ArticleFrontiers in endocrinology2022
Case report: TP53 and RB1 loss may facilitate the transformation from lung adenocarcinoma to small cell lung cancer by expressing neuroendocrine markers.
Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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9 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Patients outcomes in lung adenocarcinoma transforming to small-cell lung cancer after tyrosine kinase inhibitor therapy.World journal of surgical oncology · 2025Pooled it
- Reprogramming resistance in advanced lung cancer: epigenetic modulation to restore therapeutic vulnerability.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Durable response to ALK inhibition in low-allele-frequencyFrontiers in oncology · 2026Article
- Prevalence of Histological Transformation in First-Line Osimertinib Non-Small Cell Lung Cancers: Case Series and Literature Review.International journal of molecular sciences · 2025Review
- Mechanisms and Therapeutic Strategies to Overcome Enzalutamide Resistance in Advanced Prostate Cancer.Serican journal of medicine · 2025Article
- Whole Exome Sequencing Study Identifies Distinct Characteristics of Transformed Small Cell Lung Cancer With EGFR Mutation Compared to De Novo Small Cell and Primary Non-Small Cell Lung Cancers.Cancer medicine · 2025Article
- Transformation of lung adenocarcinoma to small cell lung cancer following osimertinib treatment: a case report and literature review.Anti-cancer drugs · 2025Review
- ALK-rearranged and EGFR wild-type lung adenocarcinoma transformed to small cell lung cancer: a case report.Frontiers in oncology · 2024Article
- Tumor grade-associated genomic mutations in Chinese patients with non-small cell lung cancer.Frontiers in oncology · 2023Article
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Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
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Abstract
Introduction: Transformation from lung adenocarcinoma (LUAD) to small cell lung cancer (SCLC) is one of the mechanisms responsible for acquired EGFR-TKIs resistance. Although it rarely happens this event determines a rapid disease deterioration and needs specific treatment. Patient and method: We report a case of 75-year-old LUAD female with a p.L858R mutation in Epidermal Growth Factor Receptor (EGFR) who presented with SCLC transformation after responding to first line osimertinib treatment for only 6 months. To understand the underlying molecular mechanism, we retrospectively sequenced the first (LUAD) and the second (SCLC) biopsy using a 56 multi-gene panel. Immunohistochemistry (IHC) staining and Fluorescence In Situ Hybridization (FISH) was applied to confirm the genetic aberrations identified. Results: EGFR p.E709A and p.L858R, Tumor Protein p53 (TP53) p.A159D and Retinoblastoma 1 (RB1) c.365-1G>A were detected in both the diagnostic LUAD and transformed SCLC samples. A high copy number gain for Proto-Oncogene C-Myc (MYC) and a Phosphoinositide 3-Kinase Alpha (PIK3CA) p.E545K mutation were found in the transformed sample specifically. Strong TP53 staining and negative RB1 staining were observed in both LUAD and SCLC samples, but FISH only identified MYC amplification in SCLC tissue. Conclusion: We consider the combined presence of MYC amplification with mutations in TP53 and RB1 as drivers of SCLC transformation. Our results highlight the need to systematically evaluate TP53 and RB1 status in LUAD patients to offer a different therapeutic strategy.
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