Open AccessRole of 18 F‐Fluorodeoxyglucose Positron Emission Tomography in Predicting Epidermal Growth Factor Receptor Mutations in Non‐Small Cell Lung Cancer
Author(s) -
Mak Raymond H.,
Digumarthy Subba R.,
Muzikansky Alona,
Engelman Jeffrey A.,
Shepard JoAnne O.,
Choi Noah C.,
Sequist Lecia V.
Publication year - 2011
Publication title -
the oncologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.176
H-Index - 164
eISSN - 1549-490X
pISSN - 1083-7159
DOI - 10.1634/theoncologist.2010-0300
Subject(s) - medicine , standardized uptake value , epidermal growth factor receptor , positron emission tomography , receiver operating characteristic , confidence interval , nuclear medicine , lung cancer , fluorodeoxyglucose , odds ratio , adenocarcinoma , cancer , oncology , pathology
Purpose. To compare 18 F‐fluorodeoxyglucose positron emission tomography (FDG‐PET) and computed tomography (CT) imaging characteristics in non‐small cell lung cancer (NSCLC) with or without epidermal growth factor receptor ( EGFR ) mutations. Methods. We retrospectively identified NSCLC patients who underwent EGFR mutation testing and pretreatment FDG‐PET and CT scans. The maximum standard uptake value (SUV max ) of the primary tumor and any metastases was measured and normalized to the SUV of blood in the pulmonary artery. We compared normalized SUV max values between EGFR ‐mutant and wild‐type patients and modeled radiographic and clinical predictors of EGFR mutation status. Receiver operator characteristic (ROC) curves were used to identify potential SUV cutoffs predictive of genotype. Results. We included 100 patients (24 EGFR ‐mutant and 76 wild‐type). There was a trend for higher normalized SUV max in the primary tumors among patients with EGFR ‐wild‐type versus mutant (median, 3.4; range, 0.6–12.8; versus median, 2.9; range, 0.4–5.0; p = .09). Normalized SUV max of nodal and distant metastases, and CT characteristics were not associated with genotype. On multivariate analysis, low normalized SUV max of the primary tumor was predictive for EGFR mutation (odds ratio, 0.72; 95% confidence interval, 0.53–0.98; p = .034). ROC curve analyses yielded an area under the curve of 0.62, and identified a potential cutoff of ≥5.0 to distinguish wild‐type from mutant tumors. Conclusions. In this retrospective study, high FDG avidity (normalized SUV max ≥5) correlated with EGFR ‐wild‐type genotype. Although genotyping remains the gold standard, further work to validate FDG‐PET as a surrogate for tumor genotype may provide useful information in patients without available tumor tissue.