Contribution of FDG PET/CT for the prediction of EGFR, KRAS Mutation and ALK Rearrangement in Patients with Non-Small Cell Lung Cancer(NSCLC)

Objectives Tumor molecular profile predicts activity of epidermal growth-factor receptor (EGFR) inhibitors in NSCLC. ALK has been identified as a novel molecular target in lung adenocarcinoma. However, tissue availability limit its assessment. We evaluated if FDG PET/CT might help to predict ALK, as well as KRAS and EFGR mutations status in NSCLC.

Methods Retrospectively, 162 NSCLC patients (98 M and 64 F; mean age 61.6±11.3) who underwent PET/CT scan for initial NSCLC staging were evaluated. ALK fluorescence in situ hybridization and EGFR and KRAS mutations were tested. SUVmax of the single hottest tumor lesion, the primary tumor, lymph nodes and distant metastases were calculated with regard to KRAS, ALK, and EGFR status.

Results From 162 patients staged, 17 (10.5%) were ALK+, 31 (19%) KRAS+, 43 (26.5%) EGFR+ and 71 (44%) had wild-type KRAS and EGFR profile (WT). No significant differences were observed in FDG uptake of EGFR+ as compared to WT. Regarding the hottest tumoral lesion, ALK+ (SUVmax 14.5±6.6) or KRAS+ (SUVmax 13.3±5.7) presented higher uptake than EGFR+ (SUVmax 9.4±5.4) and WT patients (SUVmax 10.5±4.5)(ANOVA p<0.001). The same pattern was observed in nodal metastases, ALK+ (SUVmax 7.4±3.2) or KRAS+ (SUVmax 9.2±5.7) presented higher uptake than EGFR+ (SUVmax 5.7±4.1) and WT patients (SUVmax 6.6±4.4) (ANOVA p=0.03), but not in distant metastases although patients with ALK+ presented higher uptake (SUVmax 10.5±3.3) than KRAS+ (SUVmax 8.6±4.9), EGFR+ (SUVmax 7.6±5.3) and WT (SUVmax 7.3±3.5).

Conclusions NSCLC patients with ALK and KRAS mutations presented significantly higher FDG uptake compared to those with EGFR mutation and WT, what suggests more aggressive features of ALK and KRAS mutation.