Neovascularisation of the meniscus with angiogenin. An experimental study in rabbits

King, TV; Bl, Vallee

doi:10.1302/0301-620x.73b4.1712788

Cited by 78 publications

(56 citation statements)

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“…In nonneoplastic conditions, angiogenin is a component of the intercellular matrix encircling endothelium, fibroblasts, and smooth muscle as well as the internal elastic membrane of arterioles and capillaries (6). It induces neovascularization using the chick chorioallantoic membrane, meniscus, rat cremaster muscle, and rabbit cornea models (27,37,38). Angiogenin expression is regulated by the Akt/ phosphatidylinositol 3-kinase pathway (9,39).…”

Section: Discussionmentioning

confidence: 99%

Elevated Expression of Angiogenin in Prostate Cancer and Its Precursors

Katona¹,

Neubauer

Iversen

et al. 2005

Clinical Cancer Research

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Purpose: Angiogenin is a polypeptide involved in the formation and establishment of new blood vessels necessary for growth and metastasis of numerous malignant neoplasms, including prostatic adenocarcinoma. Antiangiogenin therapy inhibits the establishment, growth, and metastasis of prostatic adenocarcinoma in animal studies. In this study, we have investigated the expression of angiogenin in prostatic adenocarcinoma, high-grade prostatic intraepithelial neoplasia, and adjacent benign prostatic epithelium in a large cohort of prostatectomy specimens. Methods: We have studied the expression of angiogenin by immunohistochemistry in prostatic adenocarcinoma, high-grade prostatic intraepithelial neoplasia, and adjacent benign prostatic tissue in 107 human total prostatectomy specimens. Results: The percentage of cells staining positively for angiogenin in benign prostatic glandular epithelium (mean = 17%) was significantly less than for high-grade prostatic intraepithelial neoplasia (mean = 58%, P < 0.001) and prostatic adenocarcinoma (mean = 60%, P < 0.001).Compared with adjacent benign prostatic epithelium, the staining intensity was significantly greater in high-grade prostatic intraepithelial neoplasia (P < 0.001) and prostatic adenocarcinoma (P < 0.001). Furthermore, staining intensity has significantly stronger in prostatic adenocarcinoma versus high-grade prostatic intraepithelial neoplasia (P = 0.0023). However, there was no correlation of angiogenin expression with various clinical and pathologic variables examined, including age at surgery, Gleason scores, pathologic stage, tumor extent, angiolymphatic invasion, extraprostatic extension, seminal vesical invasion, lymph node metastasis, surgical margin status, presence of prostatic intraepithelial neoplasia, and perineural invasion. Conclusion: Angiogenin expression in prostatic tissue increases as prostatic epithelial cells evolve from a benign to an invasive phenotype. The increasing expression of prostatic adenocarcinoma in the progression from benign prostate to high-grade prostatic intraepithelial neoplasia and ultimately to prostatic adenocarcinoma are consistent with previous studies showing the influential role that angiogenin plays in the growth, invasion, and metastasis of prostatic adenocarcinoma and many other malignant tumors.

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Section: Discussionmentioning

confidence: 99%

Elevated Expression of Angiogenin in Prostate Cancer and Its Precursors

Katona¹,

Neubauer

Iversen

et al. 2005

Clinical Cancer Research

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“…In the absence of bleeding, a different mechanism of repair may be at work (King and Vallee 1991). Clustered chondrocytes have been found near the margin of an incision in the rabbit meniscus because of an expansion of the synovial margin.…”

Section: Discussionmentioning

confidence: 99%

Meniscal repair by synovial flap transfer: Healing of the avascular zone in rabbits

Cisa

Basora

Madamas

et al. 1995

Acta Orthopaedica Scandinavica

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“…6 One of these mediators, angiogenin, is a secreted 14.1-kDa heparin-binding protein 7 that induces neovascularization in the chick chorioallantoic membrane and rabbit cornea 8 and meniscus. 9 It also stimulates the proliferation of endothelial cells in culture 10 and promotes the adhesion of both endothelial 11 and tumor 7 cells in vitro. Using antagonists of its activities, we have previously reported that angiogenin plays a crucial role in the subcutaneous (s.c.) growth of human colon, lung and fibrosarcoma tumors in athymic mice, presumably acting at an early stage of tumor development.…”

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confidence: 99%

Inhibition of prostate carcinoma establishment and metastatic growth in mice by an antiangiogenin monoclonal antibody

Olson

Byers

Key³

et al. 2002

Intl Journal of Cancer

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A neutralizing monoclonal antibody (MAb) 26-2F to human angiogenin, a potent inducer of neovascularization, has been shown previously to prevent or delay the appearance of angiogenin-secreting human colon, fibrosarcoma and lung tumor cell xenografts implanted subcutaneously (s.c.) into athymic mice. In an analogous model system, we report here that the antibody also prevents the establishment of PC-3 androgen-independent human prostate cancer tumors in, on average, 40% of treated mice (p < 0.0001, survivor analysis). Intriguingly, combining MAb 26-2F together with cisplatin and suramin, 2 therapeutic agents that together showed little antitumor activity in the aforementioned model, resulted in an even greater degree of protection (71% protected, p ‫؍‬ 0.009 compared to antibody treatment alone). This protective effect persisted several weeks after cessation of treatment. Additionally, prophylactic systemic administration of MAb 26-2F dramatically reduced by 50% the formation of spontaneous regional metastasis originating from primary growth in the prostate gland of PC-3M cells, highly metastatic variants of PC-3. Protection from metastasis was still significant when treatment with MAb 26-2F was delayed until after the primary tumor was well established. The antibody is not directly cytotoxic to either cell type, both of which secrete angiogenin in vitro and when growing as tumors in vivo, but changes the pattern of vascularity in primary tumors growing orthotopically. These findings, together with the observation that angiogenin protein and mRNA are apparently overexpressed in cancerous vs. normal human prostate tissues, demonstrate that angiogenin antagonism represents a promising new approach for preventing progression and metastasis of clinical prostate cancer.

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Neovascularisation of the meniscus with angiogenin. An experimental study in rabbits

Cited by 78 publications

References 0 publications

Elevated Expression of Angiogenin in Prostate Cancer and Its Precursors

Elevated Expression of Angiogenin in Prostate Cancer and Its Precursors

Meniscal repair by synovial flap transfer: Healing of the avascular zone in rabbits

Inhibition of prostate carcinoma establishment and metastatic growth in mice by an antiangiogenin monoclonal antibody

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