Bevacizumab plus 5-fluorouracil induce growth suppression in the CWR-22 and CWR-22R prostate cancer xenografts

Huynh, Hung

doi:10.1158/1535-7163.mct-07-0071

Cited by 10 publications

(7 citation statements)

References 37 publications

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“…These indicate that bevacizumab works well in the 2 SCC models. Moreover, the results are consistent with those obtained in previous studies with bevacizumab with 5-FU, carboplatin, and radiation in the treatment of colon, lung, breast, and prostate cancer in humans or nude mice [32,33,34]. Thus, we can use the models to investigate the underlying mechanism involved.…”

Section: Discussionsupporting

confidence: 89%

Beyond Antiangiogenesis: Intratumorally Injected Bevacizumab Plays a Cisplatin-Sensitizing Role in Squamous Cell Carcinomas in Mice

Wang

Dong

Bi³

et al. 2011

Chemotherapy

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Background: The anticancer mechanism of bevacizumab beyond antiangiogenesis remains unclear. Here, we investigated whether intratumorally injected bevacizumab could serve as an effective cisplatin sensitizer in squamous cell carcinoma (SCC) in vivo. Methods: Hela and SCC-VII experimental SCC models were established to investigate the anticancer effect of bevacizumab plus cisplatin and the underlying mechanism using immunostaining, TUNEL, and Western blot assays. Results: Bevacizumab-cisplatin therapy markedly inhibited tumor growth and significantly increased survival in both Hela- and SCC-VII-bearing mice compared with single-agent treatments and the untreated control, respectively. Immunostaining of CD34 showed that intratumorally injected bevacizumab significantly reduced microvessel density in bevacizumab-cisplatin and bevacizumab-alone groups of Hela xenografts. TUNEL assay showed that bevacizumab-cisplatin significantly promoted tumor cell apoptosis compared with single-agent treatments and untreated controls in these 2 models. Western blot showed that upregulation of cleaved caspase-3 and downregulation of Bcl-2 and p-Erk expressions are part of the molecular mechanisms beyond angiogenesis which contribute to the cooperative effect of bevacizumab plus cisplatin in the 2 SCC models. Conclusions: Bevacizumab functions not only as an angiogenesis inhibitor but also as a chemosensitizer which enhances the cytotoxicity of cisplatin and promotes apoptosis of SCC cells.

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Section: Discussionsupporting

confidence: 89%

Beyond Antiangiogenesis: Intratumorally Injected Bevacizumab Plays a Cisplatin-Sensitizing Role in Squamous Cell Carcinomas in Mice

Wang

Dong

Bi³

et al. 2011

Chemotherapy

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“…A perfect example of a similar phenomenon is that, in colon cancer, the addition of bevacizumab to cytotoxic chemotherapy improved overall survival in metastatic disease, but not in the adjuvant setting [22, 23]. Moreover, in a preclinical model, bevacizumab was found to be less active against CRPC than hormone-sensitive prostate cancer [24]. …”

Section: Discussionmentioning

confidence: 99%

Pilot Phase II Trial of Bevacizumab Monotherapy in Nonmetastatic Castrate-Resistant Prostate Cancer

et al. 2012

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Introduction/Background. Nonmetastatic castrate resistant prostate cancer (CRPC) is a challenging disease state. The objective of this study was to evaluate the efficacy and tolerability of bevacizumab in nonmetastatic CRPC patients. Patients. Patients with prostate cancer who developed PSA recurrence after local therapy were included if they had absence of bone or visceral metastases and PSA progression despite androgen deprivation therapy. Methods. Bevacizumab 10 mg/kg intravenously was administered every 14 days until PSA progression, development of metastasis, or unacceptable toxicity. Results. 15 patients were enrolled and treated with bevacizumab for a median duration of 3.1 months. Median baseline PSA was 27 ng/mL, and seven patients had Gleason Score ≥8. Five patients had declined in PSA during the treatment. Median PSA doubling time was prolonged from 4.7 months pretreatment to 6.5 months. Median time to PSA progression and new metastasis were 2.8 and 7.9 months, respectively. There were three grade 3 adverse events (one proteinuria and two hypertension) and one pulmonary embolism. There was no treatment-related mortality. Conclusion. Bevacizumab therapy had minimal impact on the disease course of nonmetastatic CRPC, and investigation of novel strategies is needed.

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“…The "normalization" of tumor vessels, accompanied by pericyte recruitment, improves drug delivery into tumors (6,7). This rationale provides a basis for the combined use of antiangiogenic drugs with radiation therapy or chemotherapy (7,32). In this study, we added COMP-Ang1, a more potent Ang1 variant (20,22), to chemotherapy with 5-FU in LLC tumors.…”

Section: Discussionmentioning

confidence: 99%

COMP-Ang1 Potentiates the Antitumor Activity of 5-Fluorouracil by Improving Tissue Perfusion in Murine Lewis Lung Carcinoma

Hwang

Lee

Kim

et al. 2009

Molecular Cancer Research

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Bevacizumab plus 5-fluorouracil induce growth suppression in the CWR-22 and CWR-22R prostate cancer xenografts

Cited by 10 publications

References 37 publications

Beyond Antiangiogenesis: Intratumorally Injected Bevacizumab Plays a Cisplatin-Sensitizing Role in Squamous Cell Carcinomas in Mice

Beyond Antiangiogenesis: Intratumorally Injected Bevacizumab Plays a Cisplatin-Sensitizing Role in Squamous Cell Carcinomas in Mice

Pilot Phase II Trial of Bevacizumab Monotherapy in Nonmetastatic Castrate-Resistant Prostate Cancer

COMP-Ang1 Potentiates the Antitumor Activity of 5-Fluorouracil by Improving Tissue Perfusion in Murine Lewis Lung Carcinoma

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