PMID- 15492846
OWN - NLM
STAT- MEDLINE
DCOM- 20050531
LR  - 20091119
IS  - 1107-3756 (Print)
IS  - 1107-3756 (Linking)
VI  - 14
IP  - 5
DP  - 2004 Nov
TI  - Co-expression of VEGF, c-Met and HGF/SF in secondary pleural tumors.
PG  - 787-91
AB  - Tumor angiogenesis is influenced by a large number of angiogenic factors among 
      which vascular endothelial growth factor (VEGF) is one of the most important 
      cytokines. Together with hepatocyte growth factor/scatter factor (HGF/SF), c-Met 
      receptor forms a paracrine signaling system. The aim was to study the 
      characterization of the proteins, VEGF, c-Met and HGF/SF with expression pattern 
      and possible co-expression in secondary pleural tumors. Biopsy specimens of the 
      pleural region from 70 patients were chosen and analyzed using 
      immunohistochemistry and in situ hybridization. In the investigated tumors, a 
      marked intracytoplasmic expression, sometimes over-expression of VEGF, c-Met and 
      HGF/SF was detected. This expression was not connected to certain tumor types or 
      a certain histogenetic origin of the tumor. These results indicate a role of 
      these factors in angiogenesis. The synthesis of VEGF and c-Met within the tumor 
      cells was established by in situ hybridization. There was a significant 
      co-expression of VEGF and c-Met/HGF. Thus, autocrine stimulation of these 
      angio-genetically effective systems may be present here. Importantly, the 
      autocrine mechanism between over-expressed c-Met and HGF/SF in malignant tumors, 
      already preferred by other authors, with demonstration of the proteins in the 
      same tumor cells, has to be assumed in the process of pleural metastatic spread. 
      Simultaneous synthesis of these three different proteins is also possible via the 
      plasminogen-urokinase system. VEGF is reported to increase vascular permeability, 
      which in turn causes pleural effusions. The results presented here may be the 
      basis for possible future palliative therapeutical strategies in malignant 
      pleural effusions.
FAU - Naim, Ramin
AU  - Naim R
AD  - Department of Otolaryngology, Head and Neck Surgery, University Hospital 
      Mannheim, D-68135 Mannheim, Germany.
FAU - Tolnay, Edina
AU  - Tolnay E
FAU - Mueller, Klaus-Michael
AU  - Mueller KM
FAU - Kuhnen, Cornelius
AU  - Kuhnen C
LA  - eng
PT  - Journal Article
PL  - Greece
TA  - Int J Mol Med
JT  - International journal of molecular medicine
JID - 9810955
RN  - 0 (HGF protein, human)
RN  - 0 (Mitogens)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 67256-21-7 (Hepatocyte Growth Factor)
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
SB  - IM
MH  - Alternative Splicing
MH  - Gene Expression Regulation, Neoplastic
MH  - Genetic Variation
MH  - Hepatocyte Growth Factor/*genetics
MH  - Humans
MH  - Immunohistochemistry
MH  - In Situ Hybridization
MH  - Mitogens/*genetics
MH  - Neoplasm Metastasis
MH  - Neovascularization, Pathologic
MH  - Pleural Neoplasms/blood supply/genetics/pathology/*secondary
MH  - Proto-Oncogene Proteins c-met/*genetics
MH  - Stromal Cells/pathology
MH  - Vascular Endothelial Growth Factor A/*genetics
EDAT- 2004/10/20 09:00
MHDA- 2005/06/01 09:00
CRDT- 2004/10/20 09:00
PHST- 2004/10/20 09:00 [pubmed]
PHST- 2005/06/01 09:00 [medline]
PHST- 2004/10/20 09:00 [entrez]
PST - ppublish
SO  - Int J Mol Med. 2004 Nov;14(5):787-91.