Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA209945 | ENA |
REPOSITORIES: ENA
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Project description:Preclinical and clinical studies have shown for decades that tumor cells demonstrate significantly enhanced sensitivity to “fever range” hyperthermia (increasing the intratumoral temperature to 42-45oC) than normal cells, although it is unknown why cancer cells exhibit this distinctive susceptibility. To address this issue, mammary epithelial cells and three malignant breast cancer lines were subjected to hyperthermic shock and microarray analysis of the global transcription changes was subsequently performed. MCF10A (mammary epithelial cells) and MCF7, MDA231, and MDA468 breast cancer cells were grow at normal growth temperatures or subjected to 30 minutes of hyperthermic (45oC) shock followed by replacement with conditioned media at normal growth temperatures. RNA was collected 4 hours after shock and subjected to microarray analysis.
2013-12-01 | E-GEOD-48398 | biostudies-arrayexpress
Project description:Preclinical and clinical studies have shown for decades that tumor cells demonstrate significantly enhanced sensitivity to “fever range” hyperthermia (increasing the intratumoral temperature to 42-45oC) than normal cells, although it is unknown why cancer cells exhibit this distinctive susceptibility. To address this issue, mammary epithelial cells and three malignant breast cancer lines were subjected to hyperthermic shock and microarray analysis of the global transcription changes was subsequently performed.
2013-12-01 | GSE48398 | GEO
Project description:The rationale underlying hyperthermia is the fact that temperatures over 42.5˚C are highly cytotoxic to tumor cells. On the other hand, although mild hyperthermia at a range from 39 to 41˚C alone did not induce cytotoxicity in tumor cells, mild hyperthermia is reported to show a synergism with radiotherapy and anti-cancer drugs. Here, the effects of mild hyperthermia (41˚C for 30 min) on the gene expression in human lymphoma U937 cells were investigated using by an Affymetrix GeneChip system. Although the cells treated with the mild hyperthermia did not induce apoptosis, a significant increase in protein levels of heat shock proteins, Hsp40 and Hsp70, was observed following activation of heat shock factor-1. At 3 h post-treatment, 938 probe sets that were differentially expressed by >1.5-fold were identified. Keywords: mild hyperthermia, gene expression, Human lymphoma U937 cell
2008-01-03 | GSE10043 | GEO
Project description:Molecular profiling was used to classify mammary tumors that develop in MTB-IGFIR transgenic mice. It was determined that the primary mammary tumors (PMT), which develop due to elevated expression of the type I insulin-like growth factor receptor (IGF-IR) in mammary epithelial cells, most closely resemble murine tumors with basal-like or mixed gene expression profiles and with human basal-like breast cancers. Downregulation of IGF-IR transgene in MTB-IGFIR tumor-bearing mice leads to the regression of most of the tumors followed by tumor re-appearance in some of the mice. These tumors that re-appear following IGF-IR transgene downregulation do not express the IGF-IR transgene and cluster with murine mammary tumors that express a mesenchymal gene expression profile and with human claudin-low breast cancers. Therefore, IGF-IR overexpression in murine mammary epithelial cells induces mammary tumors with primarily basal-like characteristics while tumors that develop following IGF-IR downregulation express a gene signature that most closely resembles human claudin-low breast tumors.
2011-10-01 | GSE32152 | GEO
Project description:Stromal and epithelial changes in breast cancer following endocrine treatment
| PRJNA252964 | ENA
Project description:LCOR regulates transcription of human mammary epithelial and breast cancer cells
| PRJNA339445 | ENA
Project description:Purpose: Leveraging genome-wide lineage-specific transcriptional profiling of human mammary luminal epithelial cells (LEPs) and myoepithelial cells (MEPs) to elucidate the molecular mechanisms underlying aging-associated breast cancer susceptibility. Methods: Human mammary luminal epithelial and myoepithelial cells were isolated from finite lifespan, non-immortalized human mammary epithelial cells (HMECs) derived from primary breast tissue of women across different age cohorts and breast cancer risk profiles. Transcriptional profiles of LEP and MEP cells were generated via RNA-sequencing performed on Illumina HiSeq 2500. RNA-Seq reads were trimmed using Trimmomatic software, and the processed reads were mapped back to the human genome (hg19) using TOPHAT2. Count matrices were generated using HTSeq. Results: Genome-wide loss of lineage fidelity is a hallmark of aging breast epithelia. Age-dependent differential expression occurred almost exclusively in luminal cells characterized by luminal epithelial cells of older women expressing markers normally expressed in myoepithelial cells. Luminal epithelial cells from histologically normal breast tissue from younger women who carry germline mutations in BRCA1, BRCA2, or PALB2 genes and who are considered to be clinically high risk for breast cancer also exhibited these hallmarks of accelerated aging. Furthermore, accelerated aging of these genetically high risk luminal epithelial cells could be predicted using a biological clock trained on gene expression and DNA methylation profiles of the luminal-specific ELF5 transcription factor. Conclusions: Our study shows that lineage-specific analysis is critical to understanding the molecular mechanisms underlying aging-associated cancer susceptibility. Our results suggest that loss of lineage fidelity is a general manifestation of epithelia that are susceptible to cancer initiation. Moreover, breast aging hallmarks identified in our study reflect a convergent biology of cancer susceptibility, regardless of the specific underlying genetic or age-dependent risk.
2021-08-19 | GSE182338 | GEO
Project description:Gene expression signatures have the capacity to identify clinically significant features of breast cancer and can predict which individual patients are likely to be resistant to neoadjuvant therapy, thus providing the opportunity to guide treatment decisions. Data used in publication: Clin Cancer Res. 2006;12:819–826. 89. Dressman et.al., Gene Expression Profiles of Multiple Breast Cancer Phenotypes and Response to Neoadjuvant Chemotherapy Combining DCE-MRI imaging and genomics have identified putative genomic biomarkers that are associated with risk for pCR following neoadjuvant chemotherapy. Furthermore, IBC gene expression profiles were associated with long term overall survival. The genomic profiles identified in this pilot study are preliminary but novel, and thus of great interest to validate as biomarkers in independent datasets. 37 breast tissue samples were collected under ultrasound guidance from patients with stage IIB/III breast cancer before four cycles of neoadjuvant liposomal doxorubicinpaclitaxel chemotherapy combined with local whole breast hyperthermia. Gene expression analysis was done using Affymetrix U133 Plus 2.0 GeneChip arrays.
2014-03-31 | E-GEOD-52322 | biostudies-arrayexpress
Project description:CK2 is an hetero-tetrameric protein made of two CK2α catalytic subunits and two regulatory CK2β subunits. The free CK2α subunit and the tetrameric holoenzyme have distinct substrate specificity profiles suggesting that the spatiotemporal organization of the individual CK2 subunits observed in living cells is crucial in the control of the many cellular processes that are governed by this pleiotropic kinase. Indeed, sub-stoichiometric expression of CK2β compared to CK2α in a subset of breast cancer tumors was correlated with the induction of EMT markers and increased epithelial cell plasticity in breast carcinoma progression. Using phosphotyrosine profiling with affinity capture and LC/MS-MS, we show that decreased expression of CK2β in MCF10A mammary epithelial cells triggers the phosphorylation of a number of tyrosine phosphorylated proteins and promotes the striking activation of the FAK1-Src-PAX1 signaling pathway. Moreover, morphometric analyses also revealed that CK2β loss increases the number and the spatial distribution of focal adhesion signaling complexes. Together, our finding allows positioning CK2β as a gatekeeper for cell spreading by restraining the focal adhesion maturation and invasion of mammary epithelial cells.
2022-07-05 | PXD030991 | Pride
Project description:Global proteomic profiling of three mammary epithelial cell types in normal human breast tissue. Primary breast specimens were obtained from 10 women undergoing reduction mammoplasties. Clinical co-variates include age (28-67), hormone status (follicular, luteal, post-menopausal) and mammary epithelial cell type (basal, luminal progenitor, mature luminal).
2021-03-12 | MSV000087042 | MassIVE