Effect of Alcohol on Tumor Growth of Hepatocellular Carcinoma with Type C Cirrhosis.

Matsuhashi, Tomohiro; Yamada, Nobuo; Shinzawa, Haruhide; Takahashi, Tsuneo

doi:10.2169/internalmedicine.35.443

Cited by 19 publications

(15 citation statements)

References 20 publications

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“…We used a model of chick embryo CAM bearing human fibrosarcoma formed by HT1080 cells and found that the administration of a physiologically relevant dose of EtOH at 0.25 g/kg per day for 9 days caused a 2.2‐fold increase in tumor volume compared with the control group. This finding was consistent with the study in humans reported by Matsuhashi et al,14 who examined the tumor volume doubling times of 35 nodules from 35 patients with hepatocellular carcinoma, as calculated through utrasonographic imaging, and found that tumor volume doubling times were reduced significantly by 50% in alcohol drinkers (80 g EtOH per day) compared with nonalcoholic patients 14. Conversely, Blank and Meadows 25.…”

Section: Discussionsupporting

confidence: 90%

“…It is worth noting that human data also suggest that alcohol consumption accelerates tumor growth. For example, Matsuhashi et al examined the tumor volume doubling times in 35 nodules from 35 patients with hepatocellular carcinoma calculated through utrasonographic imaging and found that tumor volume doubling time was reduced significantly by 50% in alcohol drinkers (80 g ethanol [EtOH] per day) compared with patients who did not drink 14…”

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confidence: 99%

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Ethanol stimulates tumor progression and expression of vascular endothelial growth factor in chick embryos

Bailey

Sartin

et al. 2005

Cancer

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BACKGROUND The mechanisms by which alcohol consumption causes cancer have not been established due to a lack of experimental studies. METHODS A chick embryo chorioallantoic membrane (CAM) model that bore human fibrosarcoma (HT1080) was used to determine whether the administration of physiologically relevant doses of ethanol could stimulate tumor growth, angiogenesis, metastasis, and vascular endothelial growth factor (VEGF) expression in tumors. HT1080 cells were inoculated onto the “upper CAM” on Day 8, saline or ethanol was administrated at a dose of 0.25g/kg per day on the CAM, and the tumors were harvested on Day 17. VEGF mRNA and protein were determined by Northern blot analysis and enzyme‐linked immunosorbent assay. Intratumoral vascular volume density (IVVD) was determined by point counting on periodic acid–Schiff‐stained sections. Intravasation of HT1080 cells was determined using human‐Alu polymerase chain reaction analysis. The effects of ethanol on VEGF expression and cell proliferation were examined in cultured HT1080 cells. RESULTS Ethanol treatment for 9 days caused a 2.2‐fold increase in tumor volume (867 ± 138 mm3 vs. 402 ± 28 mm3), a 2.1‐fold increase in IVVD (0.021 ± 0.004 mm3/mm3 vs. 0.010 mm3/mm3 ± 0.002 mm3/mm3), and a significant increase in VEGF mRNA or protein expression in tumors compared with a group of control embryos (n = 6 embryos; P < 0.01). Ethanol treatment caused an increase > 8‐fold in the intravasated HT1080 cells in the CAM group compared with the control group (n = 6 embryos; P < 0.01). Physiologically relevant levels of ethanol (10 mM and 20 mM) caused a dose‐related increase in VEGF mRNA and protein expression in cultured HT1080 cells. The ethanol–HT1080‐conditioned media increased the proliferation of endothelial cells, but not of HT1080 cells. CONCLUSIONS The findings suggest that the induction of angiogenesis and VEGF expression by ethanol represents an important mechanism of cancer progression associated with alcoholic beverage consumption. Cancer 2005. © 2004 American Cancer Society.

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Section: Discussionsupporting

confidence: 90%

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confidence: 99%

Ethanol stimulates tumor progression and expression of vascular endothelial growth factor in chick embryos

Bailey

Sartin

et al. 2005

Cancer

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“…33 This was the first human study suggesting that alcohol consumption promoted tumor growth. Conversely, Blank and Meadows reported that very high EtOH consumption (10% or 20% EtOH in drinking water) slightly reduced primary tumor size and significantly decreased body weight in melanoma-bearing mice compared with a water-drinking group.…”

Section: Discussionmentioning

confidence: 99%

Chronic alcohol consumption stimulates VEGF expression, Tumor angiogenesis and progression of melanoma in mice

Wang

Bailey²,

Shparago³

et al. 2007

Cancer Biology & Therapy

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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. Six-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 second week, all mice were inoculated subcutaneously on the right proximal dorsal with 5 x 10(5) 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/mm(2); 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 upregulation of VEGF and Flt-1, especially under the influence of EtOH.

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“…8 Previous studies have looked at the correlation between TVDT and HCC differentiation, with conflicting results. 8,11,12,27 Our sample size was too small to draw any conclusion. This was not confirmed by other studies, however.…”

Section: Discussionmentioning

confidence: 89%

Growth Rate of Hepatocellular Carcinoma

Taouli¹,

Goh²,

Lü³

et al. 2005

Journal of Computer Assisted Tomography

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Effect of Alcohol on Tumor Growth of Hepatocellular Carcinoma with Type C Cirrhosis.

Cited by 19 publications

References 20 publications

Ethanol stimulates tumor progression and expression of vascular endothelial growth factor in chick embryos

Ethanol stimulates tumor progression and expression of vascular endothelial growth factor in chick embryos

Chronic alcohol consumption stimulates VEGF expression, Tumor angiogenesis and progression of melanoma in mice

Growth Rate of Hepatocellular Carcinoma

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