title: Relationship between 18F-fluorodeoxyglucose accumulation and KRAS/BRAF mutations in colorectal cancer.
abstract: OBJECTIVE
  Positron emission tomography (PET) with (18)F-fluorodeoxyglucose (FDG) has been widely used in the management of colorectal cancer (CRC). However, the relationship between FDG accumulation and KRAS/BRAF mutations has not yet been investigated. The purpose of this study was to investigate whether KRAS/BRAF mutations affect FDG accumulation in CRC.
  
  
  METHODS
  Retrospective analysis was conducted in 51 patients with CRC who underwent FDG-PET/computed tomographic (CT) scans for staging before primary tumor resection. The maximum standardized uptake value (SUV(max)) for the primary tumor and the tumor-to-liver ratio (TLR) were calculated from FDG accumulation and compared between KRAS/BRAF mutated and wild-type groups. Expression levels of glucose transporter-1 (GLUT1) and hexokinase type-II (HXK-II) were assessed by immunohistochemical analysis.
  
  
  RESULTS
  Both SUV(max) and TLR were significantly higher in the KRAS/BRAF-mutated group compared with the wild-type group (P = 0.006 and 0.001, respectively). Multivariate analysis indicated that SUV(max) and TLR remained significantly associated with KRAS/BRAF mutations (P = 0.016 and 0.01, respectively). KRAS/BRAF status could be predicted with an accuracy of 75% when a SUV(max) cutoff value of 13 or 14 was used. GLUT1 expression in cancer cells was positively correlated with FDG accumulation and KRAS/BRAF status whereas HXK-II expression was not.
  
  
  CONCLUSIONS
  FDG accumulation was higher in CRC with KRAS/BRAF mutations. FDG-PET/CT scans may be useful for predicting the KRAS/BRAF status of patients with CRC and thus aid in determination of therapeutic strategies for patients with CRC.
authors.affiliation: Department of Surgery, Kyoto University, Kyoto, Japan. kkawada@kuhp.kyoto-u.ac.jp
authors.forename: Kenji
authors.initials: K
authors.lastname: Kawada
authors.forename: Yuji
authors.initials: Y
authors.lastname: Nakamoto
authors.forename: Mayumi
authors.initials: M
authors.lastname: Kawada
authors.forename: Koya
authors.initials: K
authors.lastname: Hida
authors.forename: Takuya
authors.initials: T
authors.lastname: Matsumoto
authors.forename: Teppei
authors.initials: T
authors.lastname: Murakami
authors.forename: Suguru
authors.initials: S
authors.lastname: Hasegawa
authors.forename: Kaori
authors.initials: K
authors.lastname: Togashi
authors.forename: Yoshiharu
authors.initials: Y
authors.lastname: Sakai
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015179:Colorectal Neoplasms / Q000235:genetics* / Q000378:metabolism*; D005260:Female; D019788:Fluorodeoxyglucose F18 / Q000378:metabolism*; D051272:Glucose Transporter Type 1 / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D009154:Mutation; D049268:Positron-Emission Tomography / Q000379:methods; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D048493:Proto-Oncogene Proteins B-raf / Q000235:genetics*; D016283:Proto-Oncogene Proteins p21(ras); D019275:Radiopharmaceuticals / Q000378:metabolism; D018631:ras Proteins / Q000235:genetics*
chemical_list: D051272:Glucose Transporter Type 1; C117307:KRAS protein, human; D011518:Proto-Oncogene Proteins; D019275:Radiopharmaceuticals; D019788:Fluorodeoxyglucose F18; C482119:BRAF protein, human; D048493:Proto-Oncogene Proteins B-raf; D016283:Proto-Oncogene Proteins p21(ras); D018631:ras Proteins