PMID- 22142567
OWN - NLM
STAT- MEDLINE
DCOM- 20121011
LR  - 20120620
IS  - 1440-1746 (Electronic)
IS  - 0815-9319 (Linking)
VI  - 27
IP  - 7
DP  - 2012 Jul
TI  - Bone marrow cells: Important role on neovascularization of hepatocellular 
      carcinoma.
PG  - 1241-51
LID - 10.1111/j.1440-1746.2011.07044.x [doi]
AB  - BACKGROUND AND AIM: Present antivascular therapies including embolization to 
      hepatocellular carcinoma (HCC) were not as satisfying as expected. The aim was to 
      explore whether or not bone marrow cells (BMCs) played an important role on 
      neovascularization in HCC. METHODS: Bone marrow-GFP(+) orthotropic HCC mice model 
      was used. In controls and HCC mice, the dynamic change of circulating BMCs and 
      serum vascular endothelial growth factor (VEGF), platelet derived growth factor 
      (PDGF) were measured by flow cytometry and enzyme linked immunosorbent assay, 
      respectively. Intrahepatic distribution of BMCs was evaluated using 
      immunofluorescent and realtime polymerase chain reaction protocols. BMCs' 
      intrahepatic differentiation and proportion in vessels was investigated by 
      immunofluorescent methods. Immunohistochemistry and western blotting were 
      performed to examine the expression of adhesion molecule in tumor tissues and 
      tumor free tissues. RESULTS: Compared with controls, the frequency of circulating 
      BMCs and serum VEGF, PDGF were much higher in HCC mice. The number of BMCs and 
      the level of CD133 gene in tumor increased significantly relative to the tumor 
      free zone. Since the early stage of HCC, BMCs have been mobilized, recruited into 
      tumor and incorporated into different types of vessels of the liver. Besides into 
      endothelial cells, BMCs also differentiated into vascular fibroblast and hepatic 
      stellate cells. Moreover with tumor growth, the proportion of BMCs in vessels 
      increased gradually. CONCLUSION: Mobilized BMCs played an important role in tumor 
      vasculogenesis of HCC. Combined blockading of bone marrow-mediated vasculogenesis 
      may improve the efficacy of current therapy to HCC patients.
CI  - (c) 2011 Journal of Gastroenterology and Hepatology Foundation and Blackwell 
      Publishing Asia Pty Ltd.
FAU - Zhu, Haitao
AU  - Zhu H
AD  - Institute of Hepatobiliary Surgery and Department of Hepatobiliary Surgery, the 
      Affiliated DrumTower Hospital, School of Medicine, Nanjing University, NanJing, 
      JiangSu Province, China.
FAU - Shao, Qianwen
AU  - Shao Q
FAU - Sun, Xitai
AU  - Sun X
FAU - Deng, Zhengming
AU  - Deng Z
FAU - Yuan, Xianwen
AU  - Yuan X
FAU - Zhou, Xiang
AU  - Zhou X
FAU - Ding, Yitao
AU  - Ding Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Australia
TA  - J Gastroenterol Hepatol
JT  - Journal of gastroenterology and hepatology
JID - 8607909
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Platelet-Derived Growth Factor)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 0 (vascular endothelial growth factor A, mouse)
SB  - IM
MH  - Animals
MH  - Bone Marrow Cells/*physiology
MH  - Bone Marrow Transplantation
MH  - Carcinoma, Hepatocellular/*blood supply/metabolism/pathology
MH  - Cell Adhesion Molecules/biosynthesis/genetics
MH  - Cell Differentiation/physiology
MH  - Cell Movement/physiology
MH  - Fibroblasts/pathology
MH  - Hepatic Stellate Cells/pathology
MH  - Liver Neoplasms/*blood supply/metabolism/pathology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Neoplasm Transplantation
MH  - Neovascularization, Pathologic/metabolism/*pathology
MH  - Platelet-Derived Growth Factor/metabolism
MH  - Up-Regulation
MH  - Vascular Endothelial Growth Factor A/blood
EDAT- 2011/12/07 06:00
MHDA- 2012/10/12 06:00
CRDT- 2011/12/07 06:00
PHST- 2011/12/07 06:00 [entrez]
PHST- 2011/12/07 06:00 [pubmed]
PHST- 2012/10/12 06:00 [medline]
AID - 10.1111/j.1440-1746.2011.07044.x [doi]
PST - ppublish
SO  - J Gastroenterol Hepatol. 2012 Jul;27(7):1241-51. doi: 
      10.1111/j.1440-1746.2011.07044.x.