ArticleHead & neck2014
HRAS mutations and resistance to the epidermal growth factor receptor tyrosine kinase inhibitor erlotinib in head and neck squamous cell carcinoma cells.
Article in Head & neck, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Survival prediction and analysis of drug-resistance genes in HER2-positive breast cancer.Heliyon · 2024Article
- Switching anti-EGFR antibody re-sensitizes head and neck cancer patient following acquired resistance to cetuximab.Cancer gene therapy · 2024Article
- New insights into RAS in head and neck cancer.Biochimica et biophysica acta. Reviews on cancer · 2023Review
- Article
- Concurrent Inhibition of ERK and Farnesyltransferase Suppresses the Growth of HRAS Mutant Head and Neck Squamous Cell Carcinoma.Molecular cancer therapeutics · 2022Article
- Review
- Targeting K-Ras and apoptosis-driven cellular transformation in cancer.Cell death discovery · 2021Review
- Major Molecular Signaling Pathways in Oral Cancer Associated With Therapeutic Resistance.Frontiers in oral health · 2020Review
- MAP2K1 is a potential therapeutic target in erlotinib resistant head and neck squamous cell carcinoma.Scientific reports · 2019Article
- Targeting the EGFR and Immune Pathways in Squamous Cell Carcinoma of the Head and Neck (SCCHN): Forging a New Alliance.Molecular cancer therapeutics · 2019Review
- Understanding the Mechanisms of Resistance inInternational journal of molecular sciences · 2019Review
- Catalytically Competent Non-transforming H-RASScientific reports · 2019Article
- Review
- HRAS-driven cancer cells are vulnerable to TRPML1 inhibition.EMBO reports · 2019Article
- Nuclear Klf4 accumulation is associated with cetuximab drug-resistance and predicts poor prognosis of nasopharyngeal carcinoma.Journal of translational medicine · 2018Article
- RAS-MAPK Reactivation Facilitates Acquired Resistance inMolecular cancer therapeutics · 2018Article
- Functional Precision Medicine Identifies Novel Druggable Targets and Therapeutic Options in Head and Neck Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- Identification of Key Genes and Pathways in Tongue Squamous Cell Carcinoma Using Bioinformatics Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- Drug-induced RAF dimerization is independent of RAS mutation status and does not lead to universal MEK dependence for cell survival in head and neck cancers.Anti-cancer drugs · 2015Article
- Genomic Correlate of Exceptional Erlotinib Response in Head and Neck Squamous Cell Carcinoma.JAMA oncology · 2015Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundThe purpose of this study was to identify mechanisms of innate resistance to an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, erlotinib, in a panel of head and neck squamous cell carcinoma (HNSCC) cell lines. Specifically, we analyzed the role of HRAS mutations in erlotinib resistance.
methodsErlotinib sensitivity was determined by methyl thiazolyl-tetrazolium (MTT) assays. Molecular signaling pathways and somatic mutations were examined. Changes in sensitivity after modulation of HRAS expression were evaluated.
resultsAll 7 cell lines were wild-type for EGFR and KRAS regardless of erlotinib sensitivity; however, 1 erlotinib-resistant cell line (HN31) harbored an HRAS G12D mutation. Downregulation of HRAS expression by small interfering RNA (siRNA) or short hairpin RNA (shRNA) in HN31 led to increased erlotinib sensitivity in vitro and in vivo. Transfection of activating HRAS-mutant (G12D and G12V) constructs into erlotinib-sensitive cell lines made them more resistant to erlotinib.
conclusionActivating HRAS mutations can confer erlotinib resistance in an HRAS mutant HNSCC cell line.
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Registered trials
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.