PMID- 18363112
OWN - NLM
STAT- MEDLINE
DCOM- 20090303
LR  - 20211020
IS  - 1357-0560 (Print)
IS  - 1357-0560 (Linking)
VI  - 25
IP  - 4
DP  - 2008
TI  - Circulating levels of vascular endothelial growth factor (VEGF), matrix 
      metalloproteinase-3 (MMP-3), and BCL-2 in malignant melanoma.
PG  - 431-6
LID - 10.1007/s12032-008-9058-y [doi]
AB  - Vascular endothelial growth factor (VEGF) is a critical regulator of angiogenesis 
      that stimulates proliferation, migration, and metastasis of melanoma. In 
      literature, all studies concerning influences of matrix metalloproteinases (MMPs) 
      and antiapoptotic proteins on VEGF-induced angiogenesis in melanoma patients have 
      been performed in tissue scale in melanoma. The objective of this study was to 
      determine the value of circulating serum VEGF and its possible mechanisms of 
      angiogenesis by circulating VEGF, MMP-3, and Bcl-2 in patients with melanoma. 
      Fifty-one patients with cutaneous melanoma pathologically verified at different 
      stages, and eighteen healthy controls were investigated. Serum VEGF, MMP-3, and 
      Bcl-2 levels were quantitatively analyzed by ELISA. The serum VEGF (P = 0.034) 
      and Bcl-2 (P = 0.005) levels were significantly higher in patients with melanoma 
      than in the control group. However, there was no significant difference in the 
      serum MMP-3 level between melanoma patients and controls (P = 0.51). The serum 
      levels of VEGF were significantly influenced only by Breslow thickness (P = 
      0.045) and mitosis (0.039) and were not positively correlated with the stage of 
      the disease. Among serum parameters, a significant relationship was found only 
      between serum levels of VEGF and MMP-3 (r = 0.32, P = 0.023). In conclusion, our 
      study demonstrates increased concentrations of VEGF and Bcl-2, but not MMP-3, in 
      serum of melanoma patients regardless of the stage of the disease. VEGF may be a 
      potential endothelial cell growth and survival factor. The mechanism of VEGF 
      regulation of angiogenesis may be in part due to enhanced proliferation and 
      survival of endothelial cells by differential expression of antiapoptotic genes 
      and in part by activation of MMPs.
FAU - Tas, Faruk
AU  - Tas F
AD  - Institute of Oncology, Istanbul University, Capa, 34390, Istanbul, Turkey. 
      faruktas2002@yahoo.com
FAU - Duranyildiz, Derya
AU  - Duranyildiz D
FAU - Oguz, Hilal
AU  - Oguz H
FAU - Camlica, Hakan
AU  - Camlica H
FAU - Yasasever, Vildan
AU  - Yasasever V
FAU - Topuz, Erkan
AU  - Topuz E
LA  - eng
PT  - Journal Article
DEP - 20080325
PL  - United States
TA  - Med Oncol
JT  - Medical oncology (Northwood, London, England)
JID - 9435512
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - EC 3.4.24.17 (Matrix Metalloproteinase 3)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Humans
MH  - Male
MH  - Matrix Metalloproteinase 3/*blood
MH  - Melanoma/*blood/pathology
MH  - Middle Aged
MH  - Proto-Oncogene Proteins c-bcl-2/*blood
MH  - Skin Neoplasms/*blood/pathology
MH  - Vascular Endothelial Growth Factor A/*blood
EDAT- 2008/03/26 09:00
MHDA- 2009/03/04 09:00
CRDT- 2008/03/26 09:00
PHST- 2007/12/26 00:00 [received]
PHST- 2008/03/07 00:00 [accepted]
PHST- 2008/03/26 09:00 [pubmed]
PHST- 2009/03/04 09:00 [medline]
PHST- 2008/03/26 09:00 [entrez]
AID - 10.1007/s12032-008-9058-y [doi]
PST - ppublish
SO  - Med Oncol. 2008;25(4):431-6. doi: 10.1007/s12032-008-9058-y. Epub 2008 Mar 25.