Breast Cancer Dataset
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE3143 | GEO | 2005/11/07
SECONDARY ACCESSION(S): PRJNA92973
REPOSITORIES: GEO
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Project description:Signatures of Oncogenic Pathway Deregulation in Human Cancers; The ability to define cancer subtypes, recurrence of disease, and response to specific therapies using DNA microarray-based gene expression signatures has been demonstrated in multiple studies. Such data is also of substantial importance to the analysis of cellular signaling pathways central to the oncogenic process. With this focus, we have developed a series of gene expression signatures that reliably reflect the activation status of several oncogenic pathways. When evaluated in several large collections of human cancers, these gene expression signatures identify patterns of pathway deregulation in tumors, and clinically relevant associations with disease outcomes. Combining signature-based predictions across several pathways identifies coordinated patterns of pathway deregulation that distinguish between specific cancers and tumor sub-types. Clustering tumors based on pathway signatures further defines prognosis in respective patient subsets, demonstrating that patterns of oncogenic pathway deregulation underlie the development of the oncogenic phenotype and reflect the biology and outcome of specific cancers. Furthermore, predictions of pathway deregulation in cancer cell lines are shown to coincide with sensitivity to therapeutic agents that target components of the pathway, underscoring the potential for such pathway prediction to guide the use of targeted therapeutics. Experiment Overall Design: RNA was extracted from human mammary epithelial cells expressing oncogenes (or GFP control) for gene array analysis. Experiment was performed in replicate.
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2009-10-06 | E-GEOD-15455 | biostudies-arrayexpress
Project description:Genome-wide mRNA expression profiles of 200 primary gastric tumors from the Singapore patient cohort. Gastric cancer (GC) is the second leading cause of global cancer mortality, with individual gastric tumors displaying significant heterogeneity in their deregulation of various oncogenic pathways. We aim to identify major oncogenic pathways in GC that robustly impact patient survival and treatment response. We used an in silico strategy based on gene expression signatures and connectivity analytics to map patterns of oncogenic pathway activation in 25 unique GC cell lines, and in 301 primary gastric cancers from three independent patient cohorts. Of 11 oncogenic pathways previously implicated in GC, we identified three predominant pathways (proliferation/stem cell, NF-kB, and Wnt/b-catenin) deregulated in the majority (>70%) of gastric tumors. Using a variety of proliferative, Wnt, and NF-kB-related assays, we experimentally validated the pathway predictions in multiple GC cell lines showing similar pathway activation patterns in vitro. Patients stratified at the level of individual pathways did not exhibit consistent differences in clinical outcome. However, patients grouped by oncogenic pathway combinations demonstrated robust and significant survival differences (e.g., high proliferation/high NF-kB vs. low proliferation/low NF-kB), suggesting that tumor behavior in GC is likely influenced by the combined effects of multiple oncogenic pathways. Our results demonstrate that GCs can be successfully taxonomized by oncogenic pathway activity into biologically and clinically relevant subgroups. Experiment Overall Design: Profiling of 200 primary gastric tumors on Affymetrix GeneChip Human Genome U133 Plus 2.0 Array. All tumors were collected with approvals from the National Cancer Centre, Singapore; the Research Ethics Review Committee; and signed patient informed consent.
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