Evidence map›Paper›PMID 39577420›Full record

ArticleCancer cell2024

Interleukin-1α release during necrotic-like cell death generates myeloid-driven immunosuppression that restricts anti-tumor immunity.

Kay Hänggi, Jie Li, Achintyan Gangadharan, Xiaoxian Liu, Daiana P Celias, Olabisi Osunmakinde, Aysenur Keske, Joshua Davis, Faiz Ahmad, Auriane Giron and 7 more

Abstract read
In one paragraph

Article in Cancer cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
–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.

3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 1 synthesis or guideline pooled it.

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4 · The record

Corrections and comments

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

17 authors.

Kay HänggiDepartment of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA. Electronic address: kay.hanggi@moffitt.org.
Jie LiDepartment of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA; Cancer Biology PhD Program, University of South Florida, Tampa, FL 33620, USA.
Achintyan GangadharanDepartment of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA; Cancer Biology PhD Program, University of South Florida, Tampa, FL 33620, USA.
Xiaoxian LiuDepartment of Biostatistics and Bioinformatics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.
Daiana P CeliasDepartment of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.
Olabisi OsunmakindeDepartment of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA; Cancer Biology PhD Program, University of South Florida, Tampa, FL 33620, USA.
Aysenur KeskeDepartment of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.
Joshua DavisDepartment of Biostatistics and Bioinformatics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.
Faiz AhmadDepartment of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Auriane GironDepartment of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.
Carmen M AnadonDepartment of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.
Alycia GardnerDepartment of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA; Cancer Biology PhD Program, University of South Florida, Tampa, FL 33620, USA.
David G DeNardoDepartment of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Timothy I ShawDepartment of Biostatistics and Bioinformatics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.
Amer A BegDepartment of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.
Xiaoqing YuDepartment of Biostatistics and Bioinformatics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.
Brian RuffellDepartment of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA; Department of Breast Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA. Electronic address: brian.ruffell@moffitt.org.

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI KENNETH Lynn WRIGHT · 1998 to 2026
$93.5M
Washington University SPORE in Pancreatic CancerP50CA272213 · NCI · WASHINGTON UNIVERSITY · PI David G DeNardo, WILLIAM G HAWKINS · 2023 to 2026
$10.7M
The Impact of Macrophage Origin on the Pathogenesis and Treatment Resistance of Pancreatic CancerR01CA177670 · NCI · WASHINGTON UNIVERSITY · PI DENARDO, DAVID G · 2014 to 2023
$3.3M
Stomal Senescence Regulator of Tumor Immunity and ProgressionR01CA286615 · NCI · WASHINGTON UNIVERSITY · PI David G DeNardo, Paolo Provenzano · 2024 to 2026
$3.2M
Re-wiring PDAC Tumor Immunity Through Dendritic CellsR01CA262506 · NCI · WASHINGTON UNIVERSITY · PI DENARDO, DAVID G, DESELM, CARL · 2021 to 2025
$2.8M
The Impact of Metastatic Site On Dendritic Cell-Driven Tumor ImmunityU01CA284086 · NCI · WASHINGTON UNIVERSITY · PI David G DeNardo, Li Ding · 2023 to 2026
$2.3M
Regulation of dendritic cell function and tumor immunity by TIM-3R01CA230610 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI RUFFELL, BRIAN · 2019 to 2023
$2.0M
NCI NIH HHS P30 CA076292NCI NIH HHS P50 CA272213NCI NIH HHS R01 CA177670NCI NIH HHS R01 CA230610NCI NIH HHS R01 CA262506NCI NIH HHS R01 CA286615NCI NIH HHS U01 CA284086
6 · The paper itself

Abstract

Necroptosis can promote antigen-specific immune responses, suggesting induced necroptosis as a therapeutic approach for cancer. Here we sought to determine the mechanism of immune activation but found the necroptosis mediators RIPK3 and MLKL dispensable for tumor growth in genetic and implantable models of breast or lung cancer. Surprisingly, inducing necroptosis within established breast tumors generates a myeloid suppressive microenvironment that inhibits T cell function, promotes tumor growth, and reduces survival. This was dependent upon the release of the nuclear alarmin interleukin-1α (IL-1α) by dying cells. Critically, IL-1α release occurs during chemotherapy and targeting this molecule reduces the immunosuppressive capacity of tumor myeloid cells and promotes CD8

Indexed as

Interleukin-1alphaNecroptosisTumor MicroenvironmentAnimalsBreast NeoplasmsCD8-Positive T-LymphocytesCell Line, TumorFemaleHumansLung NeoplasmsMiceMice, Inbred C57BLMyeloid CellsNecrosisPaclitaxelIL1A protein, humanInterleukin-1alphaPaclitaxelcancerchemotherapyimmunogenic cell deathimmunosuppressioninterleukin-1macrophagesnecroptosisnecrotic-like cell deathneutrophils

Identifiers

PMID39577420
PMCPMC11631672

What OpenQuestion holds

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Registered trials

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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.