Evidence map›Paper›PMID 41904944›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

DMAP1 Deficiency Suppresses Lung Cancer Progression by Destabilizing Replication Fork and Activating IFN Signaling-Mediated Anti-tumor Immunity.

Kan Huang, Xi Dai, Shuaihu Li, Yingxue Chen, Yaxin Yu, Lin Wang, Kun Liu, Shuhan Lyu, Chongyang Li, Yihua Sun and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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

11 authors.

Kan HuangDepartment of pathology, School of Basic Medical Sciences, Department of Thoracic Surgery, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, China.ORCID https://orcid.org/0009-0004-3697-2909
Xi DaiDepartment of pathology, School of Basic Medical Sciences, Department of Thoracic Surgery, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, China.
Shuaihu LiDepartment of pathology, School of Basic Medical Sciences, Department of Thoracic Surgery, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, China.
Yingxue ChenDepartment of Pathology and Frontier Innovation Center, School of Basic Medicine Sciences, Shanghai Pudong Hospital, Fudan University, Shanghai, China.
Yaxin YuDepartment of Pathology and Frontier Innovation Center, School of Basic Medicine Sciences, Shanghai Pudong Hospital, Fudan University, Shanghai, China.
Lin WangDepartment of Pathology and Frontier Innovation Center, School of Basic Medicine Sciences, Shanghai Pudong Hospital, Fudan University, Shanghai, China.
Kun LiuDepartment of Pathology and Frontier Innovation Center, School of Basic Medicine Sciences, Shanghai Pudong Hospital, Fudan University, Shanghai, China.
Shuhan LyuDepartment of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, USA.
Chongyang LiDepartment of Pathology and Frontier Innovation Center, School of Basic Medicine Sciences, Shanghai Pudong Hospital, Fudan University, Shanghai, China.
Yihua SunDepartment of Thoracic Surgery and State Key Laboratory of Genetic Engineering, Fudan University Shanghai Cancer Center, Shanghai, China.
Fei LiDepartment of Pathology and Frontier Innovation Center, School of Basic Medicine Sciences, Shanghai Pudong Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0002-1973-6611

Funding

China Postdoctoral Science Foundation 2024M752432Ministry of Science and Technology of the People's Republic of China 2022YFA1103900National Natural Science Foundation of China 82172744National Natural Science Foundation of China 82372794National Natural Science Foundation of China 82503107National Natural Science Foundation of China 82572985Postdoctoral Fellowship Program of CPSF GZB20240544Science and Technology Commission of Shanghai Municipality 24ZR1469100Shanghai Municipal Health Commission ZK2019C14
6 · The paper itself

Abstract

Despite substantial progress in targeted and immune therapies, lung cancer remains the leading cause of cancer-related mortality, highlighting the urgent need for novel therapeutic strategies. Through a CRISPR-based knock-out screen, we identified the DNA methyltransferase 1-associated protein 1 (DMAP1) as a critical regulator of lung cancer progression. Functional studies demonstrated that DMAP1 deficiency exerts its anti-tumor effects through attenuating tumor cell proliferation and activating T cell-mediated adaptive anti-tumor effects. Mechanistically, DMAP1 deficiency causes replication fork retardance, disturbs genome stability, and induces endogenous DNA damage, thereby activating IFN signaling-mediated anti-tumor immune response. Clinical data analyses revealed that high DMAP1 expression is associated with a "cold" tumor microenvironment and poorer overall survival in lung cancer. These findings significantly advance our knowledge of DMAP1's function in lung cancer development and offer a scientific basis for designing novel treatment approaches.

Indexed as

DNA ReplicationInterferonsLung NeoplasmsAnimalsCell Line, TumorCell ProliferationDisease ProgressionDNA DamageHumansMiceSignal TransductionTumor MicroenvironmentInterferonsDMAP1IFN signalinglung cancerreplication stresstumor immunity

Identifiers

PMID41904944
PMCPMC13271618

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.