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Homo sapiens

ABSTRACT: Microarray analysis of xenograft models in use at the Developmental Therapeutics Program of the National Cancer Institute (DTP-NCI)

OTHER RELATED OMICS DATASETS IN: E-GEOD-48433

PROVIDER: PRJNA210119 | ENA |

REPOSITORIES: ENA

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E-GEOD-48433

Project description:Microarray analysis of xenograft models in use at the Developmental Therapeutics Program of the National Cancer Institute (DTP-NCI)

2025-01-24 | E-GEOD-48433 | ExpressionAtlas

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NCI60 Expression Profiling using the Agilent Whole Human Genome Oligo Microarray

Project description:We present here a new expression profiling study of the 60 cell lines of the National Cancer Institute (NCI) Developmental Therapeutics program (DTP) drug screen (NCI-60) using the 41,000-probe Agilent Whole Human Genome Oligo Microarray. The expression levels of ∼21,000 genes were measured. The profiling study includes quadruplicate technical replicates for six cell lines and duplicates for the remaining cell lines. The resulting data sets are freely available and searchable online in the CellMiner database (http://discover.nci.nih.gov).

2010-07-31 | E-GEOD-22821 | biostudies-arrayexpress

Gene expression patterns within cell lines are predictive of chemosensitivity

Project description:We generated RNA's and measured expression of 40000 genes using spotted cDNA microarrays from the fifty nine publicly available cell lines of the NCI Developmental Therapeutics Program's NCI60 studies and an additional set of seven cell lines for which GI50 compound sensitivity data were available. All cell lines were grown to 80% confluence in RPMI 1640 supplemented with phenol red, glutamine (2 mM) and 5% fetal calf serum. This expression data, in conjunction with the compound sensitivity data sets available from the DTP, were used to empirically determine whether gene-compound correlates of a sufficiently high correlation coefficient would have a suitable low false discovery rate to support the use of a correlative approach and these datasets for early discovery approaches for new targeted therapies. A cell type comparison design experiment design type compares cells of different type for example different cell lines. Sixty six cell lines were analysed, with no repetitions. Twelve cell lines were pooled for a common reference.

2008-02-07 | E-GEOD-7947 | biostudies-arrayexpress

Clinical and prognostic relevance of squalene epoxidase in breast cancer

Project description:All cell lines were purchased from ATCC (LGC Standards S.r.l., Milan, Italy), except T-47D and MDA-MB-468 that were obtained from the National Cancer Institute Developmental Therapeutics Program (Frederick, MD).

2015-07-28 | GSE71395 | GEO

Gene expression patterns within cell lines are predictive of chemosensitivity

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Clinical and prognostic relevance of squalene epoxidase in breast cancer

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Drug tolerant persisters in erlotinib treated EGFR-mutated lung adenocarcinoma arise from pre-existing tumor cells and survive in an adapted stromal microenvironment

Project description:Targeted therapies require life-long treatment, as drug discontinuation invariably leads to tumor recurrence. Recurrence is thought to mainly be driven by minor subpopulations of drug tolerant persister (DTP) cells that survive the cytotoxic drug effect. In lung cancer, DTP studies have mainly been conducted using tumor cell line models. We conducted an in vivo DTP study using a lung adenocarcinoma (LUAD) patient-derived xenograft (PDX) tumor driven by an epidermal growth factor receptor (EGFR) mutation. Daily treatment of tumor-bearing mice for 5-6 weeks markedly shrunk the tumors and generated DTPs, which were analyzed by bulk population transcriptome.

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SAGE analysis of normal human mammary epithelial cells, breast carcinoma (malignant effusion), and breast adenocarcinoma (malignant pleural effusion)

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Role of Anlotinib-induced CCL2 decrease in anti-angiogensis and response prediction for Non-Small Cell Lung Cancer therapy

Project description:Purpose: Our previous clinical trials have been demonstrated that Anlotinib can inhibit tumor growth upon refractory advanced non-small cell lung cancer (NSCLC) patients with the possibility mechanism of anti-angiogenesis. The present study sought to reveal the underlying molecular mechanism of Anlotinib-induced anti-angiogenesis in advanced NSCLC. Experimental Design: Computed tomography (CT) was used to evaluate the treatment effect of Anlotinib upon refractory advanced NSCLC patients. Transcriptome profiling was performed to identify the key gene expression alteration in NCI-H1975 cells before and after Anlotinib treatment. NCI-H1975 derived xenograft model was applied to investigate treatment effect and verify anti-angiogenesis mechanism of Anlotinib. Results: Anlotinib induces tumor cytotoxicity on refractory advanced NSCLC patients, NCI-H1975 derived xenograft models and lung adenocarcinoma cell lines. Transcriptome profiling revealed CCL2 blockade could be responsible for Anlotinib-induced anti-angiogenesis. NCI-H1975 derived xenograft model demonstrated Anlotinib-induced CCL2 blockade play an important role in anti-angiogenesis. Conclusions: This study not only offered the first evidence that Anlotinib inhibits angiogenesis via blocking CCL2 expression, but also provided a novel theoretical basis for the application of Anlotinib in advanced NSCLC patients.

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