ArticleMolecular carcinogenesis2014
Role of PTEN in basal cell derived lung carcinogenesis.
Article in Molecular carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Loss of inducible nitric oxide synthase promotes Kras/Pten-driven lung tumorigenesis.Frontiers in cell and developmental biology · 2026Article
- CD103Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Therapeutic Implications of PTEN in Non-Small Cell Lung Cancer.Pharmaceutics · 2023Review
- Comparative Analysis of Stk11/Lkb1 versus Pten Deficiency in Lung Adenocarcinoma Induced by CRISPR/Cas9.Cancers · 2021Article
- Histologic transformation of lung adenocarcinoma to squamous cell carcinoma after chemotherapy: two case reports.Translational cancer research · 2020Article
- Development of syngeneic murine cell lines for use in immunocompetent orthotopic lung cancer models.Cancer cell international · 2020Article
- KRAS Exon 3 and PTEN Exon 7 Mutations in Small-cell Lung Cancer.Current medical science · 2019Article
- Role of KEAP1/NRF2 and TP53 Mutations in Lung Squamous Cell Carcinoma Development and Radiation Resistance.Cancer discovery · 2017Article
- Prevalence of NRAS, PTEN and AKT1 gene mutations in the central nervous system metastases of non-small cell lung cancer.Brain tumor pathology · 2017Article
- SOX2 Is the Determining Oncogenic Switch in Promoting Lung Squamous Cell Carcinoma from Different Cells of Origin.Cancer cell · 2016Article
- Smad4 loss promotes lung cancer formation but increases sensitivity to DNA topoisomerase inhibitors.Oncogene · 2016Article
- ErbB2 Pathway Activation upon Smad4 Loss Promotes Lung Tumor Growth and Metastasis.Cell reports · 2015Article
- Non-small-cell lung cancers: a heterogeneous set of diseases.Nature reviews. Cancer · 2014Review
- Loss of Lkb1 and Pten leads to lung squamous cell carcinoma with elevated PD-L1 expression.Cancer cell · 2014Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Lung adenocarcinoma (AdC) and lung squamous cell carcinoma (SCC) are the most common non-small cell lung cancer (NSCLC) subtypes, however, most genetic mouse models of lung cancer produce predominantly, if not exclusively, AdC. Whether this is secondary to targeting mutations to the distal airway cells or to the use of activating Kras mutations that drive AdC formation is unknown. We previously showed that targeting Kras(G12D) activation and transforming growth factor β receptor type II (TGFβRII) deletion to airway basal cells via a keratin promoter induced formation of both lung AdC and SCC. In this study we assessed if targeting phosphatase and tensin homologue (PTEN) deletion to airway basal cells could initiate lung tumor formation or increase lung SCC formation. We found that PTEN deletion is capable of initiating both lung AdC and SCC formation when targeted to basal cells and although PTEN deletion is a weaker tumor initiator than Kras(G12D) with low tumor multiplicity and long latency, tumors initiated by PTEN deletion were larger and displayed more malignant conversion than Kras(G12D) initiated tumors. That PTEN deletion did not increase lung SCC formation compared to Kras(G12D) activation, suggests that the initiating genetic event does not dictate tumor histology when genetic alterations are targeted to a specific cell. These studies also confirm that basal cells of the conducting airway are capable of giving rise to multiple NSCLC tumor types.
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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.