P60.08 Systemic Immune-Inflammatory Index (SII) as a Biomarker for Metastatic Non-Small Cell Lung Cancer

Abstract

Inflammation contributes to tumor development and progression. Neutrophils promote tumor metastasis by increasing vascular permeability while platelets interact with tumor cells through TGFB and NF-KB pathways promoting growth. Lymphocytes on the other hand are thought to inhibit tumor-cell division. Systemic immune-inflammatory index (SII) has been developed as a simple biomarker in solid tumors to elucidate role of inflammation in malignancy. SII has not been studied in metastatic NSCLC. This study aimed to evaluate prognostic and predictive role of SII in metastatic NSCLC. Data was obtained retrospectively for 236 patients with metastatic NSCLC between 1/1/2015-12/31/2020, who received systemic therapy. SII was calculated at treatment initiation as Platelet count x Neutrophil count/ Lymphocyte count. Overall survival (OS) and Progression Free survival (PFS) were determined as time from start of first line treatment till death and progression or death respectively. Univariate and multivariate Cox regression and Chi-squared analyses were utilized to determine significance of the findings. An optimal SII cut-off value of 1238.5 was determined using a receiver operator curve (ROC). Tobacco use was associated with higher SII (2028 vs 1399 p =0.01). Higher SII was noted for females (1952 vs 1789 p=0.49), age <70 years (1919 vs 1831 p=0.74), African-Americans vs Caucasians (2030 vs 1875 p=0.76), Chronic obstructive pulmonary disease (1987 vs 1807 p=0.49), steroid (2319 vs 1753 p=0.06) and antibiotic use (2310 vs 1791 p=0.14) within one month prior to treatment, and with coronary artery disease (2122 vs 1808 p=0.33); however these differences were not statistically significant. No statistically significant differences were noted based on histology: adenocarcinoma vs Squamous cell carcinoma vs large cell (1675.5 vs 1833.8 vs 1232.8 p=0.9). A low SII (<1238.5) was associated with improved PFS as compared to a high SII (median: 12.7 vs 7.2 months; HR 1.051, 95%CI 1.025-1.073, p<0.0001). Low SII however was not associated with improved OS (14.5 vs 12.7 months; HR 1.014; 95%CI 0.992-1.033), p=0.17). In low SII group, PFS was 11.3 vs 16.7 vs 5.9 months compared to a PFS of 6.9 vs 10.6 vs 5.9 months in high SII group for patients receiving chemotherapy vs targeted therapy vs immunotherapy respectively. SII may be a potential predictive marker for response to treatment. However, it does not appear to be a prognostic biomarker given lack of statistically significant difference in OS. SII is an easy and inexpensive tool to obtain, which makes it an appealing prediction biomarker. Future studies should evaluate the role of SII and its change following treatment, on response to immune checkpoint inhibitors.