Avaliação da mutação de EGFR e da imunoexpressão de ALK e de PD-L1 em Adenocarcinomas de Pulmão

• Ano de defesa: 2018
• Autor(a) principal: Oliveira, Ana Cláudia da Silva Mendes de
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Palavras-chave em Português: Adenocarcinoma; Neoplasias Pulmonares; Biomarcadores Tumorais; Genes erbB-1
• Link de acesso: http://www.repositorio.ufc.br/handle/riufc/39413

Lung cancer is one the most frequent cause of cancer death in Brazil and worldwide. The advent of new drugs directed towards specific molecular alterations, such as anti-tyrosine kinase for EGFR mutation (Epidermal Growth Factor Receptor) and for the rearrangement of the ALK (Anaplastic Lymphoma Kinase) gene and immunotherapy for PD-L1 (Cell Death Ligant 1 Receptor)expression brought an important gain in overall survival and in progression free survival in patients with non-small cell lung cancer (NSCLC) harboring those alterations. The present study aims to investigate the biomarkers EGFR, ALK and PD-L1 and their relationship with demographic data and histologic growth patterns in pulmonary adenocarcinomas. The study consisted in a retrospective analysis involving 173 paraffin-embedded specimens of NSCLC from the registry of the pathology laboratory during 2015 and 2016. ALK and PD-L1 expression in tumor cells were evaluated by immunohistochemical analysis using antibodies D5F3 and SP263, respectively. EGFR mutation status was assessed through sequencing. ALK expression was detected in 10.4% of samples and the population with ALK positivity was, in average, 8.8 years younger than the population not expressing ALK (p=0.0034). 22% of tumors carried mutations in EGFR. The most frequent EGFR mutation was exon 21 L858R point mutation (45.5%) followed by exon 19 deletions (36.3%). Solid predominant subtype was associated with wild-type EGFR status (P=0.047). PD-L1 tumor proportion scores (TPS) of ≥50% was documented in 18.2% of samples. No significant relationships were found between positive PD-L1 expression and driver genes (neither ALK nor EGFR).