EP1.16-32 Percentage of ALK Rearrangement as a Response Predictor in Non-Small Cell Lung Cancer Treatment

The presence of the Anaplastic Lymphoma Kinase (ALK) fusion oncogene defines a subgroup of non-small cell lung cancer (NSCLC) with clinical and pathological characteristics. It is estimated that 4 to 7% of patients have this rearrangement and it may be detected in the tumour using fluorescence in situ hybridisation (FISH), immunohistochemistry (IHC), and reverse transcription polymerase chain reaction of cDNA. As we walk to a more personalised treatment in NSCLC, we need to search every day for more predictors of response to our newer therapies, such as ALK inhibitors. Our study aimed to correlate the percentage of ALK rearrangement found as a predictor of response in NSCLC ALK-positive treatment. Designed a retrospective study with NSCLC ALK rearrangement patients in a peripheral Hospital from the last six years. Collected demographic data, histology, disease stage, the percentage of ALK rearrangement detected by FISH, lines of treatment, the response rate (RR) evaluated by RECIST 1.1 criteria, the progression-free survival (PFS) and the overall survival (OS) in patients under ALK inhibitors. Results are presented as medians and range for non-normally distributed continuous variables and as number/total for categorical data. Statistical analysis was performed using U-Mann-Whitney test, considering a significance level of 5%. Eight patients diagnosed with NSCLC ALK-positive, male (4/8), aged 64 (28-85) years, most common histology pattern was adenocarcinoma (6/8), followed by adenosquamous (2/8), mainly in stage IV (6/8) and 2 in stage IIIB, where the most frequent distant metastasis was pleural (4/6), followed by bone (2/6) and pulmonary (1/6), none of the patients had brain metastasis. All ALK-positive with % of rearrangement 68 (18-100), PD-L1 positive, but under 50%, in 1/8 patients with no other mutation found. First line therapy was mainly platinum-based chemotherapy (6/8), followed by ALK inhibitor Crizotinib (2/8). As second-line therapy, all used ALK inhibitors, mainly Crizotinib (5/7) and then Ceritinib (2/7). In third line therapy, there was only one patient with Ceritinib. RR of the patients to the first line therapy was progression disease (5/8), partial response (2/8) and stable disease (1/8). RR in the second line therapy was progression disease (4/6), stable disease (1/6) and partial response (1/6). RR in the third line was progression disease. PFS was 5,5 (2-31) months, and when we used ALK inhibitors as first line, the PFS improved to 19 months. OS was 17 (5-53) months, and with ALK inhibitors as first line was 25 months. We found that there is no statistical correlation between the percentage of ALK rearrangement and the PFS, OS or the response rate in our patients, whatever the line of therapy. Nevertheless, there is an improvement in RR, PFS and consequently in OS among patients with ALK inhibitors in first line. Besides our negative results with the the percentage of ALK rearrangement, we found in our sample an improvement in the RR, PFS and OS in patients that made in first line, ALK inhibitors rather than platinum-based chemotherapy, which is compatible with the literature and the use of ALK inhibitors in first line in NSCLC ALK-positive patients.