PMID- 19225933
OWN - NLM
STAT- MEDLINE
DCOM- 20090428
LR  - 20121115
IS  - 0914-7187 (Print)
IS  - 0914-7187 (Linking)
VI  - 23
IP  - 2
DP  - 2009 Feb
TI  - An experimental study on the antitumor effect of 131I-17-AAG in vitro and in 
      vivo.
PG  - 113-22
LID - 10.1007/s12149-008-0215-3 [doi]
AB  - OBJECTIVE: To observe the antitumor effect of 
      (131)I-17-allylamino-17-demethoxygeldanamycin ((131)I-17-AAG) in vitro/in vivo 
      and explore its antitumor mechanism with a view to its potential therapeutic 
      application. METHODS: (131)I-17-AAG was prepared by the reaction of 17-AAG with 
      Na [(131)I] in the presence of hydrogen peroxide. The effects of (131)17-AAG on 
      cell growth inhibition and cell cycle distribution in vitro were studied in 
      BEL-7402 cells lines. Following BEL-7402 tumor implantation by subcutaneous 
      xenografts into nude mice, the reagents were injected through the tail vein, and 
      the tumor volume was measured and analyzed. At the end of the experiment, tumor 
      specimens were processed for histopathological analysis. Terminal 
      deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) was used to 
      investigate apoptosis. The expression change of Akt2 was tested by Western-blot 
      analysis. RESULTS: Methyl-thiazolyl-tetrazolium assay showed inhibition rates of 
      27.7 +/- 5.3%, 57.3 +/- 4.3%, and 63.7 +/- 3.1%, in Na(131)I group, 17-AAG group, 
      and (131)I-17-AAG group, respectively. The inhibition rate in the (131)I-17-AAG 
      group differed significantly between N(a131)I group and 17-AAG group (F = 229.49, 
      P < 0.001). Following 48 h of treatment with the drug in each group, flow 
      cytometry analysis indicated that detected sub-G peaks (black) were 1.54 +/- 
      0.13%, 5.72 +/- 1.05%, 12.97 +/- 1.44%, and 20.65 +/- 1.36%, in dimethyl 
      sulfoxide (DMSO) group, Na(131)I group, 17-AAG group, and (131)I-17-AAG group, 
      respectively. Following infusion for 32 days, the tumor volumes in the 
      (131)I-17-AAG group were significantly smaller than those in the DMSO group (F = 
      24.18, P < 0.001) or the (131)I group (F = 20.68, P < 0.001). Histopathological 
      and TUNEL analyses showed that (131)I-17-AAG inhibited the proliferation of tumor 
      cells and induced apoptosis. The expression of Akt2 in (131)I-17-AAG was 
      significantly lower than that in the DMSO group or (131)I group. CONCLUSIONS: 
      (131)I-17-AAG can effectively inhibit the growth of BEL-7402 tumor cells in vitro 
      and in vivo. (131)I-17-AAG is a promising agent for the treatment of BEL-7402 
      cell tumor.
FAU - Wenyong, Tu
AU  - Wenyong T
AD  - Nuclear Medicine Technology Institution, School of Clinical Medicine, Southeast 
      University, No. 87 Dingjia Qiao Road 210009 Nanjing, Jiangsu, China.
FAU - Lu, Liu
AU  - Lu L
FAU - Daozhen, Chen
AU  - Daozhen C
FAU - Weidong, Yin
AU  - Weidong Y
FAU - Ying, Huang
AU  - Ying H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090219
PL  - Japan
TA  - Ann Nucl Med
JT  - Annals of nuclear medicine
JID - 8913398
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Benzoquinones)
RN  - 0 (Iodine Radioisotopes)
RN  - 0 (Lactams, Macrocyclic)
RN  - 0 (Radiopharmaceuticals)
RN  - 4GY0AVT3L4 (tanespimycin)
SB  - IM
MH  - Animals
MH  - Antineoplastic Agents/therapeutic use
MH  - Apoptosis/*radiation effects
MH  - Benzoquinones/*therapeutic use
MH  - Carcinoma, Hepatocellular/*pathology/*radiotherapy
MH  - Cell Line, Tumor
MH  - Iodine Radioisotopes/*therapeutic use
MH  - Lactams, Macrocyclic/*therapeutic use
MH  - Male
MH  - Mice
MH  - Mice, Nude
MH  - Radiopharmaceuticals/*therapeutic use
MH  - Treatment Outcome
EDAT- 2009/02/20 09:00
MHDA- 2009/04/29 09:00
CRDT- 2009/02/20 09:00
PHST- 2008/06/06 00:00 [received]
PHST- 2008/09/19 00:00 [accepted]
PHST- 2009/02/20 09:00 [entrez]
PHST- 2009/02/20 09:00 [pubmed]
PHST- 2009/04/29 09:00 [medline]
AID - 10.1007/s12149-008-0215-3 [doi]
PST - ppublish
SO  - Ann Nucl Med. 2009 Feb;23(2):113-22. doi: 10.1007/s12149-008-0215-3. Epub 2009 
      Feb 19.