Transcriptome differences between mature luminal and luminal progenitor cells of the breast
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA886710 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In this study, we grew primary breast epithelial cells from breast biopsies of healthy donors, five each of African Ancestry, European ancestry and those who identify as Hispanic using epithelial cell reprogramming assay growth method. Cells grown were sorted into luminal progenitors (CD49F+/EpCAM+, labelled as PP cells) and mature luminal (CD49F-/EpCAM+, labelled as NP cells) by flow cytometry. Flow sorted cells were subjected to RNA-seq.
2024-09-30 | GSE214702 | GEO
Project description:Highly purified subpopulations of primitive bipotent and committed luminal progenitor cells as well as mature luminal and myoepithelial cells from normal human mammary tissue were isolated and compared their transcriptomes obtained using the Affymetrix GeneChip Human X3P Array. Experiment Overall Design: 12 Afffymetrix array hybridizations were performed on RNA samples extracted from highly purified subpopulations of primitive bipotent and committed luminal progenitor cells as well as mature luminal and myoepithelial cells isolate from 3 different normal human mammary tissue.
2008-06-20 | E-GEOD-11394 | biostudies-arrayexpress
Project description:The goal of this study was to determine the genes regulated by ID4 in mammary epithelial subpopulations. Basal, luminal progenitor, and mature luminal mammary epithelial subpopulations were FACS-sorted from adult mice that were either WT or ID4 KO in quadruplicate. RNA-seq and differential gene expression analysis was performed.
2020-05-07 | GSE149965 | GEO
Project description:RNA-seq of FACS-enriched mammary subpopulations (basal, luminal progenitor, mature luminal) from WT and ID4 knockout mice
| PRJNA630710 | ENA
Project description:Low input proteomics on FABP7 hi/low mammary luminal progenitor cells isolated from human patient samples
2023-12-11 | MSV000093639 | MassIVE
Project description:The transcription factor c-Myb has been well characterized as an oncogene in several human tumor types, and its expression in the hematopoietic stem/progenitor cell population is essential for proper hematopoiesis. However, the role of c-Myb in mammopoeisis and breast tumorigenesis is poorly understood, despite its high expression in the majority of breast cancer cases (60-80%). We find that c-Myb high expression in human breast tumors correlates with the luminal/ER+ phenotype and a good prognosis. RNAi knock-down of endogenous c-Myb levels in the MCF7 luminal breast tumor cell line increases tumorigenesis both in vitro and in vivo, suggesting a tumor suppressor role in luminal breast cancer. We created a mammary-derived c-Myb expression signature and found it to be highly correlated with a published mature luminal mammary cell signature and least correlated with a mammary stem/progenitor lineage gene signature. These data describe, for the first time, a tumor suppressor role for the c-Myb proto-oncogene in breast cancer that has implications for understanding luminal tumorigenesis and for guiding treatment. refXsample
2010-10-15 | E-GEOD-21371 | biostudies-arrayexpress
Project description:Single-cell analysis has revolutionised genomic science in recent years. However, due to cost and other practical considerations, single-cell analyses are impossible for studies based on medium or large patient cohorts. For example, a single-cell analysis usually costs thousands of euros for one tissue sample from one volunteer, meaning that typical studies using single-cell analyses are based on very few individuals. While single-cell genomic data can be used to examine the phenotype of individual cells, cell-type deconvolution methods are required to track the quantities of these cells in bulk-tissue genomic data. Hormone receptor negative breast cancers are highly aggressive, and are thought to originate from a subtype of epithelial cells called the luminal progenitor. In this paper, we show how to quantify the number of luminal progenitor cells as well as other epithelial subtypes in breast tissue samples using DNA and RNA based measurements. We find elevated levels of cells which resemble these hormone receptor negative luminal progenitor cells in breast tumour biopsies of hormone receptor negative cancers, as well as in healthy breast tissue samples from BRCA1 (FANCS) mutation carriers. We also find that breast tumours from carriers of heterozygous mutations in non-BRCA Fanconi Anaemia pathway genes are much more likely to be hormone receptor negative. These findings have implications for understanding hormone receptor negative breast cancers, and for breast cancer screening in carriers of heterozygous mutations of Fanconi Anaemia pathway genes.
| S-EPMC8655091 | biostudies-literature
Project description:BACKGROUND: The transcription factor c-Myb has been well characterized as an oncogene in several human tumor types, and its expression in the hematopoietic stem/progenitor cell population is essential for proper hematopoiesis. However, the role of c-Myb in mammopoeisis and breast tumorigenesis is poorly understood, despite its high expression in the majority of breast cancer cases (60-80%). METHODOLOGY/PRINCIPAL FINDINGS: We find that c-Myb high expression in human breast tumors correlates with the luminal/ER+ phenotype and a good prognosis. Stable RNAi knock-down of endogenous c-Myb in the MCF7 luminal breast tumor cell line increased tumorigenesis both in vitro and in vivo, suggesting a possible tumor suppressor role in luminal breast cancer. We created a mammary-derived c-Myb expression signature, comprised of both direct and indirect c-Myb target genes, and found it to be highly correlated with a published mature luminal mammary cell signature and least correlated with a mammary stem/progenitor lineage gene signature. CONCLUSIONS/SIGNIFICANCE: These data describe, for the first time, a possible tumor suppressor role for the c-Myb proto-oncogene in breast cancer that has implications for the understanding of luminal tumorigenesis and for guiding treatment.
2010-10-15 | GSE21371 | GEO
Project description:Mammary alveologenesis is abrogated in the absence of the transcription factors STAT5A/5B that mediate cytokine signaling. To reveal the underlying causes for this developmental block we studied mammary stem and progenitor cells. While loss of STAT5A/5B did not affect the stem cell population and their ability to form mammary ducts, luminal progenitors were greatly reduced and unable to form alveoli during pregnancy. Temporally-controlled expression of transgenic STAT5A in mammary epithelium lacking STAT5A/5B restored the luminal progenitor population and rescued alveologenesis in a reversible fashion in vivo. Taken together, STAT5A is necessary and sufficient for the establishment of luminal progenitor cells. The mammary tissues from two mice of each genotype were collected 6 days (sample 9 and 11 were WT)
2009-10-21 | E-GEOD-17723 | biostudies-arrayexpress
Project description:Gene expression profiles of normal human mammary epithelial cell subsets enriched for luminal or myoepithelial characteristics on the basis of EpCAM and CD49f expression. Transcription profiles were compared between luminal- and myoepithelial-enriched human MEC subsets following 3D culture from 4 individuals. Gene expression profiles of normal human mammary epithelial cell subsets enriched for mature, luminal progenitor or bipotent progenitor-enriched characteristics on the bais of CD49f, MUC1, CD10, CD133 and Thy1 expression Transcription profiles were compared between unsorted, mature, luminal progenitor-enriched and bipotent progenitor-enriched human MEC subsets following 3D culture from 2 individuals. Four replicates of luminal-enriched human MECs and 3 replicates of myoepithelial-enriched MECs Transcription profiles of two replicates of unsorted, mature, luminal progenitor-enriched and bipotent progenitor-enriched human MEC subsets were analysed following 3D culture
2012-08-17 | E-GEOD-31429 | biostudies-arrayexpress