Evidence map›Paper›PMID 37723144›Full record

ArticleCell discovery2023

Spatial transcriptomics delineates molecular features and cellular plasticity in lung adenocarcinoma progression.

Yan Wang, Bing Liu, Qingjie Min, Xin Yang, Shi Yan, Yuanyuan Ma, Shaolei Li, Jiawen Fan, Yaqi Wang, Bin Dong and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
9.2field-weighted citation impact, top 1% of its field
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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Pooled it
  2. Cell plasticity in cancer and therapy resistance.Experimental & molecular medicine · 2026
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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

14 authors at 2 institutions in 2 countries.

Yan Wang *Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Laboratory of Molecular Oncology, Peking University Cancer Hospital & Institute, Beijing, China.
Bing Liu *Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Thoracic Surgery II, Peking University Cancer Hospital & Institute, Beijing, China.
Qingjie Min *Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Laboratory of Molecular Oncology, Peking University Cancer Hospital & Institute, Beijing, China.
Xin Yang *Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Pathology, Peking University Cancer Hospital & Institute, Beijing, China.
Shi YanKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Thoracic Surgery II, Peking University Cancer Hospital & Institute, Beijing, China.
Yuanyuan MaKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Thoracic Surgery II, Peking University Cancer Hospital & Institute, Beijing, China.
Shaolei LiKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Thoracic Surgery II, Peking University Cancer Hospital & Institute, Beijing, China.
Jiawen FanKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Laboratory of Molecular Oncology, Peking University Cancer Hospital & Institute, Beijing, China.
Yaqi WangKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Thoracic Surgery II, Peking University Cancer Hospital & Institute, Beijing, China.
Bin DongKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Central Laboratory, Peking University Cancer Hospital and Institute, Beijing, China.
Huajing TengKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Radiation Oncology, Peking University Cancer Hospital & Institute, Beijing, China.ORCID http://orcid.org/0000-0001-9952-3618
Dongmei LinKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Pathology, Peking University Cancer Hospital & Institute, Beijing, China.
Qimin ZhanKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Laboratory of Molecular Oncology, Peking University Cancer Hospital & Institute, Beijing, China. zhanqimin@bjmu.edu.cn.ORCID http://orcid.org/0000-0002-1731-938X
Nan WuKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Thoracic Surgery II, Peking University Cancer Hospital & Institute, Beijing, China. nanwu@bjmu.edu.cn.
Peking University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81988101, 81972842 and 81830086
6 · The paper itself

Abstract

Indolent (lepidic) and aggressive (micropapillary, solid, and poorly differentiated acinar) histologic subtypes often coexist within a tumor tissue of lung adenocarcinoma (LUAD), but the molecular features associated with different subtypes and their transitions remain elusive. Here, we combine spatial transcriptomics and multiplex immunohistochemistry to elucidate molecular characteristics and cellular plasticity of distinct histologic subtypes of LUAD. We delineate transcriptional reprogramming and dynamic cell signaling that determine subtype progression, especially hypoxia-induced regulatory network. Different histologic subtypes exhibit heterogeneity in dedifferentiation states. Additionally, our results show that macrophages are the most abundant cell type in LUAD, and identify different tumor-associated macrophage subpopulations that are unique to each histologic subtype, which might contribute to an immunosuppressive microenvironment. Our results provide a systematic landscape of molecular profiles that drive LUAD subtype progression, and demonstrate potentially novel therapeutic strategies and targets for invasive lung adenocarcinoma.

Identifiers

PMID37723144
PMCPMC10507052
OpenAlexW4386820164

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.