Evidence map›Paper›PMID 42753736›Full record

ArticleCancer cell2026

Myeloid reprogramming generates myeloid-derived activating cells to potentiate radiotherapy and suppress metastasis.

Fei Ji, Lei Zheng, Dapeng Chen, Peng Xia, Zhongyu Zou, Wei Liu, Jason Bugno, Emile Z Naccasha, András Piffkó, Chuangyu Wen and 14 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer cell, 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
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

24 authors.

Fei JiDepartment of Radiation and Cellular Oncology, USA; The Ludwig Center for Cancer Research, University of Chicago, Chicago, IL 60637, USA.
Lei ZhengDepartment of Chemistry, The University of Chicago, Chicago, IL 60637, USA; Howard Hughes Medical Institute, Chicago, IL 60637, USA.
Dapeng ChenDepartment of Radiation and Cellular Oncology, USA; The Ludwig Center for Cancer Research, University of Chicago, Chicago, IL 60637, USA.
Peng XiaDepartment of Chemistry, The University of Chicago, Chicago, IL 60637, USA; Howard Hughes Medical Institute, Chicago, IL 60637, USA.
Zhongyu ZouDepartment of Chemistry, The University of Chicago, Chicago, IL 60637, USA; Howard Hughes Medical Institute, Chicago, IL 60637, USA.
Wei LiuDepartment of Radiation and Cellular Oncology, USA; The Ludwig Center for Cancer Research, University of Chicago, Chicago, IL 60637, USA.
Jason BugnoDepartment of Radiation and Cellular Oncology, USA; The Ludwig Center for Cancer Research, University of Chicago, Chicago, IL 60637, USA; Committee on Clinical Pharmacology and Pharmacogenomics, University of Chicago, Chicago, IL, USA.
Emile Z NaccashaDepartment of Radiation and Cellular Oncology, USA; The Ludwig Center for Cancer Research, University of Chicago, Chicago, IL 60637, USA; Pritzker School of Medicine, The University of Chicago, Chicago, IL, USA.
András PiffkóDepartment of Radiation and Cellular Oncology, USA; The Ludwig Center for Cancer Research, University of Chicago, Chicago, IL 60637, USA.
Chuangyu WenDepartment of Radiation and Cellular Oncology, USA; The Ludwig Center for Cancer Research, University of Chicago, Chicago, IL 60637, USA.
Kangdi LiDepartment of Radiation and Cellular Oncology, USA; The Ludwig Center for Cancer Research, University of Chicago, Chicago, IL 60637, USA.
Liping XuDepartment of Radiation and Cellular Oncology, USA; The Ludwig Center for Cancer Research, University of Chicago, Chicago, IL 60637, USA.
Sean Z LuoDepartment of Radiation and Cellular Oncology, USA; The Ludwig Center for Cancer Research, University of Chicago, Chicago, IL 60637, USA.
Xiaona HuangDepartment of Radiation and Cellular Oncology, USA; The Ludwig Center for Cancer Research, University of Chicago, Chicago, IL 60637, USA.
Jiaai WangDepartment of Radiation and Cellular Oncology, USA; The Ludwig Center for Cancer Research, University of Chicago, Chicago, IL 60637, USA.
Chengwei JuDepartment of Chemistry, The University of Chicago, Chicago, IL 60637, USA; Howard Hughes Medical Institute, Chicago, IL 60637, USA.
Bei LiuDepartment of Chemistry, The University of Chicago, Chicago, IL 60637, USA; Howard Hughes Medical Institute, Chicago, IL 60637, USA.
Yiyi JiDepartment of Chemistry, The University of Chicago, Chicago, IL 60637, USA; Howard Hughes Medical Institute, Chicago, IL 60637, USA.
Han LiDepartment of Chemistry, The University of Chicago, Chicago, IL 60637, USA; Howard Hughes Medical Institute, Chicago, IL 60637, USA.
Steven J ChmuraDepartment of Radiation and Cellular Oncology, USA; The Ludwig Center for Cancer Research, University of Chicago, Chicago, IL 60637, USA.
Sean P PitrodaDepartment of Radiation and Cellular Oncology, USA; The Ludwig Center for Cancer Research, University of Chicago, Chicago, IL 60637, USA.
Hua Laura LiangDepartment of Radiation and Cellular Oncology, USA; The Ludwig Center for Cancer Research, University of Chicago, Chicago, IL 60637, USA. Electronic address: hualiang@uchicago.edu.
Chuan HeDepartment of Chemistry, The University of Chicago, Chicago, IL 60637, USA; Howard Hughes Medical Institute, Chicago, IL 60637, USA; Department of Biochemistry and Molecular Biology, University of Chicago, Chicago, IL 60637, USA. Electronic address: chuanhe@uchicago.edu.
Ralph R WeichselbaumDepartment of Radiation and Cellular Oncology, USA; The Ludwig Center for Cancer Research, University of Chicago, Chicago, IL 60637, USA. Electronic address: rweichselbaum@uchicagomedicine.org.

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

Radiation induces immunosuppressive myeloid cells that drive therapeutic resistance and metastasis. We identify TET2 as a radiation-induced regulator of myeloid-derived suppressor cells whose expression correlates with poor outcomes in advanced lung cancer patients receiving radio-immunotherapy. Following radiotherapy, myeloid-specific Tet2 deletion suppresses tumor progression and redirects monocyte differentiation toward antigen-presenting myeloid-derived activating cells (MDACs), which augment antitumor T cell responses; spatiotemporal mapping shows that this fate program initiates rapidly in the bone marrow. Mechanistically, a radiation-responsive p53-TET2 axis decreases m

Indexed as

Cellular ReprogrammingLung NeoplasmsMyeloid CellsMyeloid-Derived Suppressor CellsAnimalsCell Line, TumorDioxygenasesDNA-Binding ProteinsHumansImmunotherapyMiceNeoplasm MetastasisProto-Oncogene ProteinsTumor Suppressor Protein p53DioxygenasesDNA-Binding ProteinsProto-Oncogene ProteinsTet2 protein, mouseTumor Suppressor Protein p53chromatin-associated RNAimmunotherapyMDACsMDSCsmyeloid-derived activating cellsmyeloid-derived suppressor cellsmyeloid reprogrammingradiotherapyT cell cytotoxicityTET2

Identifiers

PMID42753736
PMCPMC13669204

What OpenQuestion holds

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Registered trials

None linked

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.