Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
20 authors.
Yu C J Chey *South Australian ImmunoGENomics Cancer Institute (SAiGENCI), The University of Adelaide, Adelaide, SA, Australia.ORCID 0000-0001-7553-5163
Bassam Kashgari *Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, VIC, Australia.
Louise McLeodCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, VIC, Australia.
Georgette A RadfordSouth Australian ImmunoGENomics Cancer Institute (SAiGENCI), The University of Adelaide, Adelaide, SA, Australia.
Linden J GearingCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, VIC, Australia.ORCID 0000-0003-3508-3056
Ruby E DawsonSouth Australian ImmunoGENomics Cancer Institute (SAiGENCI), The University of Adelaide, Adelaide, SA, Australia.
Malvika KharbandaSouth Australian ImmunoGENomics Cancer Institute (SAiGENCI), The University of Adelaide, Adelaide, SA, Australia.ORCID 0000-0001-9726-3023
Joanne LundyCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, VIC, Australia.
Daniel CroaghDepartment of Surgery (School of Clinical Sciences at Monash Health), Monash University, Clayton, VIC, Australia.ORCID 0000-0002-6430-6741
Charlotte Girard-Guyonvarc'hDivision of Rheumatology, University Hospital of Geneva, Geneva, Switzerland.ORCID 0000-0002-4901-2059
Cem GabayDivision of Rheumatology, University Hospital of Geneva, Geneva, Switzerland.ORCID 0000-0001-6853-3063
Brooke A PereiraCancer Ecosystems Program, Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Darlinghurst, Sydney, NSW, Australia.ORCID 0000-0003-3513-1214
David HerrmannCancer Ecosystems Program, Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Darlinghurst, Sydney, NSW, Australia.ORCID 0000-0002-9514-7501
Paul TimpsonCancer Ecosystems Program, Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Darlinghurst, Sydney, NSW, Australia.ORCID 0000-0002-5514-7080
John W FinnieSchool of Medicine, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, SA, Australia.
Mohamed I SaadSouth Australian ImmunoGENomics Cancer Institute (SAiGENCI), The University of Adelaide, Adelaide, SA, Australia.ORCID 0000-0002-4855-2360
Dharmesh D BhuvaSouth Australian ImmunoGENomics Cancer Institute (SAiGENCI), The University of Adelaide, Adelaide, SA, Australia.ORCID 0000-0002-6398-9157
Bernardo S FranklinInstitute of Innate Immunity, Medical Faculty, University of Bonn, Bonn, Germany.ORCID 0000-0003-2591-9833
Florian I SchmidtInstitute of Innate Immunity, Medical Faculty, University of Bonn, Bonn, Germany.ORCID 0000-0002-9979-9769
Brendan J JenkinsSouth Australian ImmunoGENomics Cancer Institute (SAiGENCI), The University of Adelaide, Adelaide, SA, Australia. brendan.jenkins@adelaide.edu.au.ORCID 0000-0002-7552-4656
Funding
U.S. Department of Defense (United States Department of Defense) PA210090
6 · The paper itself
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is driven by genetic alterations in the pancreatic epithelium (e.g., KRAS) coupled with dysregulated innate immunity that triggers tumor-promoting chronic inflammation. However, the identity of innate immune molecular regulators as therapeutic targets in PDAC is ill-defined. Here, we show in PDAC patients that elevated tumoral expression of the inflammasome adaptor protein ASC and its downstream effector Caspase-1 is primarily colocalized to the pancreatic ductal epithelium and prognostic for poor survival. In the mutant Kras-driven KPC PDAC mouse model, global and conditional (pancreatic epithelial) ablation of ASC, or nanobody-mediated targeting of extracellular ASC, suppresses pancreatic tumorigenesis. Whole transcriptome profiling and multiplex immunofluorescence reveal that the tumor-promoting activities of epithelial-derived ASC align with molecular pathways for mitochondrial respiration, metabolism (glycolysis), and immune responses. Our discovery that ASC-containing inflammasomes promote PDAC by acting as a molecular bridge between innate immunity, mitochondrial dysfunction and metabolic reprogramming provides the rationale to therapeutically target ASC in cancers.
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.
Cancer cell-intrinsic inflammasome protein ASC links innate immunity with mitochondrial metabolism in driving pancreatic cancer. · full record | OpenQuestion