ArticleFrontiers in oncology2022
Transformation of adenocarcinoma to squamous cell carcinoma as a source of EGFR-TKI resistance: A case report and literature review.
Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Lineage plasticity: a new dilemma in lung cancer treatment.Molecular biology reports · 2026Review
- Evolving treatment strategies for HER2-altered non-small-cell lung cancer: the rise of TKIs and ADCs.Frontiers in oncology · 2026Review
- Case Report: squamous transformation after long-term osimertinib in EGFR-mutant lung adenocarcinoma with retained EGFR/TP53 alterations.Frontiers in oncology · 2026Article
- Histological transformation into pulmonary sarcomatoid carcinoma from lung adenosquamous carcinoma after radical resection of EGFR gene Exon-21 L858R mutation: a case report and literature review.Frontiers in oncology · 2026Article
- Lineage Plasticity and Histologic Transformation in EGFR-TKI Resistant Lung Cancer.International journal of molecular sciences · 2025Review
- Prevalence of Histological Transformation in First-Line Osimertinib Non-Small Cell Lung Cancers: Case Series and Literature Review.International journal of molecular sciences · 2025Review
- Unraveling the immune mechanisms and therapeutic targets in lung adenosquamous transformation.Frontiers in immunology · 2025Review
- Management of oligometastatic and oligoprogressive epidermal growth factor receptor mutated non-small cell lung cancer patients: state of the art of a combined approach.Exploration of targeted anti-tumor therapy · 2024Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In general, non-small cell lung cancer patients with epidermal growth factor receptor (EGFR) mutations respond to tyrosine kinase inhibitors (TKIs). However, most patients experience resistance within 1-2 years after treatment. The histological explanation for the acquired resistance is that malignant transformation occurs during cancer treatment. To date, the transformation from adenocarcinoma to squamous cell carcinoma associated with EGFR-TKI use remains poorly reported. We report a case of stage IV lung adenocarcinoma with EGFR mutations that converted to squamous cell carcinoma due to long-term administration of EGFR-TKIs. This report strengthens histological evolution as a source of acquired drug resistance.
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