PMID- 16204727
OWN - NLM
STAT- MEDLINE
DCOM- 20060110
LR  - 20161124
IS  - 0161-5505 (Print)
IS  - 0161-5505 (Linking)
VI  - 46
IP  - 10
DP  - 2005 Oct
TI  - Different glucose uptake and glycolytic mechanisms between hepatocellular 
      carcinoma and intrahepatic mass-forming cholangiocarcinoma with increased 
      (18)F-FDG uptake.
PG  - 1753-9
AB  - (18)F-FDG uptake in malignant tumors largely depends on the presence of 
      facilitated glucose transporters, especially type 1 (Glut 1) and a rate-limiting 
      glycolytic enzyme, hexokinase (HK) type II. Low expression of Glut 1 was reported 
      in hepatocellular carcinoma (HCC), whereas high expression was found in 
      cholangiocarcinoma. Immunohistochemistry and proteome analysis were performed to 
      obtain a detailed evaluation of the mechanisms involved in glucose uptake and use 
      in these tumors. METHODS: Tumor tissues obtained from both HCC (n = 7) and 
      mass-forming cholangiocarcinoma patients (n = 7) who showed increased (18)F-FDG 
      uptake on PET were used. Immunohistochemistry for Glut 1 and HK I-III was 
      performed in all tumor tissues. To identify proteins that regulate carbohydrate 
      metabolism, a proteome analysis with matrix-assisted laser desorption 
      ionization-time of flight and enzymatic digestion in-gel were performed using 8 
      available tumor samples and 3 normal liver tissues. Of the 8 tumor samples, 4 
      were HCCs; one was an intermediate phenotype HCC, and 3 were cholangiocarcinomas. 
      The spot intensity of the proteins was calculated using proteome data; the 
      tissues then were divided into 2 groups on the basis of the protein expression 
      pattern, because the protein expression pattern of the intermediate-phenotype HCC 
      was close to that of the cholangiocarcinomas. Group A included the HCCs and group 
      B included the intermediate-phenotype HCC as well as the cholangiocarcinomas. 
      RESULTS: Immunoreactivity for Glut 1 was positive in all cholangiocarcinomas, but 
      was negative in all HCCs except the one intermediate phenotype. However, HK II 
      was positive in HCCs but was negative in 6 of the 7 cholangiocarcinomas. A total 
      of 331 protein spots with a P value of <0.05 were identified by proteome 
      analysis. Thirteen of these proteins that regulate carbohydrate metabolism were 
      selected. The pentose phosphate pathway was increased in both groups, but more 
      significantly in group B. Gluconeogenesis enzymes were decreased in both groups, 
      but the tricarboxylic acid cycle-regulating enzyme expression was variable. 
      CONCLUSION: HCCs have different glucose-regulating mechanisms from those of 
      cholangiocarcinomas, even though both tumors showed increased (18)F-FDG uptake on 
      PET scans. Further studies are required with regard to energy metabolism and 
      (18)F-FDG uptake patterns in association with various oncogenic alterations 
      regulating multiple steps of the glycolytic pathways.
FAU - Lee, Jong Doo
AU  - Lee JD
AD  - Division of Nuclear Medicine, Department of Diagnostic Radiology, Yonsei 
      University College of Medicine, Seoul, Korea. jdlee@yumc.yonsei.ac.kr
FAU - Yang, Woo Ick
AU  - Yang WI
FAU - Park, Young Nyun
AU  - Park YN
FAU - Kim, Kyung Sik
AU  - Kim KS
FAU - Choi, Jin Sub
AU  - Choi JS
FAU - Yun, Mijin
AU  - Yun M
FAU - Ko, Dooheun
AU  - Ko D
FAU - Kim, Tae-Sung
AU  - Kim TS
FAU - Cho, Arthur E H
AU  - Cho AE
FAU - Kim, Hye Mi
AU  - Kim HM
FAU - Han, Kwang-Hyub
AU  - Han KH
FAU - Im, Seung-Soon
AU  - Im SS
FAU - Ahn, Yong-Ho
AU  - Ahn YH
FAU - Choi, Chang Woon
AU  - Choi CW
FAU - Park, Jeon Han
AU  - Park JH
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Nucl Med
JT  - Journal of nuclear medicine : official publication, Society of Nuclear Medicine
JID - 0217410
RN  - 0 (Radiopharmaceuticals)
RN  - 0Z5B2CJX4D (Fluorodeoxyglucose F18)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Bile Duct Neoplasms/diagnostic imaging/metabolism
MH  - Bile Ducts, Intrahepatic/diagnostic imaging/metabolism
MH  - Carcinoma, Hepatocellular/*diagnostic imaging/*metabolism
MH  - Cholangiocarcinoma/*diagnostic imaging/*metabolism
MH  - Fluorodeoxyglucose F18/*pharmacokinetics
MH  - Glucose/*pharmacokinetics
MH  - Glycolysis
MH  - Humans
MH  - Positron-Emission Tomography/methods
MH  - Radiopharmaceuticals/pharmacokinetics
MH  - Tumor Cells, Cultured
EDAT- 2005/10/06 09:00
MHDA- 2006/01/13 09:00
CRDT- 2005/10/06 09:00
PHST- 2005/10/06 09:00 [pubmed]
PHST- 2006/01/13 09:00 [medline]
PHST- 2005/10/06 09:00 [entrez]
AID - 46/10/1753 [pii]
PST - ppublish
SO  - J Nucl Med. 2005 Oct;46(10):1753-9.