New pancreatic cancer strategy kills KRAS-mutant tumor cells and extends survival in mice
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Researchers at the University of Cologne's Center for Molecular Medicine Cologne (CMMC) have discovered a previously unknown mechanism that makes most pancreatic cancer cells susceptible to a form of programmed cell death. The team, led by Professor Dr. Silvia von Karstedt, showed that cancer cells with mutations in the KRAS gene develop a vulnerability that can be used to eliminate tumor cells in preclinical models. The findings open up new perspectives for treating pancreatic cancer. The study "Oncogenic KRAS-Driven type I Interferon Signalling Primes Pancreatic Cancer for Necroptosis" was published in the journal Nature Communications.
Pancreatic cancer is one of the most aggressive forms of cancer and has so far shown only limited response to available treatments. In approximately 90% of cases, these tumors carry mutations in the KRAS gene that drive cancer growth. Due to the aging population and the lack of effective therapies, physicians, clinicians and researchers expect pancreatic carcinoma to become one of the leading causes of cancer-related deaths worldwide in the coming years.
With the discovery of this newly identified vulnerability, a therapeutically promising approach has now been identified for treating this disease following future clinical trials.
How the weakness works
The researchers discovered that KRAS-mutated tumor cells continuously activate signals from the innate immune system. This primes the cancer cells for an inflammatory form of cell death known as necroptosis. In order to survive, tumor cells rely heavily on the protein caspase-8, which usually inhibits necroptosis. If caspase-8 is blocked, the tumor cells die.
"KRAS-mutated tumors have a previously unknown Achilles' heel," says von Karstedt, the senior author of the study. "By switching off the tumor cells' defense mechanisms, we can significantly kill these tumors."
Promising results in models
In genetically modified mouse models, the induction of necroptosis through the depletion of caspase-8 led to a significant reduction in precursor lesions—abnormal tissue from which potentially malignant tumors can develop. In addition, the researchers demonstrated that a combination drug therapy using agents already in clinical use significantly reduced tumor growth and prolonged the animals' survival.
The treatment has also shown significant efficacy in experiments using patient-derived tumor organoids—three-dimensional mini-tumors made from human pancreatic cancer tissue. This suggests that the approach could be promising for future clinical trials.
"The findings provide strong evidence that certain forms of pancreatic cancer could be specifically targeted for treatment based on their dependence on caspase-8," says first author Sofya Tishina, a postdoctoral researcher in von Karstedt's lab. "In the long term, this could help develop new therapies for patients who currently have very limited treatment options."
In addition to researchers from the University of Cologne, the study involved scientists from the German Consortium for Translational Cancer Research (DKTK), the Technical University of Munich and other national and international partners.
Publication details
Sofya Tishina et al, Oncogenic KRAS-driven type I interferon signalling primes pancreatic cancer for necroptosis, Nature Communications (2026). DOI: 10.1038/s41467-026-73189-8
Journal information: Nature Communications
Key medical concepts
Carcinoma, PancreaticNecroptosisCaspase 8type I interferon-mediated signaling pathway
Clinical categories
OncologyClinical genetics Provided by University of Cologne Who's behind this story?
Gaby Clark
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