Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Clinicopathological Observation and Initial Exploration of Characteristic Biomarkers in Apocrine Breast Carcinoma

ABSTRACT: Perform proteomic profiling comparing triple-negative apocrine carcinoma (TNAC) and luminal androgen receptor-type triple-negative breast cancer (LAR-TNBC) to elucidate their molecular distinctions and validate TNAC as a distinct entity separate from LAR-TNBC.

ORGANISM(S): Homo Sapiens

SUBMITTER: Minmin Yu

PROVIDER: PXD073549 | iProX | Mon Jan 26 00:00:00 GMT 2026

REPOSITORIES: iProX

ACCESS DATA

Json Xml

Similar Datasets

FZD7 Plays a Critical Role in Triple Negative Breast Cancer Proliferation

Project description:Breast cancer is genetically and clinically heterogeneous. Triple negative cancer (TNBC) is a subtype of breast cancer usually associated with poor outcome and lack of benefit from target therapy. A pathway analysis in a microarray study was performed using TNBC compared with non-triple negative breast cancer (non-TNBC). Overexpression of several Wnt pathway genes, such as frizzled homolog 7 (FZD7), Low density lipoprotein receptor-related protein 6 (LRP6) and transcription factor 7 (TCF7) has been observed in TNBC. Focus was given to the Wnt pathway receptor, FZD7. To validate its function, inhibition of FZD7 using FZD7shRNA was carried out. Notably decreased cell proliferation, suppressed invasiveness and colony formation in triple negative MDA-MB-231 and BT-20 cells were observed. Mechanism study indicated that these effects occurred through silencing the canonical Wnt signaling pathway, as evidenced by loss of nuclear accumulation of ï?¢-catenin and decreased transcriptional activity of TCF7. In vivo study revealed that FZD7shRNA significantly suppressed the tumor formation in xenotransplation mice due to decrease cell proliferation. Our finding suggests that FZD7 involved canonical Wnt signaling pathway is essential for tumorigenesis of TNBC. Thus, FZD7 may be a biomarker and a potential therapeutic target for triple negative breast cancer. 14 pretreatment non-triple negative breast tumors compare with 5 triple negative breast tumor.

2011-06-01 | E-GEOD-27447 | biostudies-arrayexpress

Comprehensive genomic analysis identify novel subtypes and targets of triple-negative breast cancer (198 TNBC tumors)

Project description:Recent meta-analyses suggest triple-negative breast cancer (TNBC) is a heterogenous disease. In this study we sought to define these TNBC subtypes and identify subtype-specific markers and targets. We identified and confirmed four distinct, stable TNBC subtypes: (1) Luminal-AR (LAR); 2) Mesenchymal (MES); 3) Basal-Like Immune-Suppressed (BLIS), and 4) Basal-Like Immune-Activated (BLIA). RNA profiling analysis was conducted on 198 TNBC tumors (ER-negativity defined as Allred Scale value â¤2) with >50% cellularity (discovery set: n=84; validation set: n=114)

2015-12-18 | E-GEOD-76124 | biostudies-arrayexpress

Comprehensive genomic analysis identify novel subtypes and targets of triple-negative breast cancer (67 not triple-negative tumors)

2015-12-23 | GSE76274 | GEO

Comprehensive genomic analysis identify novel subtypes and targets of triple-negative breast cancer (198 TNBC tumors)

2015-12-18 | GSE76124 | GEO

Response and resistance to BET bromodomain inhibitors in triple negative breast cancer [ChIP-Seq]

Project description:Triple negative breast cancer (TNBC) is a heterogeneous and clinically aggressive disease for which there is no targeted therapy. Here we report the preferential and high sensitivity of TNBCs to BET bromodomain inhibitors such as JQ1 manifested by cell cycle arrest in early G1, apoptosis, and induction of markers of luminal epithelial differentiation in vitro and in vivo. The sensitivity of TNBC and other tumor types to BET inhibition establishes a rationale for clinical investigation, and a motivation to understand mechanisms of resistance. After engendering acquired resistance to BET inhibition in previously sensitive TNBCs, we utilized integrative approaches to identify a unique mechanism of epigenomic resistance to this epigenetic therapy. Resistant cells remain dependent on BRD4, confirmed by RNA interference. However, TNBC cells adapt to BET bromodomain inhibition by re-recruitment of unmutated BRD4 to super-enhancers, now in a bromodomain-independent manner. Proteomic studies of resistant TNBC identify hyper-phosphorylation of BRD4 and strong association with MED1. Together, these studies provide a rationale for BET inhibition in TNBC and argue for combination strategies to anticipate clinical drug resistance. ChIP-seq in parental and JQ1 resistant triple negative breast cancer (TNBC) in response to DMSO or JQ1 treatment

2016-01-07 | E-GEOD-63581 | biostudies-arrayexpress

Response and resistance to BET bromodomain inhibitors in triple negative breast cancer [Chem-Seq]

Project description:Triple negative breast cancer (TNBC) is a heterogeneous and clinically aggressive disease for which there is no targeted therapy. Here we report the preferential and high sensitivity of TNBCs to BET bromodomain inhibitors such as JQ1 manifested by cell cycle arrest in early G1, apoptosis, and induction of markers of luminal epithelial differentiation in vitro and in vivo. The sensitivity of TNBC and other tumor types to BET inhibition establishes a rationale for clinical investigation, and a motivation to understand mechanisms of resistance. After engendering acquired resistance to BET inhibition in previously sensitive TNBCs, we utilized integrative approaches to identify a unique mechanism of epigenomic resistance to this epigenetic therapy. Resistant cells remain dependent on BRD4, confirmed by RNA interference. However, TNBC cells adapt to BET bromodomain inhibition by re-recruitment of unmutated BRD4 to super-enhancers, now in a bromodomain-independent manner. Proteomic studies of resistant TNBC identify hyper-phosphorylation of BRD4 and strong association with MED1. Together, these studies provide a rationale for BET inhibition in TNBC and argue for combination strategies to anticipate clinical drug resistance. Chem-Seq in parental and JQ1 resistant triple negative breast cancer (TNBC)

2016-01-07 | E-GEOD-63284 | biostudies-arrayexpress

miRNA expression analysis of breast cancer tissue and matched nomal tissue

Project description:Breast cancer can classify molecular subtype, luminal A, B, and HER2-positive and triple-negative breast cancer. Especially TNBC, there is no therapeutic target compared to other molecular subtypes. To investigate dysregulated miRNAs in TNBC, we performed miRNA microarray using breast cancer tissue with matched normal tissue in each subtype.

2023-06-15 | GSE154255 | GEO

H3K4ox-Mediated Chromatin Condensation Protects Breast Cancer Cells from the DNA Damage Repair Machinery

Project description:Using an H3K4ox-specific antibody, we determined that the H3K4ox modification is enriched in triple-negative breast cancer (TNBC) cells compared with luminal breast cancer subtypes—correlating with high LOXL2 levels— and, importantly, is found primarily in heterochromatin.

2019-03-06 | GSE96064 | GEO

Response and resistance to BET bromodomain inhibitors in triple negative breast cancer [RNA-Seq]

Project description:Triple negative breast cancer (TNBC) is a heterogeneous and clinically aggressive disease for which there is no targeted therapy. Here we report the preferential and high sensitivity of TNBCs to BET bromodomain inhibitors such as JQ1 manifested by cell cycle arrest in early G1, apoptosis, and induction of markers of luminal epithelial differentiation in vitro and in vivo. The sensitivity of TNBC and other tumor types to BET inhibition establishes a rationale for clinical investigation, and a motivation to understand mechanisms of resistance. After engendering acquired resistance to BET inhibition in previously sensitive TNBCs, we utilized integrative approaches to identify a unique mechanism of epigenomic resistance to this epigenetic therapy. Resistant cells remain dependent on BRD4, confirmed by RNA interference. However, TNBC cells adapt to BET bromodomain inhibition by re-recruitment of unmutated BRD4 to super-enhancers, now in a bromodomain-independent manner. Proteomic studies of resistant TNBC identify hyper-phosphorylation of BRD4 and strong association with MED1. Together, these studies provide a rationale for BET inhibition in TNBC and argue for combination strategies to anticipate clinical drug resistance. RNA-Seq in parental and JQ1 resistant triple negative breast cancer (TNBC) in response to DMSO or JQ1 treatment over time

2016-01-07 | E-GEOD-63582 | biostudies-arrayexpress

Peripheral Blood CD8+ T-Lymphocyte Immune Response in Benign and Subpopulations of Breast Cancer Patients

Project description:Peripheral blood CD8+ T-lymphocytes play a crucial role in cell-mediated immunity and tumour-related immune responses in breast cancer. The protein profile analysis of CD8+ T-lymphocytes in benign, Luminal A, Luminal B and triple-negative breast cancer (TNBC) patients in comparison to healthy control via a label-free proteomic quantification and gene set enrichment analysis (GSEA) were performed. The results confirmed that the most significantly of RNA degradation signalling pathway was down-regulated in all groups (benign, Luminal A, Luminal B, TNBC) was observed. Given the immunological role that T cells play in the treatment of disease, a better knowledge of RNA metabolism, i.e., the role that mRNA degradation pathways play in human physiology and pathology may lead to novel approaches to the therapeutic use of T cells.

2024-07-09 | PXD051985 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data