Ttf1 Ihc Predicts Egfr Status in Nsclc

Lung cancers are the leading cause of cancer-related mortality in the developed world. In recent decades, great strides have been made in treating this group of diseases, including improved surgical management, increased early detection, and newly available targeted therapies1,2. The epidermal growth factor receptor (egfr) is the most well-characterized biologic target in lung cancer3. Activating mutations in this receptor tyrosine kinase cause constitutive activation of the mitogen-activated protein kinase pathway, driving increased cellular motility, invasiveness, and resistance to apoptosis. Activating EGFR mutations are known to underlie a significant number of adenocarcinomas4, but can also be the drivers behind a smaller number of adenosquamous5 or squamous cell carcinomas harbouring adenocarcinomatous components6. Established clinical risk factors for an egfr-driven lung cancer include female sex and absence of a heavy tobacco-smoking history7. Monoclonal antibodies and small-molecule inhibitors have both been effective in blocking egfr signalling and subsequently retarding tumour growth in lung cancer and other malignancies8. Optimal outcomes are achieved when targeted therapy is delivered selectively to patients with egfr-driven lung cancers1, thus establishing the need to accurately identify lung tumours driven by egfr activation. Recent guidelines on EGFR testing in lung cancers have advocated the use of polymerase chain reaction (pcr)–based testing for all lung tumours with adenocarcinoma-like components (and discretionary testing on additional patients based on the clinical risk factors mentioned earlier)9. Up to 75% of patients with lung cancer are diagnosed with advanced or metastatic disease and therefore do not undergo surgical procedures. The initial, often scanty, tissue samples are the only material available for biomarker testing. In patients with limited or no tumour tissue available for ancillary ABSTRACT