ArticleNature communications2024
Coxsackievirus and adenovirus receptor expression facilitates enteroviral infections to drive the development of pancreatic cancer.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed.
- Early induction of the Rho-GEF ECT2 drives MEK/ERK oncogenic signaling in pancreatic ductal adenocarcinoma.Oncogene · 2026Article
- Comparative analysis of deep mutational scanning datasets in enteroviruses A and B identifies functional divergence and therapeutic targets.Nature ecology & evolution · 2026Article
- Explorative Insights into Local Immune Response to BK Virus-A Cross-Sectional Study in Urine Samples Between Transplant Recipients and Non-Immunocompromised Hosts.Medicina (Kaunas, Lithuania) · 2026Article
- Review
- Prognostic significance of advanced lung cancer inflammation index in resectable pancreatic cancer: A retrospective study.World journal of gastrointestinal surgery · 2025Article
- A vaccination strategy to prevent coxsackie virus B3-induced development of pancreatic cancer.JCI insight · 2025Article
- Comparative Analysis of Deep Mutational Scanning Datasets in Enteroviruses A and B Identifies Functional Divergence and Therapeutic Targets.Research square · 2025Article
- A Fluorescent Reporter Virus Toolkit for Interrogating Enterovirus Biology and Host Interactions.Viruses · 2025Article
- CVB3-induced P62 cleavage promotes ferroptosis through the NRF2/GPX4 axis and facilitates viral replication.Frontiers in microbiology · 2025Article
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Authors and funding
14 authors.
Funding
Abstract
The development of pancreatic cancer requires both, acquisition of an oncogenic mutation in KRAS as well as an inflammatory insult. However, the physiological causes for pancreatic inflammation are less defined. We show here that oncogenic KRas-expressing pre-neoplastic lesion cells upregulate coxsackievirus (CVB) and adenovirus receptor (CAR). This facilitates infections from enteroviruses such as CVB3, which can be detected in approximately 50% of pancreatic cancer patients. Moreover, using an animal model we show that a one-time pancreatic infection with CVB3 in control mice is transient, but in the presence of oncogenic KRas drives chronic inflammation and rapid development of pancreatic cancer. We further demonstrate that a knockout of CAR in pancreatic lesion cells blocks these CVB3-induced effects. Our data demonstrate that KRas-caused lesions promote the development of pancreatic cancer by enabling certain viral infections.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.