Anti-angiogenic Agents in Ovarian Cancer: Dawn of a New Era?

Liu, Joyce F.; Matulonis, Ursula A.

doi:10.1007/s11912-011-0194-8

Cited by 13 publications

(15 citation statements)

References 40 publications

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“…Angiogenesis plays an important role in ovarian physiology and cancer biology, and the exploration of VEGF-targeting agents in this disease has demonstrated clinical benefit (24). However, not all ovarian cancers are responsive to VEGF inhibitors (25), and initially sensitive tumors eventually develop resistance to VEGF inhibitors (26,27).…”

Section: Introductionmentioning

confidence: 99%

Dll4 Blockade in Stromal Cells Mediates Antitumor Effects in Preclinical Models of Ovarian Cancer

et al. 2015

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Section: Introductionmentioning

confidence: 99%

Dll4 Blockade in Stromal Cells Mediates Antitumor Effects in Preclinical Models of Ovarian Cancer

et al. 2015

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“…Angiogenesis is recognized as one of the principal hallmarks of various cancers (3). Indeed, tumor angiogenesis is thought to be a key process that enables ovarian cancer growth as well as dissemination in the peritoneal space, and thus one of the promising options for treating ovarian cancer is considered to be antiangiogenic therapy (4).…”

Section: Introductionmentioning

confidence: 99%

Vasohibin-2 Expressed in Human Serous Ovarian Adenocarcinoma Accelerates Tumor Growth by Promoting Angiogenesis

Takahashi

Koyanagi

Suzuki

et al. 2012

Molecular Cancer Research

106

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Vasohibin-1 (VASH1) is a VEGF-inducible endothelium-derived angiogenesis inhibitor and VASH2 is its homolog. Our previous analysis revealed that VASH1 is expressed in endothelial cells to terminate angiogenesis, whereas VASH2 is expressed in infiltrating mononuclear cells mobilized from bone marrow to promote angiogenesis in a mouse model of hypoxia-induced subcutaneous angiogenesis. To test the possible involvement of VASH2 in the tumor, we examined human ovarian cancer cells for the presence of VASH2. Immunohistochemical analysis revealed that VASH2 protein was preferentially detected in cancer cells of serous ovarian adenocarcinoma. We then used SKOV-3 and DISS, two representative human serous adenocarcinoma cell lines, and examined the role of VASH2 in the tumor. The knockdown of VASH2 showed little effect on the proliferation of cancer cells in vitro but notably inhibited tumor growth, peritoneal dissemination, and tumor angiogenesis in a murine xenograft model. Next, we stably transfected the human VASH2 gene into two types of murine tumor cells, EL-4 and MLTC-1, in which endogenous VASH2 was absent. When either EL-4 or MLTC-1 cells were inoculated into VASH2 (À/À) mice, the VASH2 transfectants formed bigger tumors when compared with the controls, and the tumor microvessel density was significantly increased. VASH2 stimulated the migration of endothelial cells, and its increased expression in cancer cells is related to the decrease of mir-200b. These results indicate that VASH2 expressed in serous ovarian carcinoma cells promoted tumor growth and peritoneal dissemination by promoting angiogenesis. Mol Cancer Res; 10(9); 1135-46. Ó2012 AACR.

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“…Epithelial ovarian cancer is the second leading cause of cancer-related death in women worldwide, and investigation of antiangiogenic agents in this disease has demonstrated antitumor activity both as a monotherapy and in combination with cytotoxic chemotherapy (22). Many questions regarding their use in treatment, their use as single agents or in combination with chemotherapy or which biomarkers predict efficacy remain unanswered (22,23).…”

Section: Discussionmentioning

confidence: 99%

“…Many questions regarding their use in treatment, their use as single agents or in combination with chemotherapy or which biomarkers predict efficacy remain unanswered (22,23).…”

Section: Discussionmentioning

confidence: 99%

Endothelial cell activation and proliferation in ovarian tumors: Two distinct steps as potential markers for antiangiogenic therapy response

2012

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Abstract. Ovarian cancer is the second leading cause of cancer-related death in women worldwide. Since most patients are diagnosed in advanced disease stages, the starting point, early steps and molecular mechanisms of ovarian cancer angiogenesis are still incompletely characterized. Most immunohistochemical studies for assessment of microvessel density (MVD) in ovarian tumors are based on CD31, CD34 and CD105 immunostaining of tumor blood vessels. Yet, the proliferative status of tumor blood vessel endothelial cells has not as yet been used in the assessment of tumor blood vessels. The present study investigated the Ki67 proliferative index of tumor blood vessel endothelial cells highlighted with the CD34 panendothelial marker and the CD105 endothelial marker in ovarian cancers by antigen co-localization with a doublestaining immunohistochemical method. Lack of co-localization of CD105 and Ki67 in all types of ovarian tumors together with the presence of CD34 + /Ki67-positive endothelial cells suggest that endothelial cell activation and proliferation are distinct steps in ovarian tumors. Differences in the proliferation index were observed in endothelial cells from blood vessels of the tumor core and those of the tumor peripheral zones. Potential specific targeting of activated and proliferating tumor blood vessels may provide clues for improving antiangiogenic therapy efficiency.

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Anti-angiogenic Agents in Ovarian Cancer: Dawn of a New Era?

Cited by 13 publications

References 40 publications

Dll4 Blockade in Stromal Cells Mediates Antitumor Effects in Preclinical Models of Ovarian Cancer

Dll4 Blockade in Stromal Cells Mediates Antitumor Effects in Preclinical Models of Ovarian Cancer

Vasohibin-2 Expressed in Human Serous Ovarian Adenocarcinoma Accelerates Tumor Growth by Promoting Angiogenesis

Endothelial cell activation and proliferation in ovarian tumors: Two distinct steps as potential markers for antiangiogenic therapy response

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