FDG Uptake in Non–Small Cell Lung Cancer Is Not an Independent Predictor of EGFR or KRAS Mutation Status

A Retrospective Analysis of 206 Patients

Lee, Seok Mo MD^*†; Bae, Sang Kyun MD^*; Jung, Soo Jin MD^‡; Kim, Chun K. MD^†

From the *Department of Nuclear Medicine, Busan Paik Hospital, Inje University College of Medicine, Busan, South Korea; †Division of Nuclear Medicine and Molecular Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; and ‡Department of Pathology, Busan Paik Hospital, Inje University College of Medicine, Busan, South Korea.

Received for publication June 18, 2015; revision accepted July 14, 2015.

Conflicts of interest and sources of funding: Supported by an education and research grant from Inje University (2008).

Correspondence to: Chun K. Kim, MD, Division of Nuclear Medicine and Molecular Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, 75 Francis St, ASB1 L1-037, Boston, MA 02115. E-mail:[email protected].

Clinical Nuclear Medicine40(12):p 950-958, December 2015. |DOI:10.1097/RLU.0000000000000975

Abstract

Purpose

Data in the literature regarding the use of¹⁸F-FDG avidity of non–small cell lung cancer (NSCLC) as an imaging biomarker to predict the status of epidermal growth factor receptor (EGFR) mutation are conflicting. Association between KRAS mutation and FDG avidity of NSCLC on PET/CT is not well known. We assessed whether the EGFR or KRAS mutation status in NSCLC can be predicted by FDG avidity by performing several different subgroup analyses to better compare with various published results.

Patients and Methods

After obtaining institutional review board approval, we enrolled patients (1) who had FDG PET/CT performed for staging of NSCLC, (2) with EGFR and KRAS mutational status of tumor identified, and (3) without uncontrolled diabetes. Univariate and multivariate regression analyses were performed to assess the relationship between the independent clinical variables (sex, age, smoking history, tumor histology, tumor size, stage, and SUV-derived variables) and the EGFR and KRAS mutation status. Separate analyses were performed for patients with adenocarcinomas.

Results

There were 206 patients (age, 33–88 years; 148 male/58 female; 71 ever-smokers/135 never-smokers; 135 adenocarcinoma/71 squamous cell carcinoma; 22 stage I-II/184 stage III-IV; tumor size, 1.2–15.0 cm; SUV_max, 2.9–36.4; EGFR mutations present in 47; KRAS mutations present in 20). In multivariate analysis, sex, smoking history, histology, and tumor size were significantly associated with EGFR mutation but none of the SUV-derived variables was. Likewise, no correlation was found between the SUV-derived variables and KRAS mutation.