ArticlePloS one2012
KIT (CD117) expression in a subset of non-small cell lung carcinoma (NSCLC) patients.
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 9 papers.
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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.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- SLPI⁺ AT2-Like Cells Orchestrate Lung Adenocarcinoma Invasion via Wnt Pathway Activation and Stromal Crosstalk in a Spatially Defined Margin Niche.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Evaluating the Histologic Grade of Digital Squamous Cell Carcinomas in Dogs and Copy Number Variation of KIT Ligand-A Correlation Study.Veterinary sciences · 2023Article
- Potential of Stem Cells and CART as a Potential Polytherapy for Small Cell Lung Cancer.Frontiers in cell and developmental biology · 2021Review
- Targeting c-kit inhibits gefitinib resistant NSCLC cell growth and invasion through attenuations of stemness, EMT and acquired resistance.American journal of cancer research · 2020Article
- Lung Cancers: Molecular Characterization, Clonal Heterogeneity and Evolution, and Cancer Stem Cells.Cancers · 2018Review
- The Mesenchymal State Predicts Poor Disease-Free Survival in Resectable Non-Small Cell Lung Cancer.The Annals of thoracic surgery · 2017Article
- CD117 expression is a predictive marker for poor prognosis in patients with non-small cell lung cancer.Oncology letters · 2017Article
- A breast cancer stem cell niche supported by juxtacrine signalling from monocytes and macrophages.Nature cell biology · 2014Article
- Dynamic Interactions Between Cancer Stem Cells And Their Stromal Partners.Current pathobiology reports · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
We have previously described the expression of CD44, CD90, CD117 and CD133 in NSCLC tumors, adjacent normal lung, and malignant pleural effusions (MPE). Here we describe the unique subset of tumors expressing CD117 (KIT), a potential therapeutic target. Tumor and adjacent tissue were collected from 58 patients. Six MPE were obtained before therapy. Tissue was paraffin embedded for immunofluorescent microscopy, disaggregated and stained for flow cytometry or cryopreserved for later culture. The effect of imatinib on CD117(high)/KIT+ tumors was determined on first passage cells; absolute cell counts and flow cytometry were readouts for drug sensitivity of cell subsets. Primary tumors divided into KIT(neg) and KIT+ by immunofluorescence. By more sensitive flow cytometric analysis, CD117+ cytokeratin+ cells were detected in all tissues (1.1% of cytokeratin+ cells in normal lung, 1.29% in KIT "negative" tumors, 40.7% in KIT+ tumors, and 0.4% in MPE). In KIT+/CD117(high), but not KIT+/CD117(low) tumors, CD117 was overexpressed 3.1-fold compared to normal lung. Primary cultures of CD117(high) tumors were sensitive to imatinib (5 µM) in short term culture. We conclude that NSCLC tumors divide into CD117(low) and CD117(high). Overexpression of CD117 in CD117(high) NSCLC supports exploring KIT as a therapeutic target in this subset of patients.
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