Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Comparison of mouse epithelial tumor initiating cells to mesenchymal tumor initiating cells generated by EMT

ABSTRACT: The differentiation of stem-like cells of tumors may contribute to the cellular heterogeneity of breast cancers. We report the propagation of highly enriched mouse mammary cancer stem cells that retain the potential to differentiate both in vivo and in culture and their use to identify chemical compounds that influence both self-renewal and differentiation. We identify epithelial tumor initiating cells (ETIC) that expresses lineage markers of both basal and luminal mammary cell lineages and retains the potential to generate heterogeneous tumors similar to the tumor of origin from even single cells. ETIC can progress through a Rho associated coil-coil protein kinase 1 (ROCK1) dependent, epithelial to mesenchymal transition to generate a second cell type capable of initiating tumors of limited heterogeneity. The propagation of ETIC will increase the opportunities for identifying new therapeutic compounds that may inhibit or prevent progression of some types of breast cancer. These data compare the gene expression pattern of ETIC and MTIC. Total RNA obtained from ETIC and MTIC cells, allowing the comparison of gene expression patterns and the selection of potential targets.

ORGANISM(S): Mus musculus

SUBMITTER: Roy Williams

PROVIDER: E-GEOD-33433 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Similar Datasets

Project description:Along with the two hallmark pathologies—intracellular neurofibrillary tangles (NFTs) and extracellular amyloid plaques—transcriptional studies suggest that Alzheimer's disease (AD) results from dysfunction of many cellular pathways including synaptic transmission, cytoskeletal dynamics, and apoptosis. While these studies consistently point to the same pathways involved in AD, there is no consensus on which genes in each pathway are disease-relevant, much less on whether these genes play causative roles or are downstream effects of disease progression. To address these issues, we have performed a large-scale transcriptional analysis in brain of individuals with advanced AD and non-demented controls, focusing specifically on CA1 and the relatively less affected CA3. For comparisons between regions and across disease status, we find consistency in both pathway enrichment as well as specific differentially expressed genes across several studies. Furthermore, genes that show decreased expression with AD progression also tend to show enrichment in CA3 (and vice versa), suggesting that transcription levels in a region may reflect that region's vulnerability to disease. In particular, we find several strong candidate vulnerability (ABCA1, MT1H, PDK4, RHOBTB3) and protection (FAM13A1, LINGO2, UNC13C) genes based on expression patterns. We have also applied weighted gene coexpression network analysis (WGCNA) to explore the pathophysiology of AD from a systems perspective, finding modules for major cell types, which each show distinct disease-relevant expression patterns. In particular, a microglial module shows increased expression in the brain of non-demented controls harboring early NFT pathology, suggesting that microglial activation is an early event in AD progression. Total RNA obtained from 60um sections of frozen human hippocampus was collected using scalpel dissection. Control and AD brains were matched for all non-disease characteristics as closely as possible. CA1 and CA3 dissections for a given individual were taken from the same section. Several region- and disease-related comparisons were performed.

Dataset Information

Comparison of mouse epithelial tumor initiating cells to mesenchymal tumor initiating cells generated by EMT

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure