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The Biological Activity of Cediranib (AZD2171) in Gastro-Intestinal Stromal Tumours(GIST).

ABSTRACT: To determine the anti-tumour activity and biological effects of cediranib (AZD2171) at a dose of 45mg, primarily in Gastrointestinal Stromal Tumour (GIST) patients who are resistant to imatinib mesylate (current standard therapy) and also in patients with metastatic Soft Tissue Sarcoma (STS) resistant to standard therapy.

DISEASE(S): Soft Tissue Sarcomas,Sarcoma,Advanced Cancer,Metastatic Gastro-intestinal Stromal Tumours,Cancer,Gastrointestinal Stromal Tumors

PROVIDER: 2033358 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Expression data for Cediranib in Metastatic ASPS

Project description:Gene expression from pre- and post- Cediranib treated patients with metastatic Alveolar Soft Part Sarcoma (ASPS)

2013-07-01 | GSE32569 | GEO

A Phase I/II Study of Cediranib (AZD2171) in Japanese Metastatic Colorectal Cancer Patients in Combination With FOLFOX

Project description:This Study is in two parts, the first part is to make sure that combining a potential new treatment, cediranib (AZD2171), with a standard treatment (FOLFOX) for metastatic colorectal cancer is safe. Once this part is complete and it is decided that it is safe to continue the Study will the go on to look at the efficacy of the two drugs together. This will be done by studying two treatment options. One will be the standard treatment alone (FOLFOX) + dummy cediranib (AZD2171) tablets and the other will be the standard treatment (FOLFOX) + real cediranib (AZD2171) tablets. Using dummy tablets means the study is ‘blinded’ and that non-one can tell the difference between the two treatment groups. This kind of study design is done to try to avoid the chance that the results might be biased in some way. The overall aim of the second part of the study is to see if adding cediranib (AZD2171) to a standard treatment for Metastatic Colorectal Cancer (mCRC), in this case FOLFOX, gives better results. That is, it’s better than giving standard treatment alone in helping to prevent progression of mCRC.

| 2041551 | ecrin-mdr-crc

Expression data for Cediranib in Metastatic ASPS

Project description:Gene expression from pre- and post- Cediranib treated patients with metastatic Alveolar Soft Part Sarcoma (ASPS) Paired tumor biopsies from 6 patients were collected. Samples were collected at baseline and 3 to 5 days following treatment. The patients are all enrolled in the replicate cohort of a National Cancer Institute (NCI)-sponsered investigational new drug application with institutional review board approval, and all participants provided written informed consent. ClinicalTrials.gov number, NCT00942877. The timing of the tumor biopsies was based on clinical observations of increased tumor pain associated with an inflammatory-like response in peripheral tumor lesions, usually within the second week of treatment. Tumor biopsies were obtained in the first week of treatment before the development of clinical signs and symptoms to evaluate gene expression changes. The time points are labeled "pre" and "post" to denote their relationship to treatment.

2013-07-01 | E-GEOD-32569 | biostudies-arrayexpress

Genome wide analysis of mouse gastrointestinal stromal tumors (GIST) in a mouse model of spontaneous GIST.

2011-12-31 | GSE30416 | GEO

Genome wide analysis of mouse gastrointestinal stromal tumors (GIST) in a mouse model of spontaneous GIST.

Project description:Analysis of mouse GIST tumors at the gene expression level. The purpose of the study was to identify immunomodulatory genes in mouse GIST tumors after in vivo treatment with the specific tyrosine kinase inhibitor imatinib mesylate. Total RNA obtained from mouse GIST tumors after in vivo treatment with imatinib or vehicle control injected intraperitoneally.

2011-12-31 | E-GEOD-30416 | biostudies-arrayexpress

microRNA profiling by array of human breast cancer cell lines exposed to Cediranib

Project description:We investigated the effect of Cediranib in human mammary carcinoma cell lines Hs578T, MDA-MB-231 and T47D by cellular and molecular assays. The cellular assays determined the ability to inhibit cell growth (IC50) by MTS assay, cell migration and invasion. Furthermore, using a microRNA-array and qRT-PCR approach we assessed the comparative expression of microRNAs following Cediranib treatment

2014-05-05 | E-MTAB-2126 | biostudies-arrayexpress

Calu6 and LoVo xenograft mRNA expression profiles in response to cediranib treatment

Project description:Calu6 and LoVo xenograft mRNA expression profiles in response to cediranib treatment

2013-09-09 | E-MTAB-1627 | biostudies-arrayexpress

Gene expression signature predictive of rapid response to imatinib mesylate in Gastrointestinal Stromal Tumor (GIST)

Project description:Gene expression profiling using oligonucleotide microarrays performed on tumor samples obtained before and after imatinib mesylate (IM) therapy. Rapid responding (to IM) samples were compared to non-responding/stable disease samples as measured by CT scan measurements to identify a gene signature that can predict rapid response to IM.

2009-11-24 | GSE15966 | GEO

Cediranib/AZD2171 inhibits bone and brain metastasis in a preclinical model of advanced prostate cancer.

Project description:Late stage or aggressive cancers exhibit metastatic growth at multiple sites, and the characterization of treatment response in various organs to drugs with potentially wide-ranging efficacy is needed. Tumor cells that induce angiogenesis are a common characteristic of metastatic disease, and clinically, antiangiogenic therapies have shown value in the setting of advanced cancer. However, recent preclinical studies have suggested that exposure to antiangiogenic drugs can increase tumor invasiveness and metastasis, making it important to determine which contexts antiangiogenic therapy is most appropriate. We describe here the effects of cediranib, a receptor tyrosine kinase inhibitor, in a model of advanced prostate cancer metastatic to skeleton and brain. Treatment with cediranib decreased metastatic tumor burden in the brain and bone, decreased cerebral vasogenic edema, and improved survival, despite increasing the invasive histology of brain metastases. Short-duration cediranib treatment given at the time of tumor cell dissemination was sufficient to inhibit the establishment and subsequent growth of bone metastases, although brain metastases were subject to rebound growth after the discontinuation of cediranib. Distinct growth patterns at different organ sites in the same animal showed that certain tumor microenvironments such as bone may be most amenable to interventions by anti-vascular endothelial growth factor (VEGF) therapies. In addition, anti-VEGF treatment may be of utility in decreasing the rapid growth of solid brain metastases and vasogenic edema in patients with advanced cancer, leading to reduced morbidity and associated clinical benefit.

| S-EPMC2989818 | biostudies-literature

Combination testing of cediranib (AZD2171) against childhood cancer models by the pediatric preclinical testing program.

Project description:BackgroundCediranib (AZD2171) is a potent small molecule inhibitor of vascular endothelial growth factor (VEGF) receptors. Cediranib has demonstrated single agent activity in several adult cancers and is being studied in combination with standard cytotoxic agents in multiple disease settings.ProceduresCediranib was tested in vivo against six childhood tumor xenograft models (four sarcomas, one glioblastoma, one neuroblastoma) alone or combined with cyclophosphamide (two models), vincristine (three models) or cisplatin (one model), each administered at its maximum tolerated dose, or rapamycin (six models).ResultsThe combination of cediranib with standard cytotoxic agents was superior to the cytotoxic agent used alone for a single xenograft (one of the three xenografts evaluated for the vincristine-cediranib combination). The cediranib-cyclophosphamide combination was inferior to single agent cyclophosphamide in time to event for both models studied and was significantly inferior for one of the models. Cediranib combined with rapamycin was superior to each of the agents used alone in two of the six models and was determined to be additive or supra-additive with rapamycin in four models, although the effects were not large.ConclusionsCediranib combined with cytotoxic chemotherapy agents demonstrated little or no benefit (and in one case was significantly inferior) compared to chemotherapy alone for the six pediatric cancer xenografts studied. By contrast, the combination of cediranib with rapamycin was additive or supra-additive in four of the six models in terms of prolongation of time to event, though tumor regressions were not observed for this combination.

| S-EPMC3253323 | biostudies-literature

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