Our paper is out today at Nature Communications. Chaitanya Parikh in our lab developed an all-in-one cytokine and antigen mRNA therapy that can produce pancreatic cancer cures in 50% of mice! Excited to take this technology into patients with our company ImmunoScript. www.nature.com/articles/s41...

Multiplexed cytokine and antigen mRNA administration generates durable anti-tumor immunity against pancreatic cancer - Nature Communications

Pancreatic ductal adenocarcinoma (PDAC) displays dismal immunotherapy outcomes in part through a lack of cytokine and antigen signals needed for anti-tumor immunity. The authors here develop a cocktai...

nature.com

Our lab is recruiting both a postdoc and research technician to start in May/June! If you know anyone interested in investigating mechanisms of metastasis and immune suppression in cancer through developing innovative mouse models and studying senescence, please spread the word! Links below.

Unexpected news to end 2025. I have been promoted to Associate Professor @umasschan.bsky.social! Thanks to all the colleagues, mentors, and collaborators here and abroad who have contributed to my and the lab's development, as well as our amazing lab members who make doing science such a thrill!

Thanks again for the invite! Had a blast and learned a ton. The future of senescence research is bright.

SENESCEL@senescel.org · 9mo ago

We now have Marcus Ruscetti from @umasschan.bsky.social after the lunch break speaking at #SENESCEL25 in Barcelona

What are the genetic determinants of immune suppression and immunotherapy resistance in cancer? In a recent study from our lab, Kat Murphy developed innovative genetically engineered mouse models of late-stage prostate cancer to address this question. aacrjournals.org/cancerres/ar...

Could not be more proud of Kat and all she has accomplished in graduate school and beyond! Be sure to also check out her recent paper in Cancer Research elucidating genetic mechanisms of immune suppression and immunotherapy resistance in prostate cancer. aacrjournals.org/cancerres/ar...

UMass Chan Medical School@umasschan.bsky.social · 9mo ago

PhD candidate Katherine “Kat” Murphy has received an NIH grant to research mutations found in a late-stage type of castration-resistant prostate cancer in the lab of Marcus Ruscetti, PhD: direc.to/nDnJ #ProstateCancer #CancerResearch #PhD @marcus-ruscetti.bsky.social @uofmass.bsky.social

How can senescent cells, which are damaged and growth arrested, both block tumor initiation as well as fuel its growth? A recent study published in Cancer Discovery @aacrjournals.bsky.social from Lin Zhou in the lab uncovered some new insights into this puzzle. aacrjournals.org/cancerdiscov...

Now online in Cancer Discovery @aacrjournals.bsky.social: p21-Positive Senescent Stromal Cells Promote Prostate Cancer Immune Suppression & Progression that Can Be Reversed by Senolytic Therapy - by Lin Zhou, @marcus-ruscetti.bsky.social, and colleagues doi.org/10.1158/2159... @umasschan.bsky.social

Congrats to postdoc @nikitab.bsky.social for being awarded an AACR Scholar-in-Training award for this year's #AACRPan25 conference. Be sure to check out her poster # B049 today from 6-9pm!

*NEW paper alert* In a recent study from our former postdoc Shreya Chowdhury and in collaboration with Kate Fitzgerald, we identified PPT1 as a negative regulator of STING in tumor cells whose targeting could reactivate T cell immunity in ovarian and prostate cancers. www.pnas.org/doi/10.1073/...

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

This month our lab is celebrating 5 years! Couldn't be more thrilled with and proud of the group we have. Great scientists and human beings all around. Also super excited about the science coming out of the lab. Stay tuned for a few new studies dropping in the upcoming weeks.

Congrats @nikitab.bsky.social !

PitarresiLab@pitarresilab.bsky.social · 12mo ago

Congrats to postdoc @nikitab.bsky.social for winning the Margaret Foti @theaacr.bsky.social Scholar-in-Training Award for next month's Pancreatic AACR conference! If you see her at the conference, be sure to ask her about her work on PDAC cachexia, bioRxiv link below! biorxiv.org/content/10.1...

www.nytimes.com/interactive/...

Read the Letter

Researchers at academic institutions nationwide say that U.S. science is being dismantled.

nytimes.com

Why do we even have to do this? I wondered the whole time at Stand for Science. 🧪 But it was inspiring to see so many people committed to fighting for truth, science, and justice!

#standupforscience Boston

Congrats to Haruka from the Atukorale and Ruscetti labs for passing her qualifying exam to become a Ph.D. candidate yesterday! We are proud mentors and can't wait to see what you can accomplish through engineering LNPs for drug delivery in pancreatic cancer!

Happy to highlight work from Zhao et al., who developed 4! new mouse models to trace and genetically manipulate different p16+ senescent cell types that will be invaluable to the field. Check out my spotlight @Dev_Cell and original article in @cellcellpress.bsky.social www.cell.com/developmenta...

Lineage tracing senescence in vivo shows not all senescent cells are created equal

Understanding the impact of senescence on disease is limited by the lack of tools to lineage label senescent cells. In a recent Cell issue, Zhao et al. create mouse models to genetically manipulate and trace p16+ cells, identifying contrasting roles for senescent macrophages and endothelial cells (ECs) in liver fibrosis.

cell.com

Happy to share our recent review on cellular senescence and its impact on tumor immune surveillance authored by Lin Zhou and Boyang Ma in the lab, out now online at Trends in Cancer. Lots of exciting developments in the field over the past few years worth checking out! www.cell.com/trends/cance...

Cellular senescence offers distinct immunological vulnerabilities in cancer

Chronic damage following oncogene induction or cancer therapy can produce cellular senescence. Senescent cells not only exit the cell cycle but communicate damage signals to their environment that can trigger immune responses. Recent work has revealed that senescent tumor cells are highly immunogenic, leading to new ways to activate antitumor immunosurveillance and potentiate T cell-directed immunotherapies. However, other studies have determined that heterogeneous senescent stromal cell populations contribute to immunosuppression and tumor progression, sparking the development of senotherapeutics to target senescent cells that evade immune detection. We review current findings that provide deeper insights into the mechanisms contributing to the dichotomous role of senescence in immune modulation and how that can be leveraged for cancer immunotherapy.

cell.com

Always wonderful to see how our lab family grows each year. Happy Holidays from the Ruscetti and @pitarresilab.bsky.social groups!

🧪1/ 🚨New paper on ecDNAs from our lab! We reveal a strategy to engineer extrachromosomal DNA (ecDNA) amplifications in cells & mice. Let's dive in! Let’s dive in! 🧵👇 www.nature.com/articles/s41...

Engineered extrachromosomal oncogene amplifications promote tumorigenesis - Nature

Large extrachromosomal DNAs are engineered using a CRISPR- and Cre–loxP-based approach and shown to drive cancer in mouse models, with potential applications in determining the role of oncogene a...

nature.com

First post on @bsky.app! Excited to engage with the scientific community, share our lab's research on tumor immunology and cellular senescence, and highlight the work and accomplishments of our inspiring lab members on this platform.

I'm thrilled to share our latest research, published in Nature Communications. This work highlights how pancreatic cancer cells hijack cell polarity proteins to regulate macropinocytosis and tumor metabolism, shedding light on potential therapeutic vulnerabilities. www.nature.com/articles/s41...

Cell polarity proteins promote macropinocytosis in response to metabolic stress - Nature Communications

Cancer cells rely on macropinocytosis to survive in a nutrient-deprived environment. Here, Lambies et al. identified various members of the cell polarity protein network as essential regulators of mac...

nature.com

No better 1st post on this platform than this - the Pitarresi and Ruscetti labs at UMass Chan raising awareness on World Pancreas Cancer Day. Surely a long way to go but fueled by a singular purpose of defeating this deadly malignancy!