title: Alterations of tumor suppressor genes (Rb, p16, p27 and p53) and an increased FDG uptake in lung cancer.
abstract: OBJECTIVE
  The FDG uptake in lung cancer is considered to reflect the degree of malignancy, while alterations of some tumor suppressor genes are considered to be related to the malignant biological behavior of tumors. The aim of this study is to examine the relationship between FDG-PET and alterations in the tumor suppression genes of lung cancer.
  
  
  METHODS
  We examined 28 patients with primary lung cancer who underwent FDG-PET before surgery consisting of 17 patients with adenocarcinoma, 10 with squamous cell carcinoma and 1 with large cell carcinoma. The FDG-PET findings were evaluated based on the standardized uptake value (SUV). Alterations in the tumor suppressor genes, Rb, p16, p27 and p53, were evaluated immunohistochemically.
  
  
  RESULTS
  The FDG uptake in lung cancer with alteration in each tumor suppressor gene tended to be higher than in those genes without alterations, although the differences were not significant. In 15 tumors with alterations in either tumor suppressor genes, the FDG uptake was 6.83 +/- 3.21. On the other hand, the mean FDG uptake was 1.95 in 2 tumors without alterations in any genes. The difference in the FDG uptake between the 2 groups was statistically significant (p < 0.001).
  
  
  CONCLUSIONS
  In conclusion, the presence of abnormalities in the tumor suppressor genes, which results in an accelerated cell proliferation, is thus considered to increase the FDG uptake in lung cancer.
authors.affiliation: Department of Clinical Radiology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. msasaki@radiol.med.kyushu-u.ac.jp
authors.forename: Masayuki
authors.initials: M
authors.lastname: Sasaki
authors.forename: Kenji
authors.initials: K
authors.lastname: Sugio
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Kuwabara
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Koga
authors.forename: Makoto
authors.initials: M
authors.lastname: Nakagawa
authors.forename: Tao
authors.initials: T
authors.lastname: Chen
authors.forename: Koichiro
authors.initials: K
authors.lastname: Kaneko
authors.forename: Kazutaka
authors.initials: K
authors.lastname: Hayashi
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Shioyama
authors.forename: Shuji
authors.initials: S
authors.lastname: Sakai
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Honda
mesh_terms: D000328:Adult; D000368:Aged; D002277:Carcinoma / Q000000981:diagnostic imaging / Q000378:metabolism; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000378:metabolism; D005260:Female; D019788:Fluorodeoxyglucose F18 / Q000493:pharmacokinetics*; D015972:Gene Expression Regulation, Neoplastic; D016147:Genes, Tumor Suppressor; D006801:Humans; D008175:Lung Neoplasms / Q000000981:diagnostic imaging* / Q000378:metabolism*; D008297:Male; D008840:Microfilament Proteins / Q000378:metabolism; D008875:Middle Aged; D009124:Muscle Proteins; D019275:Radiopharmaceuticals / Q000493:pharmacokinetics; D016160:Retinoblastoma Protein / Q000378:metabolism; D014055:Tomography, Emission-Computed / Q000379:methods*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D025521:Tumor Suppressor Proteins / Q000378:metabolism*
chemical_list: D019941:Cyclin-Dependent Kinase Inhibitor p16; D008840:Microfilament Proteins; D009124:Muscle Proteins; D019275:Radiopharmaceuticals; D016160:Retinoblastoma Protein; C058992:Tagln protein, mouse; D016159:Tumor Suppressor Protein p53; D025521:Tumor Suppressor Proteins; D019788:Fluorodeoxyglucose F18