Researchers at the University of Nebraska Medical Center are among the authors of a newly posted preprint that identifies a KRAS-MAPK signaling pathway as a driver of CD73 expression in pancreatic ductal adenocarcinoma, and reports preclinical tumor control improvement with a two-drug combination.
Study authors and findings
The preprint, titled “Oncogenic KRAS-MAPK signaling sustains a CD73 dependent therapeutic vulnerability in pancreatic cancer,” lists Khadija Turabi as the lead author and includes UNMC faculty Jennifer M. Bailey-Lundberg and Kathleen E. DelGiorno among the contributors. The full author list named in the preprint includes Urvinder Kaur Sardarni, Katherine E. Ankenbauer, Sabrina M. Torbit and several others.
“New preprint with Kathy Delgiorno: KRAS-MAPK signaling sustains CD73 expression in PDAC. Daraxonrasib + quemliclustat enhaces tumor control and reshapes the tumor immune landscape. Led by Khadija! Congrats to Urvinder Kaur, Katherine Ankenbauer and the team!” — Jennifer Bailey-Lundberg, associate professor, UNMC
The post announcing the preprint was shared on X by Jennifer Bailey-Lundberg, an associate professor in UNMC’s Department of Pathology, Microbiology and Immunology. Her message highlighted three points summarized in the paper’s title and her post: that KRAS-MAPK signaling promotes CD73 expression in pancreatic ductal adenocarcinoma (PDAC), that the combination of daraxonrasib and quemliclustat produced improved tumor control in the preclinical work, and that the regimen appeared to alter the tumor immune microenvironment.
What the preprint reports and what remains to be learned
- The preprint links oncogenic KRAS-MAPK activity to sustained CD73 expression in PDAC, a disease commonly abbreviated as PDAC in the oncology literature.
- Laboratory results reported in the preprint indicate that combining daraxonrasib and quemliclustat enhanced tumor control and reshaped the tumor immune landscape in the study’s experimental models.
- The paper is a preprint, meaning it has been posted publicly before formal peer review; subsequent peer-reviewed publication and independent replication are necessary to verify and extend the findings.
Pancreatic ductal adenocarcinoma is the most common form of pancreatic cancer and is frequently the subject of laboratory and clinical research because of its aggressive behavior and limited effective treatments. The preprint’s focus on a KRAS-driven mechanism is consistent with longstanding interest in KRAS mutations and their downstream signaling pathways in PDAC biology.
The OncoDaily item that first flagged the preprint quoted Bailey-Lundberg’s social-media message and reproduced the preprint title and author list. The study names experimental agents daraxonrasib, a MAPK-pathway targeted inhibitor, and quemliclustat, an agent that can affect pathways linked to CD73 biology; the preprint reports combined effects on tumor control and immune features in the models used.
Because the work is currently available as a preprint, peer review and eventual journal publication will provide further detail on the experimental design, statistical analysis, reproducibility and potential paths for clinical translation. The corresponding authors named on the paper, and UNMC officials, would be the sources for subsequent updates about peer-reviewed publication, clinical development plans or institutional support for follow-on studies.
