Evidence map›Paper›PMID 39141316›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2025

Loss of histone deubiquitinase Bap1 triggers anti-tumor immunity.

Hong Chang, Mingxia Li, Linlin Zhang, Meng Li, Swee Hoe Ong, Zhiwei Zhang, Jie Zheng, Xiang Xu, Yu Zhang, Jing Wang and 8 more

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. BAP1 regulates HSF1 activity and cancer immunity in pancreatic cancer.Journal of experimental & clinical cancer research : CR · 2024
    Article
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

18 authors.

Hong Chang *Department of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China.
Mingxia Li *Department of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China.
Linlin ZhangDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China.
Meng LiWellcome Sanger Institute, Hinxton, Cambridge, CB10 1HH, UK.
Swee Hoe OngWellcome Sanger Institute, Hinxton, Cambridge, CB10 1HH, UK.
Zhiwei ZhangDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China.
Jie ZhengDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China.
Xiang XuDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China.
Yu ZhangDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China.
Jing WangDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China.
Xingjie LiuDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China.
Kairui LiDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China.
Yao LuoDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China.
Haiyun WangDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China.
Zhichao MiaoTranslational Research Institute of Brain and Brain-Like Intelligence, Department of Anesthesiology, Shanghai Fourth People's Hospital Affiliated to Tongji University School of Medicine, Shanghai, 200081, China.
Xi ChenDepartment of Biology, Southern University of Science and Technology, 1088 Xueyuan Avenue, Shenzhen, 518055, China.
Jie ZhaDepartment of Hematology, The First Affiliated Hospital of Xiamen University and Institute of Hematology, School of Medicine, Xiamen University, Xiamen, China. zhajie@xmu.edu.cn.
Yong YuDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China. yy3@tongji.edu.cn.

Funding

National Key Research and Development Program of China 2021YFA1100903, 2021YFA1100900National Natural Science Foundation of China 82371736
6 · The paper itself

Abstract

purposeImmunotherapy using PD-L1 blockade is effective in only a small group of cancer patients, and resistance is common. This emphasizes the importance of understanding the mechanisms of cancer immune evasion and resistance.

methodsA genome-scale CRISPR-Cas9 screen identified Bap1 as a regulator of PD-L1 expression. To measure tumor size and survival, tumor cells were subcutaneously injected into both syngeneic WT mice and immunocompromised mice. The phenotypic and transcriptional characteristics of Bap1-deleted tumors were examined using flow cytometry, RNA-seq, and CUT&Tag-seq analysis.

resultsWe found that loss of histone deubiquitinase Bap1 in cancer cells activates a cDC1-CD8

conclusionThe histone deubiquitinase Bap1 could be used as a biomarker for tumor stratification and as a potential therapeutic target for cancer immunotherapies.

Indexed as

NeoplasmsTumor Suppressor ProteinsUbiquitin ThiolesteraseAnimalsB7-H1 AntigenCD8-Positive T-LymphocytesCell Line, TumorGene Expression Regulation, NeoplasticHumansMiceMice, Inbred C57BLTumor MicroenvironmentB7-H1 AntigenBAP1 protein, humanBAP1 protein, mouseTumor Suppressor ProteinsUbiquitin ThiolesteraseAnti-tumor immunityBap1PD-L1Tumor microenvironment

Identifiers

PMID39141316
PMCPMC11850471

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

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.