P2.13: Testing Profiles in NSCLC Biopsy Samples: Multi-Institutional Study in Cordoba

Abstract

Background: ALK activation is generally produced due to formation of fusion genes involving EML4, being described in 3 to 10% of NSCLC. ALK+ tumors present more frequently in young, non smoker patients, with female predominance and are generally adenocarcinomas. ALK alterations have been described in all clinical and pathologic subtypes and these should not be the sole indicators to search for the fusion. This determination describes a subgroup with different biological behavior and effective directed therapy. The ALK Break Apart FISH Probe Kit (Abbott Molecular, Des Plaines, IL) and the VENTANA ALK (D5F3) CDx Assay has become an FDA-approved companion diagnostic for targeted therapy. The FISH assay is fraught with technical challenges; including FISH signal instability and scoring difficulties. Consequently, the assay is prone to false negatives and false positives. Two case reports are presented with different diagnostic results in ALK status by IHC and FISH and diverse clinical responses to directed therapy. Method: ALK IHC testing was performed using the Ventana anti-ALK (D5F3) Rabbit monoclonal antibody (Roche, CE-IVD) used in combination with the OptiView DAB IHC Detection kit and OptiView Amplification Kit as a fully automated IHC assay on the Ventana BenchMark XT automated slide stainer. ALK FISH testing was performed using the Vysis ALK Break Apart Probe kit (2p23/ALK translocation detection, Abbott, CE-IVD). Results: We examined 308 NSCLC cases and compared the FISH results to ALK IHC. Of 8 (3%) cases identified as positive expression, only 6 have ALK rearrangement. Case 1: 54 years old male, 30 pack/year smoker, evaluated in October 2015 presenting fever and cough. CT