulation of iron-catalyzed lipid peroxides in membrane lipid acyl chains and subsequent loss of membrane integrity.1 Despite thorough investigation of its mechanisms in cultured cells, induction of ferroptosis has unresolved clinical utility in cancer therapy. Here, we systematically evaluate ferroptosis induction via multiple mechanisms, in both cell and tumor models, using focused genetic screens, genetic loss-of-function systems, and pharmacological perturbations. Through this analysis we identify cancer cell line subsets with distinct responses to canonical ferroptosis inducers and suppressors and define the underpinnings of each. Inhibition of central in vitro ferroptosis suppressors GPX4, GCLC, or SLC7A11 across these multiple models fails to impact established tumor growth. In contrast, deficiency in the cytosolic thioredoxin reductase and pharmacologic GCLC inhibition potently induces tumor regression and triggers a form of non-ferroptotic cell death regulated by cystine availability and translation. These analyses further reveal that the principal essential function of environmental cystine in cultured cells is to support selenoprotein function, identified through investigating our finding that beta-mercaptoethanol supports exponential growth in cystine-free conditions. Thus, while ferroptosis activation may be efficacious alone or in combination with other therapies in specific tumor contexts, cell culture systems greatly overestimate the potential anti-cancer effects of ferroptosis induction via the GPX4 axis. ### Competing Interest Statement The authors have declared no competing interest. NIH Common Fund, R01CA286141, R01GM132491, P30CA016087

biorxiv.org

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

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.

tinyurl.com

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

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...

rdcu.be

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.

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

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.

Our paper on regulation of BCAA catabolism by mitochondrial calcium signaling is out! Mitochondrial calcium signaling regulates branched-chain amino acid catabolism in fibrolamellar carcinoma | Science Advances www.science.org/doi/10.1126/...

Mitochondrial calcium signaling regulates branched-chain amino acid catabolism in fibrolamellar carcinoma

Mitochondrial Ca2+ signaling regulates branched-chain amino acid catabolism in an adolescent liver cancer.

science.org