GEO DataSets

(Submitter supplied) RUNX1 encodes a RUNX family transcription factor (TF) and was recently identified as a novel mutated gene in human luminal breast cancers. We found that Runx1 is expressed in all subpopulations of murine mammary epithelial cells (MECs) except the secretory alveolar luminal cells. Conditional knockout of Runx1 in MECs by MMTV-Cre led to a decrease in luminal MECs, largely due to a profound reduction in the estrogen receptor (ER)-positive mature luminal subpopulation, a phenotype that could be rescued by loss of either Trp53 or Rb1. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

6 Samples

Download data: CEL

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

21 Samples

Download data: CEL

(Submitter supplied) The purpose of this microarray experiment was to obtain reference gene expression patterns of a number of epithelial cell populations [mammary stem cells (MASC), luminal progenitors (LP), alveolar luminal stem/progenitor cells (WC virgin-these are mammary epithelial cells genetically marked by Wap-Cre in virgin females), mature luminal cells (ML, mainly represent ductal luminal cells in virgin females), and alveolar luminal cells (WC preg – these are alveolar cells genetically marked by Wap-Cre during mid-gestation)] present in the mammary gland of wildtype adult mice on a C57BL6 genetic background.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

15 Samples

Download data: CEL

(Submitter supplied) Mammary stem and progenitor cells are essential for mammary gland homeostasis and are also candidates for cells of origin of mammary tumors. Here, we provide evidence that the protein kinase p38a is required for the differentiation of luminal progenitor cells through modulation of the transcription factors Runx1 and Foxa1. Moreover, using a mouse model for breast cancer initiated by luminal cells, we show that p38a downregulation in mammary epithelial cells reduces tumorigenesis, which correlates with reduced numbers of tumor-initiating cells. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL11180

16 Samples

Download data: CEL

(Submitter supplied) Breast cancer is a heterogeneous disease comprised of at least five major subtypes. Luminal subtype tumors confer a more favorable patient prognosis, which is in part, attributed to the Estrogen Receptor-α (ER) positivity and anti-hormone responsiveness of these tumors. Expression of the forkhead box transcription factor, FOXA1, also correlates with the luminal subtype and patient survival, but is present in a subset of ER-negative tumors. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL4133

20 Samples

Download data: TXT

(Submitter supplied) Mutations in ARID1A, a subunit of the SWI/SNF chromatin remodelling complex, are the most common somatic alteration of the SWI/SNF complex across all cancers including oestrogen receptor positive (ER)+ breast cancer. We have recently reported that ARID1A inactivating mutations are present at a high frequency in advanced endocrine resistant ER+ breast cancer. In parallel, to identify mechanisms of resistance to endocrine therapy in breast cancer, we performed an epigenome CRISPR/CAS9 knockout screen that identified ARID1A as the top candidate whose loss determines resistance to the ER degrader fulvestrant. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

32 Samples

Download data: TXT

(Submitter supplied) Mutations in ARID1A, a subunit of the SWI/SNF chromatin remodelling complex, are the most common somatic alteration of the SWI/SNF complex across all cancers including oestrogen receptor positive (ER)+ breast cancer. We have recently reported that ARID1A inactivating mutations are present at a high frequency in advanced endocrine resistant ER+ breast cancer. In parallel, to identify mechanisms of resistance to endocrine therapy in breast cancer, we performed an epigenome CRISPR/CAS9 knockout screen that identified ARID1A as the top candidate whose loss determines resistance to the ER degrader fulvestrant. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

17 Samples

Download data: BW

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing

Platform:

GPL11154

103 Samples

Download data: BW

(Submitter supplied) Mutations in ARID1A, a subunit of the SWI/SNF chromatin remodelling complex, are the most common somatic alteration of the SWI/SNF complex across all cancers including oestrogen receptor positive (ER)+ breast cancer. We have recently reported that ARID1A inactivating mutations are present at a high frequency in advanced endocrine resistant ER+ breast cancer. In parallel, to identify mechanisms of resistance to endocrine therapy in breast cancer, we performed an epigenome CRISPR/CAS9 knockout screen that identified ARID1A as the top candidate whose loss determines resistance to the ER degrader fulvestrant. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

10 Samples

Download data: TXT

(Submitter supplied) Mutations in ARID1A, a subunit of the SWI/SNF chromatin remodelling complex, are the most common somatic alteration of the SWI/SNF complex across all cancers including oestrogen receptor positive (ER)+ breast cancer. We have recently reported that ARID1A inactivating mutations are present at a high frequency in advanced endocrine resistant ER+ breast cancer. In parallel, to identify mechanisms of resistance to endocrine therapy in breast cancer, we performed an epigenome CRISPR/CAS9 knockout screen that identified ARID1A as the top candidate whose loss determines resistance to the ER degrader fulvestrant. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

24 Samples

Download data: BW

(Submitter supplied) Mutations in ARID1A, a subunit of the SWI/SNF chromatin remodelling complex, are the most common somatic alteration of the SWI/SNF complex across all cancers including oestrogen receptor positive (ER)+ breast cancer. We have recently reported that ARID1A inactivating mutations are present at a high frequency in advanced endocrine resistant ER+ breast cancer. In parallel, to identify mechanisms of resistance to endocrine therapy in breast cancer, we performed an epigenome CRISPR/CAS9 knockout screen that identified ARID1A as the top candidate whose loss determines resistance to the ER degrader fulvestrant. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

20 Samples

Download data: BW

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens; Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing

Platforms:

GPL17021 GPL16791

26 Samples

Download data: BED

(Submitter supplied) About 75% of all breast cancers express the nuclear hormone receptor oestrogen receptor α (ERα). However, the majority of mammary tumors from genetically engineered mouse models are ERα-negative. To model ERα-positive breast cancer in mice, we exogenously introduced expression of mouse and human ERα in an existing p53-deficiency driven breast cancer mouse model. After initial ERα expression during development of the mammary gland, expression was reduced or lost in adult glands and p53-deficient mammary tumors. more...

Organism:

Homo sapiens; Mus musculus

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL17021 GPL16791

18 Samples

Download data: TXT

(Submitter supplied) About 75% of all breast cancers express the nuclear hormone receptor oestrogen receptor α (ERα). However, the majority of mammary tumors from genetically engineered mouse models are ERα-negative. To model ERα-positive breast cancer in mice, we exogenously introduced expression of mouse and human ERα in an existing p53-deficiency driven breast cancer mouse model. After initial ERα expression during development of the mammary gland, expression was reduced or lost in adult glands and p53-deficient mammary tumors. more...

Organism:

Mus musculus; Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL16791 GPL17021

8 Samples

Download data: BED

(Submitter supplied) Effect of RUNX1 depletion in the presence or absence of Estradiol

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

12 Samples

Download data: IDAT, TXT

(Submitter supplied) Comparative analysis of RUNX1 and RUNX2 responsiveness in the presence or absence of E2

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

24 Samples

Download data: IDAT, TXT

(Submitter supplied) The transcription factor RUNX1 exhibits recurrent loss-of-function mutations in estrogen receptor-positive (ER+) breast cancer (BCa). Its knockdown in vitro decreased AXIN1 expression in estrogen-dependent manner. Consistently, RUNX1 and AXIN1 mRNA levels are strongly correlated in ER+, not ER- tumors. RUNX1 occupies AXIN1’s second intron in living cells, abutting an ERa-binding site. Potentially promoting BCa progression, decreased AXIN1 expression after RUNX1 knockdown associated with upregulation of b-catenin, and this was preventable by AXIN stabilizers. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL16791

3 Samples

Download data: BED

(Submitter supplied) The tumor suppressor gene p53 is frequently mutated in human breast cancer and is a marker for poor prognosis and resistance to chemotherapy. Transplantation of p53-null mouse mammary epithelium into syngeneic wild-type mice leads to normal mammary gland development followed by spontaneous mammary tumors that recapitulate many of the phenotypic, molecular, and genetic features of human breast cancer. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6096

6 Samples

Download data: CEL

(Submitter supplied) To assess how the TOX3 nuclear protein can modulate gene expression in luminal epithelial cells, MCF7 cells were transfected with a TOX3 expression vector or vector control. In both instances, GFP was coexpressed, allowing isolation of transfected cells by flow cytometry before transcriptome analysis. Experiments were carried out under estrogen depleted conditions, and cells isolated 48 hours after transfection.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6244

4 Samples

Download data: CEL

(Submitter supplied) The mammary luminal cell compartment is heterogeneous. In adult virgin mice, it contains clonogenic luminal progenitors and non-clonogenic luminal cells expressing estrogen and progesterone receptors that can be discrimated by their cell surface expression of ICAM-1. We have separated ICAM1+ luminal progenitors and ICAM- non-clonogenic luminal cells and analyzed their transcriptomic profiles. After showing that the luminal progenitor population overexpressed Met, Trp53 and numerous p53 target genes, we analyzed how the p53 and Met signaling pathways cooperate to control the function and plasticity of luminal progenitors.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL17400

14 Samples

Download data: CEL