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Microarray analysis of mouse gene expression in metronomic cyclophosphamide-treated human glioma U251 xenografts implanted in scid mice

ABSTRACT: 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 mouse microarray analysis to identify responsive mouse (host) cell-specific factors.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE60866 | GEO | 2015/05/04

SECONDARY ACCESSION(S): PRJNA259777

REPOSITORIES: GEO

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Microarray analysis of human gene expression in metronomic cyclophosphamide-treated human glioma U251 xenografts implanted in scid mice

2015-05-04 | GSE60867 | GEO

Microarray analysis of human gene expression in metronomic cyclophosphamide-treated human glioma U251 xenografts implanted in scid mice

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.

2015-05-04 | E-GEOD-60867 | biostudies-arrayexpress

Microarray analysis of mouse gene expression in metronomic cyclophosphamide-treated human glioma U251 xenografts implanted in scid mice

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 mouse microarray analysis to identify responsive mouse (host) 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 mouse expression microarrays comparing cyclophosphamide-treated RNA to untreated control tumor RNA.

2015-05-04 | E-GEOD-60866 | biostudies-arrayexpress

Microarray analysis of mouse gene expression in metronomic cyclophosphamide-treated rat glioma 9L xenografts implanted in scid mice

2015-05-04 | GSE60864 | GEO

Microarray analysis of mouse gene expression in metronomic cyclophosphamide-treated rat glioma 9L xenografts implanted in scid mice

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 rat 9L gliosarcoma xenografts by mouse microarray analysis to identify responsive mouse (host) cell-specific factors. Rat glioma 9L 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 fourth cyclophosphamide treatment. Tumor RNA was then analyzed on two color Agilent mouse expression microarrays comparing cyclophosphamide-treated RNA to untreated control tumor RNA.

2015-05-04 | E-GEOD-60864 | biostudies-arrayexpress

RNA-seq analysis of immunogenic actions of metronomic cyclophosphamide treatment: dependence of gene responses on tumor model, mouse host, and drug schedule

Project description:RNA-seq analysis was performed using RNA isolated from three tumor models (GL261 glioma, LLC Lewis lung carcinoma, B16F10 melanoma) implanted subcutaneousy in C57BL/6 mice, or in ICR scid mice. Mice were untreated or were treated with cyclophosphamide (CPA) given on a 6-day repeating metronomic schedule (CPA/6d), except as noted. Results from these global transcriptome analysis indicated substantial elevation of basal GL261 immune infiltration and strong activation by CPA/6d treatment of GL261 immune stimulatory pathways and their upstream regulators, but without preferential depletion of negative immune regulators compared to LLC and B16F10 tumors. In LLC tumors, where CPA/6d treatment was found to be anti-angiogenic, CPA/6d suppressed VEGFA target genes and down regulated cell adhesion and leukocyte transendothelial migration genes. In GL261 tumors implanted in adaptive immune-deficient scid mice, where CPA/6d-induced GL261 regression is incomplete and late tumor growth rebound can occur, T cell receptor signaling and certain cytokine-cytokine receptor responses seen in B6 mice were deficient. Extending the CPA treatment interval from 6 to 9 days (CPA/9d) â which results in a strong but transient natural killer cell response followed by early tumor growth rebound â induced fewer cytokines and increased expression of drug metabolism genes. Taken together, these findings elucidate molecular response pathways activated by intermittent metronomic CPA treatment and identify deficiencies that characterize immune-unresponsive tumor models and drug schedules. RNA isolated from various tumor cell lines implanted s.c in C57BL/6 mice or scid mice, untreated or treated with cyclophosphamide (CPA) given on a metronomic schedule, were prepared and used for stranded or unstranded RNA-seq.

2016-08-01 | E-GEOD-71491 | biostudies-arrayexpress

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

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

2012-12-30 | GSE27930 | GEO

Gene expression in metronomic cyclophosphamide-treated glioma xenografts

Project description:Gene expression in metronomic cyclophosphamide-treated glioma xenografts

| PRJNA259797 | ENA

RNA-seq analysis of immunogenic actions of metronomic cyclophosphamide treatment: dependence of gene responses on tumor model, mouse host, and drug schedule

Project description:RNA-seq analysis was performed using RNA isolated from three tumor models (GL261 glioma, LLC Lewis lung carcinoma, B16F10 melanoma) implanted subcutaneousy in C57BL/6 mice, or in ICR scid mice. Mice were untreated or were treated with cyclophosphamide (CPA) given on a 6-day repeating metronomic schedule (CPA/6d), except as noted. Results from these global transcriptome analysis indicated substantial elevation of basal GL261 immune infiltration and strong activation by CPA/6d treatment of GL261 immune stimulatory pathways and their upstream regulators, but without preferential depletion of negative immune regulators compared to LLC and B16F10 tumors. In LLC tumors, where CPA/6d treatment was found to be anti-angiogenic, CPA/6d suppressed VEGFA target genes and down regulated cell adhesion and leukocyte transendothelial migration genes. In GL261 tumors implanted in adaptive immune-deficient scid mice, where CPA/6d-induced GL261 regression is incomplete and late tumor growth rebound can occur, T cell receptor signaling and certain cytokine-cytokine receptor responses seen in B6 mice were deficient. Extending the CPA treatment interval from 6 to 9 days (CPA/9d) − which results in a strong but transient natural killer cell response followed by early tumor growth rebound − induced fewer cytokines and increased expression of drug metabolism genes. Taken together, these findings elucidate molecular response pathways activated by intermittent metronomic CPA treatment and identify deficiencies that characterize immune-unresponsive tumor models and drug schedules.

2016-08-01 | GSE71491 | GEO

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