Evidence map›Paper›PMID 40356247›Full record

ArticleClinical and translational medicine2025

Lysine-specific demethylase 1 deletion reshapes tumour microenvironment to overcome acquired resistance to anti-programmed death 1 therapy in liver cancer.

Chen Liang, Mu Ye, Lei Yu, Peng-Fei Zhang, Xiao-Jun Guo, Xian-Long Meng, Hai-Ying Zeng, Shu-Yang Hu, Dao-Han Zhang, Qi-Man Sun and 14 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and translational medicine, 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. Review
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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

24 authors.

Chen LiangDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID 0009-0005-0932-5148
Mu YeShanghai Institute of Infectious Disease and Biosecurity, Fudan University, Shanghai, China.
Lei YuDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Shanghai, China.
Peng-Fei ZhangLiver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai, China.
Xiao-Jun GuoDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Shanghai, China.
Xian-Long MengDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Shanghai, China.
Hai-Ying ZengDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China.
Shu-Yang HuLiver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai, China.
Dao-Han ZhangLiver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai, China.
Qi-Man SunDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Shanghai, China.
Ying-Hao ShenDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Shanghai, China.
Jia-Bin CaiDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Shanghai, China.
Shuang-Qi LiKey Laboratory of Medical Epigenetics and Metabolism, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Zhen ChenClinical Research Unit, Institute of Clinical Science, Zhongshan Hospital, Fudan University, Shanghai, China.
Ying-Hong ShiDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Shanghai, China.
Ai-Wu KeLiver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai, China.
Yujiang G ShiKey Laboratory of Medical Epigenetics and Metabolism, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Jian ZhouDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Shanghai, China.
Jia FanDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Shanghai, China.
Fei-Zhen WuKey Laboratory of Medical Epigenetics and Metabolism, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Xiao-Yong HuangDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Shanghai, China.
Guo-Ming ShiDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID 0000-0003-3817-9117
Zheng TangLiver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai, China.
Jia-Cheng LuDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID 0000-0001-9557-264X

Funding

Fudan Undergraduate Research Opportunities Program 202410246112Shanghai Sailing Program 24YF2705000the Key Disease Joint Research Program of Xuhui District XHLHGG202102the National Natural Science Foundation of China 81972232the National Natural Science Foundation of China 82072575the National Natural Science Foundation of China 82403964the National Science and Technology Major Project of China 2023ZD0511500the Outstanding Resident Clinical Postdoctoral Program of Zhongshan Hospitalthe Program of Shanghai Academic Research Leader 22XD1402700
6 · The paper itself

Abstract

backgroundImmune checkpoint blockade, particularly targeting programmed death 1 (PD-1) and programmed death ligand 1 (PD-L1), shows promise in treating hepatocellular carcinoma (HCC). However, acquired resistance, especially in patients with 'hot tumours', limits sustained benefits. Lysine-specific demethylase 1 (LSD1) plays a role in converting 'cold tumours' to 'hot tumours', but its involvement in PD-1 inhibitor resistance in HCC is unclear.

methodsLSD1 and PD-L1 expression, along with CD8

resultsLSD1 overexpression in HCC patients correlated with reduced PD-L1 expression, less CD8

conclusionLSD1 deletion reshapes the TME, enhances CD8 KEY POINTS: Uncovering the synthetic lethality resulting from LSD1 deletion and PD1 inhibitor co-administration, evaluating their combined effects on tumour growth and TME remodelling. Elucidating the mechanism underlying the combined therapy of LSD1 deletion with PD1 inhibition for HCC. Exploring the implications of LSD1, CD74 and effector CD8

Indexed as

Carcinoma, HepatocellularDrug Resistance, NeoplasmHistone DemethylasesLiver NeoplasmsTumor MicroenvironmentAnimalsB7-H1 AntigenCD8-Positive T-LymphocytesCell Line, TumorFemaleHumansImmune Checkpoint InhibitorsMaleMiceProgrammed Cell Death 1 ReceptorB7-H1 AntigenHistone DemethylasesImmune Checkpoint InhibitorsKDM1A protein, humanProgrammed Cell Death 1 Receptoracquired resistancehepatocellular carcinomaimmune checkpoint blockadelysine‐specific demethylase 1programmed death ligand 1programmed death protein 1tumour microenvironment

Identifiers

PMID40356247
PMCPMC12069797

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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.