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Research Paper
Chronic Alcohol Consumption Stimulates VEGF Expression, Tumor Angiogenesis and Progression of Melanoma in Mice
Wei Tan, Amelia P. Bailey, Megan Shparago, Brandi Busby, Jordan Covington, James W. Johnson, Emily Young and Jian-Wei Gu
volume 6 | issue 8
August 2007Pages: 1211 - 1217
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The mechanisms of alcohol-induced cancer in humans are unclear. We used the immunocompetent mice implanted with B16F10 cells to evaluate the effects of physiologically relevant EtOH intake on tumor growth and angiogenesis of melanoma. 6-wk-old male mice (C57BL/6J) were given 1% EtOH in drinking water for 12-hrs during the night which was then replaced with regular water during the remaining 12-hrs each day for 4 wks (n=10). The control mice received regular drinking water only. In the 2nd wk, all mice were inoculated subcutaneously on the right proximal dorsal with ~5×105 B16F10 cells. In the end, the tumors were isolated for measuring tumor size, average microvascular density (AMVD) using CD31 immunohistochemistry, and the expression of VEGF and its receptor (Flt-1) using Northern blot, ELISA, and immunohistochemistry. EtOH intake caused a 2.16-fold increase in tumor weight over the control (4.81±0.39 vs. 2.23±0.48 g; n=10; P=0.003), a 2.02-fold increase in AMVD (60.63±5.56 vs. 30.01±7.41/mm2; P=0.0014), and a significant increase in VEGF mRNA and protein expression plus Flt-1 protein levels in melanoma compared to the control group (P<0.01). These results suggest that progression of melanoma growth and angiogenesis may be mediated by up-regulation of VEGF and Flt-1, especially under the influence of EtOH.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.




