Article in Nature immunology, 2025. 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
11 authors.
Andrew Kent *Division of Hematology, University of Colorado School of Medicine, Aurora, CO, USA.
Kristel Joy Yee Mon *Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell University, New York, NY, USA.ORCID 0000-0001-7355-4811
Zachary HutchinsJill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell University, New York, NY, USA.
Gregory PutzelJill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell University, New York, NY, USA.
Dmitry ZhigarevJill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell University, New York, NY, USA.ORCID 0000-0002-8227-3875
Alexander GrierJill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell University, New York, NY, USA.
Baosen JiaJill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell University, New York, NY, USA.
Roderik M KortleverThe Francis Crick Institute, London, UK.
Gaetan BarbetJill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell University, New York, NY, USA.ORCID 0000-0002-0152-3650
J Magarian BlanderJill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell University, New York, NY, USA. jmblander@med.cornell.edu.ORCID 0000-0001-9207-1700
Funding
Toll-like receptor control of endocytic antigen cross-presentationR01AI170832 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI Julie Magarian Blander · 2023 to 2026
$2.7M
Mobilizing TAP-independent CD8 T cells through non-canonical cross-presentationR01AI170897 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI Julie Magarian Blander · 2023 to 2026
$2.7M
Multidisciplinary Research Training in Gastroenterology and HepatologyT32DK116970 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI Randy S Longman · 2019 to 2026
$2.3M
Immunology Training GrantT32AI007605 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI LIRA, SERGIO A. · 2001 to 2017
$2.2M
Toll-like Receptor Control of MHC Class I EndocytosisR21AI159772 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI BLANDER, JULIE MAGARIAN · 2022 to 2023
$466k
Modulating XIAP for the Treatment of Inflammatory Bowel DiseaseR21AI178327 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI BLANDER, JULIE MAGARIAN, LARISCH, SARIT · 2023 to 2024
$399k
Consequences of NLRC4/NAIP5 Inflammasome Signaling on Adaptive Immunity and TumorF30CA174313 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI KENT, ANDREW T · 2013 to 2015
$123k
Cancer Research UK 29210Cancer Research UK CC2229Cancer Research UK (CRUK) A29210Division of Cancer Prevention, National Cancer Institute (NCI Division of Cancer Prevention) T32AI007605Division of Intramural Research, National Institute of Allergy and Infectious Diseases (Division of Intramural Research of the NIAID) AI159772Division of Intramural Research, National Institute of Allergy and Infectious Diseases (Division of Intramural Research of the NIAID) AI170832Division of Intramural Research, National Institute of Allergy and Infectious Diseases (Division of Intramural Research of the NIAID) AI170897Division of Intramural Research, National Institute of Allergy and Infectious Diseases (Division of Intramural Research of the NIAID) AI178327NCI NIH HHS F30 CA174313NIAID NIH HHS R01 AI170832NIAID NIH HHS R01 AI170897NIAID NIH HHS R21 AI159772NIAID NIH HHS R21 AI178327NIAID NIH HHS T32 AI007605NIDDK NIH HHS T32 DK116970Robert Wood Johnson Foundation (RWJF) 74260United States - Israel Binational Science Foundation (BSF) 2021299U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases) T32DK116970
6 · The paper itself
Abstract
The inflammasome plays multifaceted roles in cancer, but less is known about its function during premalignancy upon initial cell transformation. We report a homeostatic function of the inflammasome in suppressing malignant transformation through Ras inhibition. We identified increased hematopoietic stem cell (HSC) proliferation within the bone marrow of inflammasome-deficient mice. HSCs within an inflammasome-deficient stroma expressed a Ras signature associated with increased Ras pathway- and cancer-related transcripts and heightened levels of cytokine, chemokine and growth factor receptors. Stromal inflammasome deficiency established a poised Ras-dependent mitogenic state within HSCs, which fueled progeny B cell lymphomagenesis upon Myc deregulation in a spontaneous model of B cell lymphoma, and shortened its premalignant stage leading to faster onset of malignancy. Thus, the stromal inflammasome preserves tissue balance by restraining Ras to disrupt the most common oncogenic Myc-Ras cooperation and establish a natural defense against transition to malignancy. These findings should inform preventative therapies against hematological malignancies.
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.
A stromal inflammasome Ras safeguard against Myc-driven lymphomagenesis. · full record | OpenQuestion