Hypoxia-induced angiogenesis and vascular endothelial growth factor secretion in human melanoma

Tumour cells exposed to hypoxia in vitro can show increased expression of several selected genes, including the gene encoding the vascular endothelial growth factor (VEGF), suggesting that hypoxia followed by reoxygenation might promote the malignant progression of tumours. An in vitro/in vivo study...

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Bibliographic Details
Published in:British journal of cancer 1998-03, Vol.77 (6), p.897-902
Main Authors: Rofstad, EK, Danielsen, T
Format: Article
Language:English
Subjects:
Aerobiosis
Animals
Biological and medical sciences
Biomedical and Life Sciences
Biomedicine
Cancer Research
Capillaries - pathology
Cell Hypoxia - physiology
Drug Resistance
Endothelial Growth Factors - biosynthesis
Epidemiology
experimental-oncology
Female
Gene Expression Regulation, Neoplastic
Humans
Kinetics
Lymphokines - biosynthesis
Medical sciences
Melanoma - blood supply
Melanoma - pathology
Melanoma - physiopathology
Mice
Mice, Inbred BALB C
Mice, Nude
Molecular Medicine
Multiple tumors. Solid tumors. Tumors in childhood (general aspects)
Neovascularization, Pathologic - physiopathology
Oncology
Skin - blood supply
Skin Neoplasms - blood supply
Skin Neoplasms - pathology
Skin Neoplasms - physiopathology
Transplantation, Heterologous
Tumor Cells, Cultured
Tumors
Vascular Endothelial Growth Factor A
Vascular Endothelial Growth Factors
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Summary:Tumour cells exposed to hypoxia in vitro can show increased expression of several selected genes, including the gene encoding the vascular endothelial growth factor (VEGF), suggesting that hypoxia followed by reoxygenation might promote the malignant progression of tumours. An in vitro/in vivo study was conducted to investigate whether hypoxia can increase the angiogenic potential of tumour cells through increased VEGF secretion. Four human melanoma cell lines (A-07, D-12, R-18, U-25) were included in the study. Cell cultures were exposed to hypoxia (oxygen concentration
ISSN:0007-0920
1532-1827
DOI:10.1038/bjc.1998.148