GEO DataSets

(Submitter supplied) Transcriptional profiling of breast cell lines comparing breast cell line mixed reference with individual breast cell lines. Goal was to characterize breast cell line subtypes.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL7264

51 Samples

Download data: TXT

(Submitter supplied) HER2 targeting with trastuzumab has changed the prognosis of breast cancer patients carrying amplification and/or overexpression of this oncogene. Despite this progress, however, resistance to trastuzumab occurs in the vast majority of patients. Newer anti-HER2 therapies, like the dual tyrosine-kinase inhibitor (TKI) lapatinib, show antitumor activity in a limited proportion of patients, indicating that HER2 can be still exploited as a target after trastuzumab failure. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL4133

2 Samples

Download data: TXT

(Submitter supplied) PD-0332991 is a selective inhibitor of the CDK4/6 kinases with the ability to block retinoblastoma (Rb) phosphorylation in the low nanomolar range. Here we investigate the role of CDK4/6 inhibition in human ovarian cancer. We examined the effects of PD-0332991 on proliferation, cell-cycle, apoptosis, and Rb phosphorylation using a panel of 40 established human ovarian cancer cell lines. Molecular markers for response prediction, including p16 and Rb, were studied using gene expression profiling, Western blot, and arrayCGH. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6480

40 Samples

Download data: PDF, TXT

(Submitter supplied) Targeting HER2 with lapatinib (L), trastuzumab (T), or the LT combination, is effective in HER2+ breast cancer (BC), but de novo and acquired resistance commonly occur. The purpose of this experiment was to investigate the somatic alterations found in Lapatinib and/or Trastuzumab resistant cells lines.

Organism:

Homo sapiens

Type:

Genome variation profiling by SNP array; SNP genotyping by SNP array

Platform:

GPL16104

4 Samples

Download data: TXT

(Submitter supplied) We have used ChIP-seq to profile binding of the estrogen receptor (ER) to chromatin in response to two mTOR inhibitors, i.e. everolimus (RAD001) and vistusertib (AZD2014). Two hours of treatment with these inhibitors significantly affected mTOR signaling, but surprisingly did not affect binding of ER to chromatin. This suggests that these mTOR inhibitors work through largely ER-independent mechanisms.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL16791

24 Samples

Download data: NARROWPEAK

(Submitter supplied) Gene expression levels were determined with control or PD-0332991 treatment

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

12 Samples

Download data: TXT

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

Organism:

Homo sapiens

Type:

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

Platform:

GPL17303

15 Samples

Download data: BED, BW

(Submitter supplied) We performed SMAD2 ChIP-seq analysis in T47D cells with/without Palbociclib treatment. To validate whether the changes in SMAD2 binding to the genome indeed resulted in changes in target gene expression, we performed RNA-seq transcriptome analyses in T47D with/without ActA stimulation and Palbo treatment.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17303

4 Samples

Download data: BW, FPKM_TRACKING

(Submitter supplied) Inhibitors for cyclin-dependent kinase (CDK) 4 and CDK6 have been established as effective therapeutic options for hormone receptor (HR)-positive, HER2-negative advanced breast cancer. Although the CDK4/6 inhibitors mainly target the cyclin D-CDK4/6-retinoblastoma tumor suppressor protein (RB) axis, little is known about clinical impact of inhibiting phosphorylation of other CDK4/6 target proteins. Here, we have focused on other CDK4/6 targets, SMAD proteins. We showed that a CDK4/6 inhibitor Palbociclib and Activin-SMAD2 signaling cooperatively inhibited cell cycle progression of a luminal-type breast cancer cell line T47D. Mechanistically, Palbociclib enhanced SMAD2 binding to the genome through inhibiting linker phosphorylation of the SMAD2 protein by CDK4/6. Comparison of the SMAD2 ChIP-seq data of T47D with those of a triple-negative breast cancer cell line Hs578T indicated that Palbociclib augments different SMAD2-mediated program defined based on types of cells, and enhances SMAD2 binding to the target regions on the genome without affecting its binding pattern. Collectively, the CDK4/6 inhibitor facilitates the cytostatic effects of Activin-SMAD2, while it also enhances its tumor promoting effects depending on types of breast cancer.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL17303

6 Samples

Download data: BED, BW

(Submitter supplied) Inhibitors for cyclin-dependent kinase (CDK) 4 and CDK6 have been established as effective therapeutic options for hormone receptor (HR)-positive, HER2-negative advanced breast cancer. Although the CDK4/6 inhibitors mainly target the cyclin D-CDK4/6-retinoblastoma tumor suppressor protein (RB) axis, little is known about clinical impact of inhibiting phosphorylation of other CDK4/6 target proteins. Here, we have focused on other CDK4/6 targets, SMAD proteins. We showed that a CDK4/6 inhibitor Palbociclib and Activin-SMAD2 signaling cooperatively inhibited cell cycle progression of a luminal-type breast cancer cell line T47D. Mechanistically, Palbociclib enhanced SMAD2 binding to the genome through inhibiting linker phosphorylation of the SMAD2 protein by CDK4/6. Comparison of the SMAD2 ChIP-seq data of T47D with those of a triple-negative breast cancer cell line Hs578T indicated that Palbociclib augments different SMAD2-mediated program defined based on types of cells, and enhances SMAD2 binding to the target regions on the genome without affecting its binding pattern. Collectively, the CDK4/6 inhibitor facilitates the cytostatic effects of Activin-SMAD2, while it also enhances its tumor promoting effects depending on types of breast cancer.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL17303

5 Samples

Download data: BED, BW

(Submitter supplied) In order to better understand signaling events following receptor dimerization involving HER2, we have generated an experimental system in which ErbB dimerization can be controlled. We used gene expression microarrays to identify genes and pathways that are differentially activated by HER2 homodimers and HER2 containing heterodimers.

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS4361

Platform:

GPL6244

12 Samples

Download data: CEL, CHP

Analysis of mammary epithelial MCF10A/HER2/FKBP/HA cells treated with AP1510 to induce the chimeric HER2-FKBP molecule to homodimerize, or with TGFα or heregulin to induce heterodimerization with EGFR or HER3. Results provide insight into signaling events following HER2 receptor dimerization.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 4 agent sets

Platform:

GPL6244

Series:

GSE22288

12 Samples

Download data: CEL, CHP

(Submitter supplied) Agilent gene expression arrays were used for intrinsic subtyping and to measure changes after anastrozole (C1D1) and after combination of anastrazole and palbociclib (C1D15).

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6480

118 Samples

Download data: TXT

(Submitter supplied) These data provide scientific information to understand the mechanism of action of lapatinib resistance in HER2-positive patients and to test the combination of HER2-targeted agents and GSK1363089 (foretinib) in the clinic by using an acquired lapatinib-resistant cell line.

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS4083

Platform:

GPL570

18 Samples

Download data: CEL

(Submitter supplied) The accurate mapping of recurring DNA copy number aberrations (CNAs), a hallmark feature of the cancer genome, has facilitated the discovery of tumor suppressor genes and oncogenes. Microarray-based assays designed to detect these chromosomal copy number alterations on a genome-wide and high-resolution scale have emerged as a cornerstone technology in the genomic era. The diversity of commercially-available platforms prompted a systematic comparison of five copy number profiling assays for their ability to detect 2-fold copy number gain and loss (4n or 1n, respectively) as well as focal high-amplitude CNAs. more...

Organism:

Homo sapiens

Type:

Genome variation profiling by genome tiling array; Genome variation profiling by SNP array

8 related Platforms

151 Samples

Download data: CEL, TXT

Analysis of BT474 (lapatinib-sensitive) and BT474-J4 (acquired lapatinib-resistance) HER2+ breast cancer cells treated with lapatinib, foretinib or both. Foretinib restored lapatinib-sensitivity in BT474-J4. Results provide insight into molecular basis of acquired lapatinib-resistance in BC cells.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 4 agent, 2 cell line, 2 genotype/variation sets

Platform:

GPL570

Series:

GSE16179

18 Samples

Download data: CEL

(Submitter supplied) Here we characterise the response of models of ER-positive breast cancer to treatment with the small molecule MDM2 inhibitor NVP-CGM097, a dihydroisoquinolinone derivative currently evaluated in a phase I clinical trial. We show that NVP-CGM097 reduces tumour cell viability of in vitro and in vivo models of endocrine sensitive, endocrine resistant and palbociclib (CDK4/6 inhibitor) resistant p53 wildtype (p53wt) ER-positive breast cancer. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

29 Samples

Download data: CSV

(Submitter supplied) Despite effective strategies, therapy resistance in HER2+ breast cancer remains a challenge. While the Mevalonate pathway (MVA) is suggested to promote cell growth and survival, including in HER2+ models, its potential role in resistance to HER2-targeted therapy is unknown. Using HER2+ breast cancer parental (P) cell models (AU565, SKBR3, and UACC812), we have established anti-HER2-resistant derivatives made resistant to lapatinib (LR) or lapatinib plus trastuzumab (LTR). more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

15 Samples

Download data: TXT

(Submitter supplied) miR-16 is a potent tumor suppressor in ErbB-2 positive breast cancer. The primary objetive of this study was to identify previously uncharacterized putative mRNA targets of miR-16 in ErbB-2 postitive breast cancer cells. To achieve our objective we studied the effects of exogenously expressed miR-16 on the gene expression profile of primary cultures of ErbB-2 positive murine breast cancer tumors. The C4HD tumor line displays high levels of estrogen receptor and progesterone receptor, overexpresses ErbB-2 and ErbB-3, exhibits low ErbB-4 levels, and lacks EGF-R expression.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL7202

6 Samples

Download data: TXT

(Submitter supplied) Array-CGH experiments of HER2+ breast cancer cell lines grown under standard conditions.

Organism:

Homo sapiens

Type:

Genome variation profiling by genome tiling array

Platform:

GPL4091

11 Samples

Download data: TXT