title: Metabolic phenotype of stage IV lung adenocarcinoma: relationship with epidermal growth factor receptor mutation.
abstract: OBJECTIVE
  Epidermal growth factor receptor (EGFR) mutation status is important in treatment stratification of stage IV lung adenocarcinoma. We evaluated the relationship between the SUV max measured on PET/CT and EGFR mutations and the value of SUV max in predicting EGFR mutations.
  
  
  METHODS
  Seventy-one stage IV lung adenocarcinoma patients with verified EGFR mutations (48 EGFR mutant, 23 EGFR wild-type) having pretreatment PET/CT were retrospectively reviewed. SUV max values of the primary tumors (n = 71), nodal (n = 246), and distant metastases (n = 618) were compared between EGFR-mutant and EGFR wild-type adenocarcinoma by Mann-Whitney U test. The receiver operating characteristics curve and logistic regression were performed for factors, SUV max, age, sex, and smoking status. The significant predictors were assessed individually and in combination in discriminating EGFR mutation status. Statistical significance was assumed at P < 0.05 RESULTS: The metastases in EGFR-mutant adenocarcinoma had lower SUV max than EGFR wild-type adenocarcinoma (nodal SUV max 3.4 vs 5.5, distant metastasis SUV max 3.4 vs 4.7, respectively; both P < 0.001). No statistical significant difference was observed in the primary tumors SUV max between the 2 groups (SUV max 7.4 vs 8.1, P = 0.311). A receiver operating characteristics-derived SUV max less than or equal to 7.2 in metastasis could separate EGFR-mutant from EGFR wild-type adenocarcinoma (area under the curve, 0.71-0.74; P < 0.05). SUV max was a significant independent predictor, and when combined with age, sex, and smoking status, it is highly predictive of EGFR mutation status (area under the curve, 0.90).
  
  
  CONCLUSIONS
  Low SUV max in the metastasis favors the presence of EGFR mutations in stage IV lung adenocarcinoma, and SUV max is an independent predictor of EGFR mutations.
authors.affiliation: From the Departments of *Diagnostic Radiology, †Clinical Oncology, and ‡Pathology, Queen Mary Hospital, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, China.
authors.forename: Elaine Yuen Phin
authors.initials: EY
authors.lastname: Lee
authors.forename: Pek-Lan
authors.initials: PL
authors.lastname: Khong
authors.forename: Victor Ho Fun
authors.initials: VH
authors.lastname: Lee
authors.forename: Wenshu
authors.initials: W
authors.lastname: Qian
authors.forename: Xue
authors.initials: X
authors.lastname: Yu
authors.forename: Maria Pik
authors.initials: MP
authors.lastname: Wong
mesh_terms: D000230:Adenocarcinoma / Q000000981:diagnostic imaging* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D000077192:Adenocarcinoma of Lung; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D066246:ErbB Receptors / Q000235:genetics* / Q000378:metabolism; D005260:Female; D019788:Fluorodeoxyglucose F18 / Q000493:pharmacokinetics; D006801:Humans; D008175:Lung Neoplasms / Q000000981:diagnostic imaging* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D064847:Multimodal Imaging; D009154:Mutation; D009367:Neoplasm Staging; D010641:Phenotype; D049268:Positron-Emission Tomography; D019275:Radiopharmaceuticals / Q000493:pharmacokinetics; D012189:Retrospective Studies; D014057:Tomography, X-Ray Computed
chemical_list: D019275:Radiopharmaceuticals; D019788:Fluorodeoxyglucose F18; D066246:ErbB Receptors