Synergistic effect of retinoids and interferon α on tumor‐induced angiogenesis: Anti‐angiogenic effect on HPV‐harboring tumor‐cell lines

Majewski, S.; Szmurło, A.; Marczak, Maria; Jabłońska, Stefania; Bollag, W.

doi:10.1002/ijc.2910570115

Cited by 108 publications

(46 citation statements)

References 16 publications

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“…Indeed, Majewski et al 51 showed antiangiogenic activity of retinoids in a mouse model of tumorinduced angiogenesis and Pienta et al 52 demonstrated that HPR is a potent inhibitor of prostate cancer and EC growth in vitro and inhibits angiogenesis in the CAM assay.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of neuroblastoma-induced angiogenesis by fenretinide

et al. 2001

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Retinoids are a class of natural or synthetic compounds that participate in the control of cell proliferation, differentiation and fetal development. The synthetic retinoid fenretinide (HPR) inhibits carcinogenesis in various animal models. Retinoids have also been suggested to be effective inhibitors of angiogenesis. The effects of HPR on certain endothelial cell functions were investigated in vitro, and its effects on angiogenesis was studied in vivo, by using the chorioallantoic membrane (CAM) assay. HPR inhibited vascular endothelial growth factor-(VEGF-) and fibroblast growth factor-2-(FGF-2)-induced endothelial cell proliferation without affecting endothelial motility; moreover, HPR inhibited growth factor-induced angiogenesis in the CAM assay. Furthermore, a significant antiangiogenic potential of HPR has also been observed in neuroblastoma (NB) biopsy-induced angiogenesis in vivo. We previously demonstrated that supernatants derived from NB cell lines stimulated endothelial cell proliferation. In the present study, we found that this effect was abolished when NB cells were incubated in the presence of HPR. VEGF-and FGF-2-specific ELISA assays, performed on both NB cells derived from conditioned medium and cellular extracts, indicated no consistent effect of HPR on the level of these angiogenic cytokines. Moreover, RT-PCR analysis of VEGF and FGF-2 gene expression confirmed the above lack of effect. HPR was also able to significantly repress the spontaneous growth of endothelial cells, requiring at least 48 -72 hr of treatment with HPR, followed by a progressive accumulation of cells in G 1 at subsequent time points. Finally, immunohistochemistry experiments performed in the CAM assay demonstrated that endothelial staining of both VEGF receptor 2 and FGF-2 receptor-2 was reduced after implantation of HPR-loaded sponges, as compared to control CAMs. These data suggest that HPR exerts its antiangiogenic activity through both a direct effect on endothelial cell proliferative activity and an inhibitory effect on the responsivity of the endothelial cells to the proliferative stimuli mediated by angiogenic growth factors.

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Section: Discussionmentioning

confidence: 99%

Inhibition of neuroblastoma-induced angiogenesis by fenretinide

et al. 2001

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“…Antiangiogenic effects of IFN (α, β, or γ) have also been observed in different clinical circumstances. 47,48 Quantifying Immune Therapy Benefit…”

Section: Subcutaneous Il-2mentioning

confidence: 99%

Immunotherapy of Metastatic Renal Cell Cancer

Fishman

Seigne

2002

Cancer Control

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“…Initially, the direct cytostatic effect of IFN-a was thought to be the major mechanism by which it inhibits tumor growth (33,34,48); however, subsequent studies revealed that inhibition of angiogenesis and induction of tumor cell apoptosis are other IFN-a mediated antitumor effects (7,10,(49)(50)(51)(52). Our in vitro studies revealed that B16F10 melanoma cells are more sensitive to the cytostatic effects of IFN-a, whereas the CT26 colon carcinoma cells are more sensitive to the proapoptotic properties of rmIFN-a in vitro.…”

Section: Discussionmentioning

confidence: 99%

Administration of IFN-α Enhances the Efficacy of a Granulocyte Macrophage Colony Stimulating Factor–Secreting Tumor Cell Vaccine

Prell

Li²,

Lin³

et al. 2005

Cancer Research

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IFN-A is approved for the treatment of multiple cancers. Its pleiotropic properties include inhibition of proliferation and angiogenesis and induction of apoptosis. Type I IFNs also exert immunomodulatory effects, which make it an appropriate candidate to combine with cancer vaccines. The studies reported herein show that 50% of mice reject established B16 tumors following treatment with the combination of a granulocyte macrophage colony-stimulating factor-secreting tumor cell vaccine (B16.GM) and subclinical doses of recombinant murine IFN-A delivered at the vaccine site. Similarly, 80% of mice treated with the combination reject established B16 tumors when recombinant murine IFN-A is given at the challenge site, suggesting that in the latter case its antiproliferative, proapoptotic, and antiangiogenic properties may be involved in controlling tumor growth. In contrast, fewer than 10% of mice reject the tumors when either one is used as a monotherapy. Furthermore, a 30-fold increase in the frequency of melanoma-associated antigen (Trp-2 and gp100) specific T cells was observed in mice treated with the combination when compared with unvaccinated controls. These data show that IFN-A combined with a granulocyte macrophage colonystimulating factor-secreting tumor cell vaccine significantly enhances vaccine potency and may represent a potential new approach for tumor immunotherapy. (Cancer Res 2005; 65(6): 2449-56)

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Synergistic effect of retinoids and interferon α on tumor‐induced angiogenesis: Anti‐angiogenic effect on HPV‐harboring tumor‐cell lines

Cited by 108 publications

References 16 publications

Inhibition of neuroblastoma-induced angiogenesis by fenretinide

Inhibition of neuroblastoma-induced angiogenesis by fenretinide

Immunotherapy of Metastatic Renal Cell Cancer

Administration of IFN-α Enhances the Efficacy of a Granulocyte Macrophage Colony Stimulating Factor–Secreting Tumor Cell Vaccine

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