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Transformation to a squamous cell carcinoma phenotype of an EGFR-mutated NSCLC patient after treatment with an EGFR-tyrosine kinase inhibitor
  1. Justine L Kuiper1,
  2. Merle I Ronden1,
  3. Annemarie Becker1,
  4. Daniëlle A M Heideman2,
  5. Peter van Hengel3,
  6. Bauke Ylstra2,
  7. Erik Thunnissen2,
  8. Egbert F Smit1,4
  1. 1Department of Pulmonary Diseases, VU University Medical Center, Amsterdam, The Netherlands
  2. 2Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands
  3. 3Department of Pulmonary Diseases, Flevo Hospital, Almere, The Netherlands
  4. 4Department of Pulmonary Diseases, The Netherlands Cancer Institute, Amsterdam, The Netherlands
  1. Correspondence to Justine L Kuiper, Department of Pulmonary Diseases, VU University Medical Center, P.O. Box 7057, Amsterdam 1007 MB, The Netherlands; jl.kuiper{at}vumc.nl

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Activating mutations in the epidermal growth factor receptor (EGFR) are detected in approximately 10% of Caucasian and up to 50% of Asian patients with non-small cell lung cancer (NSCLC).1 EGFR-tyrosine kinase inhibitors (TKIs) constitute the preferred first-line treatment for these patients. Unfortunately, all patients eventually develop resistance to EGFR-TKI after a median of 13 months.2 Several different resistance mechanisms have been demonstrated in biopsies of recurrent tumours after EGFR-TKI treatment. Among these are the T790M secondary resistance mutation on EGFR exon 20 and amplification of alternative pathways such as hepatocyte growth factor receptor (MET) and human epidermal growth factor receptor 2 (HER2), but also morphological changes with epithelial-to-mesenchymal transition and transformation to a small cell lung cancer (SCLC) phenotype.2

Here we report a case with transformation to a squamous cell carcinoma (SqCC) phenotype. To the best of our knowledge, …

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