caa a22 4500 445335386 CHVBK 20180317142753.0 cr unu---uuuuu 170323e20111001xx s 000 0 eng 10.1245/s10434-011-1621-7 doi (NATIONALLICENCE)springer-10.1245/s10434-011-1621-7 EGFR and p53 Status of Pulmonary Pleomorphic Carcinoma: Implications for EGFR Tyrosine Kinase Inhibitors Therapy of an Aggressive Lung Malignancy [Elektronische Daten] [Yih-Leong Chang, Chen-Tu Wu, Jin-Yuan Shih, Yung-Chie Lee] Background: Pleomorphic carcinomas of the lung are uncommon malignant tumors composed of carcinomatous and sarcomatous components and are distinguished from other non-small-cell lung carcinomas by a more aggressive clinical course with early distant metastases and far worse survival. Epidermal growth factor receptor (EGFR) and p53 are common genes involved in the pathogenesis of non-small-cell lung carcinomas, but their roles in pleomorphic carcinomas are unclear. The potential clinical activity of EGFR-targeted therapy is also unknown. Methods: A total of 42 pleomorphic carcinomas were identified to investigate somatic mutations of EGFR and p53. Genomic DNA was extracted from microdissected cells of paraffin-embedded tumor tissues. Somatic mutations in EGFR (exons 18-21) and p53 (exons 5-8) were examined. Results: EGFR mutations were detected in 10 of 42 cases. Five of these patients had point mutations in exon 21 majorly with L858R; this mutation was found in both adenocarcinomatous and sarcomatous components in 1 case. The other 5 cases harbored 4 deletions and 1 mutation in exon 19. p53 mutations were found in 12 patients. Notably, identical mutation was observed in carcinomatous and sarcomatous components in 3 patients, and this finding strongly supported the theory of monoclonal histogenesis. Conclusions: The occurrence (23.8%) of EGFR mutations, including the exons 19 and 21 mutations observed frequently in our series, suggests that the patients with inoperable pleomorphic carcinomas are likely to benefit from treatment with EGFR tyrosine kinase inhibitors. Society of Surgical Oncology, 2011 Chang Yih-Leong Department of Pathology, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan aut Wu Chen-Tu Department of Pathology, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan aut Shih Jin-Yuan Department of Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan aut Lee Yung-Chie Department of Surgery, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan aut Annals of Surgical Oncology Springer-Verlag 18/10(2011-10-01), 2952-2960 1068-9265 18:10<2952 2011 18 10434 https://doi.org/10.1245/s10434-011-1621-7 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1245/s10434-011-1621-7 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Chang Yih-Leong Department of Pathology, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan aut NATIONALLICENCE 700 1- Wu Chen-Tu Department of Pathology, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan aut NATIONALLICENCE 700 1- Shih Jin-Yuan Department of Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan aut NATIONALLICENCE 700 1- Lee Yung-Chie Department of Surgery, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan aut NATIONALLICENCE 773 0- Annals of Surgical Oncology Springer-Verlag 18/10(2011-10-01), 2952-2960 1068-9265 18:10<2952 2011 18 10434 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer