ArticleScience (New York, N.Y.)2026
Chronic type II interferon promotes tumor growth through mitochondrial RNA-induced type I interferon and prostaglandin synthesis.
Melissa A Johnson, Siva Karthik Varanasi, Kailash Chandra Mangalhara, Kathryn Lande, Gladys R Rojas, Pau B Esparza-Moltó, Mack B Reynolds, Neva Olliffe, Karl Wessendorf-Rodriguez, Sagnika Ghosh and 12 more
Abstract read
In one paragraphArticle in Science (New York, N.Y.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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 registryThe 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.
3 · Its place in the literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
22 authors.
Kathryn LandeSalk Institute for Biological Studies, La Jolla, CA, USA.
Funding
Viral Vector Core (VVC)P30CA014195 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Alan Saghatelian · 1985 to 2026
$82.8MProject 4: Interrogating and harnessing age-related IFN signaling and innate immunity in HCC prevention and therapyP01AG073084 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI PETER D. ADAMS, GERALD SHADEL · 2021 to 2026
$13.6MPathways in Biological Sciences Training ProgramT32GM133351 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Matthew Daugherty, Randolph Y. Hampton · 2020 to 2026
$9.9MSalk Institute Cancer Training GrantT32CA009370 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Diana Clare Hargreaves, Jan Karlseder · 1986 to 2026
$8.6MSan Diego Nathan Shock CenterP30AG068635 · NIA · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI SHADEL, GERALD · 2020 to 2024
$6.0M(PQ5) Mitochondrial Heterogeneity in Melanoma Tumor and Immune ResponsesR01CA216101 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI GERALD SHADEL · 2018 to 2026
$5.0MMitochondria-to-Nucleus Signaling in Colorectal CancerR01CA228211 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI HARGREAVES, DIANA CLARE, SHADEL, GERALD · 2020 to 2024
$2.6MThe Role of the Tumor Suppressor ARID1A in R loop Homeostasis and Tumor ImmunityR01CA285867 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Diana Clare Hargreaves · 2024 to 2026
$1.7MMetabolic heterogeneity of tissue resident memory T cells in the liverR21AI151562 · NIAID · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI KAECH, SUSAN M · 2020 to 2021
$529kMitochondrial Regulation of Interferon Response in MelanomaF31CA278581 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI JOHNSON, MELISSA · 2023 to 2025
$106kMechanism of cardioprotective mitochondrial oxidative stress priming in doxorubicin-induced cardiotoxicityF30HL178290 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Matthew P Donnelly · 2025 to 2026
$98kNCI NIH HHS F31 CA278581NCI NIH HHS P30 CA014195NCI NIH HHS R01 CA216101NCI NIH HHS R01 CA228211NCI NIH HHS R01 CA285867NCI NIH HHS T32 CA009370NHLBI NIH HHS F30 HL178290NIAID NIH HHS R21 AI151562NIA NIH HHS P01 AG073084NIA NIH HHS P30 AG068635NIGMS NIH HHS T32 GM133351
6 · The paper itselfAbstract
Interferons (IFNs) are proinflammatory cytokines that promote immune cell engagement to eliminate malignant cells. Paradoxically, chronic interferon signaling can also activate anti-inflammatory mechanisms that allow cancer cells to evade the immune system. In this study, we sought to determine the cellular mechanisms underlying this switch from antitumorigenic to protumorigenic interferon activity. We show that chronic type II interferon (IFN-II) exposure distinctively induced tumor growth by activating a type I interferon (IFN-I) response mediated by release of double-stranded mitochondrial RNA (ds-mtRNA) into the cytoplasm. This IFN-I signal synergized with IFN-II to enhance tumor growth by increasing immunosuppressive prostaglandin E
Indexed as
DinoprostoneInterferon-gammaInterferon Type IMelanomaMelanoma, ExperimentalRNA, MitochondrialAnimalsCell Line, TumorCyclooxygenase 2ImmunotherapyMiceMice, Inbred C57BLRNA, Double-StrandedSignal TransductionCyclooxygenase 2DinoprostoneInterferon-gammaInterferon Type IPtgs2 protein, mouseRNA, Double-StrandedRNA, Mitochondrial
Identifiers
PMID42721225
PMCPMC13634221
What OpenQuestion holds
Textmetadata
Read underepoch 390