ArticlePloS one2012
Alveolar type II cells possess the capability of initiating lung tumor development.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 123 citations in OpenAlex.
- Mapping the dialogue: Decoding alveolar stem-niche interactions.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
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- Hippo signaling differentially regulates distal progenitor subpopulations and their transitional states to construct the mammalian lungs.Nature communications · 2026Article
- Cellular Aging Signatures in the Plasma Proteome Record Human Health and Disease.bioRxiv : the preprint server for biology · 2026Article
- PDLIM2 in Lung Adenocarcinoma Metastasis.bioRxiv : the preprint server for biology · 2025Article
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- SMAD2 linker phosphorylation impacts overall survival, proliferation, TGFβ1-dependent gene expression and pluripotency-related proteins in NSCLC.British journal of cancer · 2025Article
- APOBEC affects tumor evolution and age at onset of lung cancer in smokers.Nature communications · 2025Article
- A Recurrent Small Cell Lung Carcinoma Harboring an EML4-ALK Fusion Mutation with Sustained Response to Ensartinib: A Case Report.Current oncology (Toronto, Ont.) · 2025Article
- Proteogenomic characterization reveals tumorigenesis and progression of lung cancer manifested as subsolid nodules.Nature communications · 2025Article
- Acquisition of discrete immune suppressive barriers contributes to the initiation and progression of preinvasive to invasive human lung cancer.bioRxiv : the preprint server for biology · 2025Article
- Targeting nanoparticles to lung cancer-derived A549 cells based on changes on interstitial stiffness in biomimetic models.iScience · 2024Article
- A Multi-Omics Study of Epigenetic Changes in Type II Alveolar Cells of A/J Mice Exposed to Environmental Tobacco Smoke.International journal of molecular sciences · 2024Article
- Cell of origin alters myeloid-mediated immunosuppression in lung adenocarcinoma.bioRxiv : the preprint server for biology · 2024Article
- Mitochondrial respiratory function is preserved under cysteine starvation via glutathione catabolism in NSCLC.Nature communications · 2024Article
- CRTAC1 identified as a promising diagnosis and prognostic biomarker in lung adenocarcinoma.Scientific reports · 2024Article
- Exhaled breath condensate contains extracellular vesicles (EVs) that carry miRNA cargos of lung tissue origin that can be selectively purified and analyzed.Journal of extracellular vesicles · 2024Article
- Article
- Rare case report: a case of histological type transformation of lung cancer caused by neoadjuvant immunotherapy.Frontiers in oncology · 2024Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Identifying cells of tumor origin is a fundamental question in tumor biology. Answers to this central question will not only advance our understanding of tumor initiation and progression but also have important therapeutic implications. In this study, we aimed to uncover the cells of origin of lung adenocarcinoma, a major subtype of non-small cell lung cancer. To this end, we developed new mouse models of lung adenocarcinoma that enabled selective manipulation of gene activity in surfactant associated protein C (SPC)-expressing cells, including alveolar type II cells and bronchioalveolar stem cells (BASCs) that reside at the bronchioalveolar duct junction (BADJ). Our findings showed that activation of oncogenic Kras alone or in combination with the removal of the tumor suppressor p53 in SPC⁺ cells resulted in development of alveolar tumors. Similarly, sustained EGF signaling in SPC⁺ cells led to alveolar tumors. By contrast, BASCs failed to proliferate or produce tumors under these conditions. Importantly, in a mouse strain in which Kras/p53 activity was selectively altered in type II cells but not BASCs, alveolar tumors developed while BADJs retained normal architecture. These results confirm and extend previous findings and support a model in which lung adenocarcinoma can initiate in alveolar type II cells. Our results establish the foundation for elucidating the molecular mechanisms by which lung cancer initiates and progresses in a specific lung cell type.
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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.