Ascites revisited: a novel role for tamoxifen

Donovan, D; Harmey, J.; Redmond, H. P.; Bouchier‐Hayes, David

doi:10.1016/s0748-7983(97)93461-2

Cited by 5 publications

(6 citation statements)

References 2 publications

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“…In our study, there was a 23% reduction in serum VEGF levels after 3 months tamoxifen therapy ( P = 0·051). Our results were similar to the results of Maity's [27] and Donovan's [28] studies. A decrease in serum VEGF levels may be a result of reduced angiogenic activity by tamoxifen treatment.…”

Section: Discussionsupporting

confidence: 92%

“…Donovan et al . [28] reported that tamoxifen reduced preoperative serum VEGF levels by 30% in breast cancer patients. It has been suggested that tamoxifen has additional effects on angiogenesis mediated by reducing levels of potently proangiogenic cytokine VEGF [29].…”

Section: Discussionmentioning

confidence: 99%

“…[27] suggested that tamoxifen induces hypoxia in breast carcinoma cells by inhibiting VEGF expression, resulting in decreased angiogenesis. Donovan et al [28] reported that tamoxifen reduced preoperative serum VEGF levels by 30% in breast cancer patients. It has been suggested that tamoxifen has additional effects on angiogenesis mediated by reducing levels of potently proangiogenic cytokine VEGF [29].…”

Section: Discussionmentioning

confidence: 99%

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Effect of tamoxifen on serum IL-18, vascular endothelial growth factor and nitric oxide activities in breast carcinoma patients

Coşkun¹,

Günel²,

Sancak³

et al. 2004

Clinical and Experimental Immunology

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SUMMARY Vascular endothelial growth factor (VEGF) is a multi‐functional cytokine that has been suggested to be a major angiogenic factor in breast cancer. Nitric oxide (NO) is a potent biological molecule that partipicates in the multi‐step process of carcinogenesis. Interleukin (IL)‐18 has been shown to have potent anti‐tumour effects. In this study, we investigated the effect of tamoxifen therapy on serum VEGF, NO and IL‐18 activity in breast cancer patients. Serum levels of VEGF, nitrate + nitrite and IL‐18 were measured in 34 postmenopausal breast cancer patients before and 3 months after the tamoxifen therapy. Both serum VEGF and IL‐18 levels decreased after tamoxifen therapy (P = 0·051, P < 0·05, respectively). Serum VEGF levels increased in patients with endometrial thickness, while patients without endometrial thickness had a significant reduction in serum VEGF levels after therapy (P < 0·05). Serum nitrate + nitrite levels increased after the therapy, but this was not statistically significant (P > 0·05). A decrease in serum VEGF levels with tamoxifen therapy may be a reflection of reduced angiogenic activity in patients without endometrial thickness. The negative effect of tamoxifen therapy on IL‐18, which is known to have a potent antitumour activity, may be related to the decreased tumour growth by induction of NO and reduction of VEGF activity as a feedback mechanism.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Effect of tamoxifen on serum IL-18, vascular endothelial growth factor and nitric oxide activities in breast carcinoma patients

Coşkun¹,

Günel²,

Sancak³

et al. 2004

Clinical and Experimental Immunology

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“… 18 Furthermore, Donovan et al proposed additional effects of tamoxifen on angiogenesis that occur in conjunction with decreased levels of the proangiogenic cytokine VEGF. 22 In contrast, other authors have reported an agonistic effect of tamoxifen on VEGF expression, despite antagonistic effects on tumor growth. 9 Tamoxifen has been shown to induce angiogenesis by increased expression of VEGF messenger ribonucleic acid in rat uterus.…”

Section: Discussionmentioning

confidence: 90%

Effect of varying doses of tamoxifen on ovarian histopathology, serum VEGF, and endothelin 1 levels in ovarian hyperstimulation syndrome: an experimental study

Pala¹,

Atılgan²,

Ozkan³

et al. 2015

DDDT

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ObjectiveTo examine the effects of low-to-high doses of tamoxifen on ovarian histopathology, serum VEGF, and endothelin 1 levels in ovarian hyperstimulation syndrome (OHSS) in an experimental setting.Materials and methodsA total of 20 female Wistar albino rats, 22 days of age, were randomly divided into four groups. Follicle-stimulating hormone 10 IU was administered subcutaneously in 15 rats on 4 consecutive days, with OHSS induction on day 5 by 30 IU of human chorionic gonadotropin. Group 1 (n=5) comprised 35-day-old control rats, group 2 (n=5) 35-day-old OHSS rats, group 3 (n=5) 27-day-old OHSS rats receiving 1 mg/kg of oral tamoxifen for 7 days, group 4 (n=5) 27-day-old OHSS rats receiving 3 mg/kg of oral tamoxifen for 7 days. All rats were decapitated on day 35. Serum VEGF, endothelin 1, and ovarian follicular reserve were assessed in all rats. Kruskal–Wallis variance analysis and the Mann–Whitney U-test were used for statistical comparisons. A Bonferroni correction was performed to control the inflation of significance, with a significance level set at a P-value of less than 0.025.ResultsDespite higher serum VEGF, endothelin 1, follicular reserve, and angiogenesis and fibrosis of the corpus luteum in the OHSS group compared to controls, these differences were not significant (P>0.025, Mann–Whitney U-test). There was a significant reduction in the ovarian follicular reserve in tamoxifen groups compared to controls (P<0.025, Mann–Whitney U-test), while angiogenesis of the corpus luteum, number of atretic follicles, fibrosis, and serum VEGF were significantly higher in rats receiving tamoxifen (P<0.025, Mann–Whitney U-test). Also, significantly lower follicular reserve and fibrosis were observed among rats in the low-dose tamoxifen group in comparison with rats in the high-dose tamoxifen group (P<0.025, Mann–Whitney U-test). No groups had a significant change in endothelin 1 levels (P>0.025, Mann–Whitney U-test).ConclusionTamoxifen 1 g and 3 g resulted in a dose-dependent increase in VEGF and endothelin 1 levels, and ovarian follicle reserves were significantly reduced in our experimental model.

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“…It influences cytokines involved in the regulation of angiogenesis, including IGF [21], TGF‐β[22] and bFGF [23]. It has been demonstrated to reduce serum VEGF in patients with breast [24] and gastric carcinoma [25]. Tamoxifen reduces VEGF‐mediated endothelial cell proliferation and migration in vivo [20].…”

Section: Introductionmentioning

confidence: 99%

Neoadjuvant antiangiogenic therapy with tamoxifen does not impair gastrointestinal anastomotic repair in the rat

et al. 2003

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Ascites revisited: a novel role for tamoxifen

Cited by 5 publications

References 2 publications

Effect of tamoxifen on serum IL-18, vascular endothelial growth factor and nitric oxide activities in breast carcinoma patients

Effect of tamoxifen on serum IL-18, vascular endothelial growth factor and nitric oxide activities in breast carcinoma patients

Effect of varying doses of tamoxifen on ovarian histopathology, serum VEGF, and endothelin 1 levels in ovarian hyperstimulation syndrome: an experimental study

Neoadjuvant antiangiogenic therapy with tamoxifen does not impair gastrointestinal anastomotic repair in the rat

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Ascites revisited: a novel role for tamoxifen

Cited by 5 publications

References 2 publications

Effect of tamoxifen on serum IL-18, vascular endothelial growth factor and nitric oxide activities in breast carcinoma patients

Effect of tamoxifen on serum IL-18, vascular endothelial growth factor and nitric oxide activities in breast carcinoma patients

Effect of varying doses of tamoxifen on ovarian histopathology, serum VEGF, and endothelin 1 levels in ovarian hyperstimulation syndrome: an&nbsp;experimental study

Neoadjuvant antiangiogenic therapy with tamoxifen does not impair gastrointestinal anastomotic repair in the rat

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Effect of varying doses of tamoxifen on ovarian histopathology, serum VEGF, and endothelin 1 levels in ovarian hyperstimulation syndrome: an experimental study