Evidence map›Paper›PMID 39601163›Full record

ArticleClinical and translational medicine2024

Single-cell dissection reveals immunosuppressive F13A1+ macrophage as a hallmark for multiple primary lung cancers.

Chenglin Yang, Jiahao Qu, Jingting Wu, Songhua Cai, Wenyi Liu, Youjun Deng, Yiran Meng, Liuqing Zheng, Lishen Zhang, Li Wang and 1 more

Abstract read
In one paragraph

Article in Clinical and translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Integrated multi-omics profiling reveals the potential role of maternal systemic immune dysregulation driven by monocyte/macrophage in preeclampsia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. World journal of gastroenterology · 2025
    Article
  10. Article
  11. 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

11 authors.

Chenglin YangNational Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, China.
Jiahao QuNational Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, China.
Jingting WuNational Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, China.
Songhua CaiNational Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, China.
Wenyi LiuNational Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, China.
Youjun DengNational Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, China.
Yiran MengDepartment of R&D, Hangzhou Repugene Technology Co., Ltd., Hangzhou, China.
Liuqing ZhengDepartment of R&D, Hangzhou Repugene Technology Co., Ltd., Hangzhou, China.ORCID 0009-0003-6324-3595
Lishen ZhangDepartment of R&D, Hangzhou Repugene Technology Co., Ltd., Hangzhou, China.
Li WangDepartment of R&D, Hangzhou Repugene Technology Co., Ltd., Hangzhou, China.
Xiaotong GuoNational Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, China.

Funding

Medical Scientific Research Foundation of Guangdong Province, China A2022204National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen SZ2020ZD01SanMing Project of Medicine in Shenzhen SZSM202211011Shenzhen High-level Hospital Construction FundShenzhen Key Medical Discipline Construction Fund SZXK075
6 · The paper itself

Abstract

backgroundThe increasing prevalence of multiple primarylung cancers (MPLCs) presents challenges to current diagnostic and clinicalmanagement approaches. However, the molecular mechanisms driving MPLCdevelopment and distinguishing it from solitary primary lung cancers (SPLCs)remain largely unexplored.

methodsWe performed a comparative single-cell RNAsequencing (scRNA-seq) analysis on tumour and adjacent para-tumour tissues fromMPLC and SPLC patients to comparatively evaluate their immunological landscapes.Additionally, multiplex immunofluorescence (mIF) staining and independentvalidation datasets were used to confirm findings.

resultsMPLCs and SPLCs share significant similarities in genetic, transcriptomic and immune profiles, suggesting common therapeutic strategies such as EGFR-TKIs andICIs. Notably, an immunosuppressive macrophage subtype, F13A1+ Macrophage (Mϕ), is specifically enriched in MPLCs. This subtype overexpresses M2 macrophagemarkers and exhibits up-regulation of SPP1-CD44/CCL13-ACKR1 interactions, indicatingits role in shaping the immunosuppressive tumour microenvironment and promotingtumour growth in MPLCs.

conclusionsThis study unveils shared molecular mechanismsbetween MPLCs and SPLCs, while identifying MPLC-specific cellular and molecularfeatures, such as the role of F13A1+ macrophages. The findings provide novelinsights into MPLC pathogenesis, supporting the development of targetedtherapeutic strategies. KEY POINTS: Comparative scRNA-seq analysis reveals significant similarities in genetic, transcriptomicand immune profiles between MPLCs and SPLCs. Identification of a unique immunosuppressive F13A1+ macrophage subtype, preferentially enriched in MPLCs, linked to immune evasion and tumourprogression. SPP1-CD44/CCL13-ACKR1 interactions are crucial in MPLC tumour microenvironment, indicating potential targets for therapeutic intervention.

Indexed as

Lung NeoplasmsMacrophagesHumansSingle-Cell AnalysisTumor MicroenvironmentF13A1+ MϕMPLCscRNA‐seqSPLC

Identifiers

PMID39601163
PMCPMC11600049

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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.