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EVALUATION IN A MOUSE PROSTATE CANCER XENOGRAFT MODEL OF THE EFFECTIVENESS OF CYCLOPHOSPHAMIDE METRONOMIC REGIMEN

ABSTRACT: The aim of this study was to evaluate in a mouse prostate cancer xenograft model the effectiveness of cyclophosphamide metronomic regimen, as single agent or in combination with standard docetaxel therapy. We used a human prostate cancer cell line to establish tumours in mice and we treated the animals with the combination of 50 mg/kg of cyclophosphamide (per os) and 30 or 10 mg/kg of docetaxel (intraperitoneally) or with the two drugs alone. We found that metronomic cyclophosphamide alone is as efficient as docetaxel in blocking tumor growth (respectively 18% and 21% of the tumor volume reached by control group in 25 days of treatment). Immunohistochemical analysis on tumours and in vitro proliferation and FACS analyses revealed that cyclophosphamide acts downregulating cell proliferation, both in vitro and in vivo. Through microarray analysis we found the upregulation of p21 that probably together with an action on the micro-environment may explain the induction of apoptosis seen in tumor xenografts. Moreover, we found 107 genes differentially expressed upon treatment with the active metabolite of cyclophosphamide and associated with functions such as cellular movement, growth, and proliferation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE27930 | GEO | 2012/12/30

SECONDARY ACCESSION(S): PRJNA137851

REPOSITORIES: GEO

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EVALUATION IN A MOUSE PROSTATE CANCER XENOGRAFT MODEL OF THE EFFECTIVENESS OF CYCLOPHOSPHAMIDE METRONOMIC REGIMEN

Project description:The aim of this study was to evaluate in a mouse prostate cancer xenograft model the effectiveness of cyclophosphamide metronomic regimen, as single agent or in combination with standard docetaxel therapy. We used a human prostate cancer cell line to establish tumours in mice and we treated the animals with the combination of 50 mg/kg of cyclophosphamide (per os) and 30 or 10 mg/kg of docetaxel (intraperitoneally) or with the two drugs alone. We found that metronomic cyclophosphamide alone is as efficient as docetaxel in blocking tumor growth (respectively 18% and 21% of the tumor volume reached by control group in 25 days of treatment). Immunohistochemical analysis on tumours and in vitro proliferation and FACS analyses revealed that cyclophosphamide acts downregulating cell proliferation, both in vitro and in vivo. Through microarray analysis we found the upregulation of p21 that probably together with an action on the micro-environment may explain the induction of apoptosis seen in tumor xenografts. Moreover, we found 107 genes differentially expressed upon treatment with the active metabolite of cyclophosphamide and associated with functions such as cellular movement, growth, and proliferation. Cells (2 x 10^6) were seeded in T150 flasks and then treated with vehicle (ctrl), with inactive cyclophosphamide (trt) or with 5.5 M-NM-<M of active 4-Hydro peroxy cyclophosphamide (trtA) for 10, 24, and 48 hours.

2012-12-30 | E-GEOD-27930 | biostudies-arrayexpress

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Project description:Cyclophosphamide (CPA) treatment on a six-day repeating metronomic schedule induces a dramatic, innate immune cell-dependent regression of implanted gliomas. However, little is known about the underlying mechanisms of innate immune cell mobilization and recruitment, or about the role of DNA damage and cell stress response pathways in eliciting the anti-tumor immune responses linked to tumor regression. To address these questions, we compared untreated and 6-day metronomic cyclophosphamide-treated human U251 glioblastoma xenografts by human microarray analysis to identify responsive tumor cell-specific factors. Human glioma U251 tumors were implanted sc in scid immunodeficient mice then treated with cyclophosphamide at 140 mg/kg every 6 days. Tumors were collected 6 days after the second cyclophosphamide treatment and also 6 days after the third cyclophosphamide treatment. Tumor RNA was then analyzed on two color Agilent human expression microarrays comparing cyclophosphamide-treated RNA to untreated control tumor RNA.

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