PMID- 18632807
OWN - NLM
STAT- MEDLINE
DCOM- 20081014
LR  - 20181201
IS  - 0161-5505 (Print)
IS  - 0161-5505 (Linking)
VI  - 49
IP  - 8
DP  - 2008 Aug
TI  - Colorectal tumor cells treated with 5-FU, oxaliplatin, irinotecan, and cetuximab 
      exhibit changes in 18F-FDG incorporation corresponding to hexokinase activity and 
      glucose transport.
PG  - 1386-94
LID - 10.2967/jnumed.107.047886 [doi]
AB  - The purpose of this study was to determine therapy-induced changes in 18F-FDG 
      incorporation at the colorectal tumor cell level in response to conventional and 
      novel chemotherapy agents and examine how these changes relate to factors 
      involved in 18F-FDG incorporation. METHODS: SW620 cells were treated with 
      inhibitory concentration of 50% (IC50) doses (determined by MTT) of 
      5-fluorouracil (5-FU), oxaliplatin, and irinotecan; HCT-8 cells were treated with 
      IC50 doses of irinotecan, cetuximab, and irinotecan plus cetuximab. 18F-FDG 
      incorporation, glucose transport, hexokinase (HK) activity, adenosine 
      triphosphate (ATP) content, annexin V binding, and cell cycle distribution were 
      determined after 24-, 48-, and 72-h treatments. Eight-hour treatments with and 
      without subsequent incubation in drug-free medium were also examined. A 
      clonogenic assay was used to determine the tumor-forming ability of treated 
      cells. RESULTS: Apoptosis was evident in SW620 cells, especially after treatment 
      with irinotecan and 5-FU. 18F-FDG incorporation was increased in SW620 cells 
      after 24- or 48-h treatments with some agents and in HCT-8 cells after irinotecan 
      treatment but was decreased in all 72-h treatments or cell-line combinations 
      including cetuximab. Treatment of SW620 cells for 8 h followed by 64 h in 
      drug-free medium also resulted in decreased 18F-FDG incorporation. Decreased 
      18F-FDG incorporation broadly corresponded to glucose transport in HCT-8 cells 
      and to HK activity in SW620 cells. Inhibition of glucose transport decreased 
      18F-FDG incorporation into HCT-8 but not into SW620 cells. ATP levels were 
      decreased by oxaliplatin treatment and increased at 48 or 72 h after irinotecan 
      treatment. CONCLUSION: 18F-FDG incorporation is modulated by therapy-induced 
      changes in both glucose transport and HK activity depending on the tumor cell. 
      Colorectal cells treated with IC50 doses of cetuximab also exhibit decreased 
      18F-FDG.
FAU - Sharma, Rituka I
AU  - Sharma RI
AD  - School of Medical Sciences (Biomedical Physics), University of Aberdeen, 
      Foresterhill, Aberdeen, United Kingdom.
FAU - Smith, Tim A D
AU  - Smith TA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080716
PL  - United States
TA  - J Nucl Med
JT  - Journal of nuclear medicine : official publication, Society of Nuclear Medicine
JID - 0217410
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Organoplatinum Compounds)
RN  - 0 (Radiopharmaceuticals)
RN  - 04ZR38536J (Oxaliplatin)
RN  - 0Z5B2CJX4D (Fluorodeoxyglucose F18)
RN  - 7673326042 (Irinotecan)
RN  - EC 2.7.1.1 (Hexokinase)
RN  - IY9XDZ35W2 (Glucose)
RN  - PQX0D8J21J (Cetuximab)
RN  - U3P01618RT (Fluorouracil)
RN  - XT3Z54Z28A (Camptothecin)
SB  - IM
MH  - Antibodies, Monoclonal/pharmacology
MH  - Antibodies, Monoclonal, Humanized
MH  - Antineoplastic Agents/*pharmacology
MH  - Biological Transport
MH  - Camptothecin/analogs & derivatives/pharmacology
MH  - Cell Line, Tumor
MH  - Cell Survival/drug effects
MH  - Cetuximab
MH  - Colorectal Neoplasms
MH  - Drug Interactions
MH  - Fluorodeoxyglucose F18/*metabolism
MH  - Fluorouracil/pharmacology
MH  - Glucose/*metabolism
MH  - Hexokinase/*metabolism
MH  - Humans
MH  - Irinotecan
MH  - Organoplatinum Compounds/pharmacology
MH  - Oxaliplatin
MH  - Radiopharmaceuticals/metabolism
EDAT- 2008/07/18 09:00
MHDA- 2008/10/15 09:00
CRDT- 2008/07/18 09:00
PHST- 2008/07/18 09:00 [pubmed]
PHST- 2008/10/15 09:00 [medline]
PHST- 2008/07/18 09:00 [entrez]
AID - jnumed.107.047886 [pii]
AID - 10.2967/jnumed.107.047886 [doi]
PST - ppublish
SO  - J Nucl Med. 2008 Aug;49(8):1386-94. doi: 10.2967/jnumed.107.047886. Epub 2008 Jul 
      16.