Kate O'Donnell
kateodonnell-lab.bsky.social
Kate O'Donnell
@kateodonnell-lab.bsky.social
Scientist in the Department of Molecular Biology at UT Southwestern Medical Center. We investigate mechanisms of tumorigenesis.

https://labs.utsouthwestern.edu/odonnell-lab
And check out exciting new work from the Oliver lab
@tgoliver.bsky.social showing that KLF4 promotes a KRT13+hillock-like state in squamous lung cancer👇:
www.biorxiv.org/content/10.1...
KLF4 promotes a KRT13+ hillock-like state in squamous lung cancer
Lung squamous cell carcinoma (LUSC) is basal-like subtype of lung cancer with limited treatment options. While prior studies have identified tumor-propagating cell states in squamous tumors, the broad...
www.biorxiv.org
November 11, 2025 at 6:36 PM
Finally, we are grateful for our funding sources:
DoD, ALA, CPRIT, NCI, Welch Foundation, and V Foundation.
November 11, 2025 at 6:21 PM
This work was led by my student Hari Shankar Sunil (who defended his thesis last week and is now officially Dr. Sunil). Special THANKS to all our AMAZING collaborators: Trudy Oliver @tgoliver.bsky.social, Jinming Gao, Tae Hyun Hwang, Ralph DeBerardinis @rjdlab.bsky.social, John Minna, et al.
November 11, 2025 at 6:21 PM
Collectively, our results demonstrate that TMPRSS11B promotes an acidified and immunosuppressive microenvironment. This work also nominates this enzyme as a promising therapeutic target in squamous lung cancer.
November 11, 2025 at 6:21 PM
Utilizing ultra-pH-sensitive nanoparticle imaging and in vivo metabolite analysis, we identify regions of acidification, elevated lactate, and enrichment of immunosuppressive macrophages in LUSC tumors.
November 11, 2025 at 6:21 PM
RNA FISH and spatial transcriptomics in the Rosa26-Sox2-Ires-GfpLSL/LSL; Nkx2-1fl/fl; Lkb1fl/fl (SNL) model reveal an enrichment of Tmprss11b expression in lung squamous tumors (LUSCs), specifically in Krt13+ hillock-like cells.
November 11, 2025 at 6:21 PM
In our new study, we show that TMPRSS11B depletion reduces tumor burden and triggers an infiltration of immune cells in immunocompetent mice.
November 11, 2025 at 6:21 PM
We initially identified TMPRSS11B in a Sleeping Beauty transposon mutagenesis screen (PMID:30463017). Our prior work showed that TMPRSS11B promotes the transformation of human bronchial epithelial cells and enhances lactate export from human lung squamous cell carcinoma cells.
November 11, 2025 at 6:21 PM
Congratulations Trudy and Abbie, et al! Beautiful work!
September 23, 2025 at 3:56 PM
Congratulations Niladri!!
August 29, 2025 at 9:27 PM
Congratulations!!!
August 14, 2025 at 4:16 AM
Congratulations Debbie! Exciting news!
July 18, 2025 at 2:10 PM
It was a pleasure to speak to our SURF students - thank you for the invite Dr. Diaz!
July 17, 2025 at 9:48 PM
A special thanks to ALL our collaborators for their important contributions to this work and to NIH/NCI, CPRIT, V Foundation, Welch Foundation, and DoD for their support, and I’m excited that our submission was selected for the cover (credit: Jose Cabrera)!
July 17, 2025 at 8:57 PM
Collectively, our studies uncover a novel mechanism by which two immune checkpoint proteins are coordinately regulated and suggest a new therapeutic strategy for lung cancer patients.
July 17, 2025 at 8:57 PM
Finally, we showed that ISR activation accelerates tumorigenesis and inhibits T cell function, effects that can be overcome by combining PD-1 and TIGIT blockade with the ISR inhibitor ISRIB.
July 17, 2025 at 8:57 PM
Our analysis of primary human lung tumors identified a significant correlation between PD-L1 and CD155 expression. This is particularly interesting because other groups have shown that CD155 expression is associated with resistance to anti-PD-1 therapy in lung cancer.
July 17, 2025 at 8:57 PM
Here we sought to uncover additional immune checkpoint proteins regulated by the ISR to elucidate mechanisms of tumor immune escape. We show that CD155 and PD-L1 are coordinately induced by the ISR, enhancing translation of both immune checkpoints through bypass of inhibitory uORFs in their 5' UTRs.
July 17, 2025 at 8:57 PM
The ISR is an adaptive pathway hijacked by cancer cells to survive cellular stresses in the tumor microenvironment. We previously showed that ISR activation potently induces Programmed Death Ligand 1 (PD-L1), leading to suppression of anti-tumor immunity (Suresh et al, Nature Cancer, 2020).
July 17, 2025 at 8:57 PM
The Integrated Stress Response (ISR) Pathway Coordinates Translational Control of Multiple Immune Checkpoints in Lung Cancer url: aacrjournals.org/cancerres/ar...
The Integrated Stress Response Pathway Coordinates Translational Control of Multiple Immune Checkpoints in Lung Cancer
The integrated stress response represents a targetable axis to improve the efficacy of immunotherapy in lung cancer by inhibiting the coordinated translational regulation of the PD-L1/PD-1 and CD155/T...
aacrjournals.org
July 17, 2025 at 8:57 PM