Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA269723 | ENA |
REPOSITORIES: ENA
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Project description:Triple negative breast cancer is an aggressive phenotypic breast cancer characterized by ER negative, PR negative and Her2 negative immunohistochemistry status. We embarked on a study to explore the transcriptome of Kenyan TNBC patients and identify potential biomarkers specific to Kenyan population. The transcriptome sequencing of tumors from Kenyan TNBC patients and comparisons with African American and Caucasian TNBC transcriptomes revealed several interesting targets and dysregulated pathways.
2021-04-28 | GSE142258 | GEO
Project description:To identify novel molecular targets for triple negative breast cancer (TNBC), we have employed whole genome microarray expression profiling. We purified 30 surgically resected breast cancer tissue diagnosed triple negative by means of immunohistochemical staining and 13 normal mammary ductal cells with lasermicrobeam microdissection system (PALM MicroBeam, Carl Zeiss MicroImaging Co., Ltd), performed whole human genome microarray, and compared gene expression levels of TNBC, normal mammary ductal cells, and normal vital organs to develop molecular targets with a minimum risk. Gene expression levels of 30 TNBC, 13 normal mammary ductal cells, and 4 normal vital tissues were evaluated. to clarify the molecular mechanism involved in TNBC, we analyzed gene expression profiles of 30 TNBC as well as 13 normal epithelial ductal cells purified by laser microbeam microdissection, and identified 301 transcripts that were significantly up-regulated and 321 transcripts that were significantly down-regulated in TNBC. In addition, gene-expression profiles analysis of normal human vital organs including heart, lung, liver, and kidney allowed us to identify 90 cancer-specific genes involved in breast carcinogenesis such as NEK2, PBK, DTL, MELK and GPSM2. Among them, we focused on cell cycle regulators, asp (abnormal spindle) homolog, microcephaly associated (Drosophila) (ASPM) and centromere protein K (CENPK) as novel therapeutic targets for TNBC.
2012-12-21 | E-GEOD-38959 | biostudies-arrayexpress
Project description:Triple-negative breast cancer (TNBC) is a highly aggressive form of breast cancer that exhibits extremely high levels of genetic complexity and yet a relatively uniform transcriptional program. We postulate that TNBC might be highly dependent on uninterrupted transcription of a key set of genes within this gene expression program and might therefore be exceptionally sensitive to inhibitors of transcription. Utilizing a novel kinase inhibitor and CRISPR/Cas9-mediated gene editing, we show here that triple-negative but not ER/PR+ breast cancer cells are exceptionally dependent on CDK7, a transcriptional cyclin-dependent kinase. TNBC cells are unique in their dependence on this transcriptional CDK and suffer apoptotic cell death upon CDK7 inhibition. An “Achilles cluster” of TNBC-specific genes are extremely sensitive to CDK7 inhibition and frequently associated with super-enhancers. We conclude that CDK7 mediates transcriptional addiction to a vital cluster of genes in TNBC and CDK7 inhibition may be useful therapy for this challenging cancer. Expression microarrays in H3K27ac in triple-negative breast cancer +/- treatment with covalent CDK7 inhibitor THZ1 treatment
2015-09-24 | E-GEOD-69106 | biostudies-arrayexpress
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
Project description:To identify novel molecular targets for triple negative breast cancer (TNBC), we have employed whole genome microarray expression profiling. We purified 30 surgically resected breast cancer tissue diagnosed triple negative by means of immunohistochemical staining and 13 normal mammary ductal cells with lasermicrobeam microdissection system (PALM MicroBeam, Carl Zeiss MicroImaging Co., Ltd), performed whole human genome microarray, and compared gene expression levels of TNBC, normal mammary ductal cells, and normal vital organs to develop molecular targets with a minimum risk.
2012-12-21 | GSE38959 | GEO
Project description:The genomic studies was designed to identify genes differentially expressed in tumor versus normal breast tissue. We aimed at identifying novel Antibody Drug Conjugate (ADC) targets that could be used to treat Triple Negative Breast Cancer (TNBC). Comparative genomic studies between normal breast and TNBC tissues, together with proteomic and bioinformatic analyses resulted in the elaboration of a catalog of potential ADC targets.
2021-10-12 | GSE185645 | GEO
Project description:An TMT-based quantitative phosphoproteome analysis using liquid chromatography–coupled tandem mass spectrometry was performed to acquire proteome-wide expression data on Triple-negative Breast Cancer (TNBC) cells treated with time-course Rocaglamide A.
2025-01-04 | PXD048247 | JPOST Repository
Project description:An iTRQA-based quantitative proteome analysis using liquid chromatography–coupled tandem mass spectrometry was performed to acquire proteome-wide expression data on Triple-negative Breast Cancer (TNBC) cells treated with Rocaglamide A for 24 hours.
2024-12-08 | PXD047648 | JPOST Repository
Project description:Triple-negative breast cancer (TNBC) is characterized by lack of receptors, estrogen (ER), progesterone, and Her2, and standard receptor-targeted therapies are ineffective. FOXC1, a transcriptional factor aberrantly overexpressed in many cancers, drives growth, metastasis, and stem-cell-like properties in TNBC. However, the molecular function of FOXC1 is unknown, partly due to heterogeneity of TNBC. Here, we show that although FOXC1 regulates many cancer hallmarks in TNBC, its function is varied in different cell lines, highlighted by the differential response to CDK4/6 inhibitors upon FOXC1 loss. Despite this functional heterogeneity, we show that FOXC1 regulates key oncogenes and tumor suppressors and identify a set of core FOXC1 peaks conserved across TNBC cell lines. We identify the ER-associated and drug-targetable nuclear receptor NR2F2 as a cofactor of FOXC1. Finally, we show that core FOXC1 targets in TNBC are parallelly regulated by the pioneer factor FOXA1 and the nuclear receptor NR2F2 in ER+ breast cancer.
2024-07-03 | PXD053261 | Pride
Project description:We report the application of ChIP-seq, which combines chromatin immunoprecipitation (ChIP) with massively parallel DNA sequencing, to map genome-wide XBP1 binding sites in different breast cancer cell lines. We showed that HIF1M-NM-1 motif was enriched in XBP1 binding sites in triple negative breast cancer (TNBC) cell lines, but not enriched in ER positive breast cancer cell line. We also demonstrated that different breast cancer cell lines of the same sub-type had similar XBP1 binding sites, whereas different breast cancer sub-types had majorly different XBP1 binding sites. Finally, a model was applied to integrate XBP1 ChIP-seq data with expression data to predict XBP1's direct targets in TNBC cell line; the predicted direct targets were shown to be predictive of patient survival, and the prediction power was specific to TNBC patients. The above evidence indicates that XBP1 performs important functions in TNBC by interacting with HIF1M-NM-1, and such regulation mechanism is specific to TNBC, which is later proved by follow-up experiments.This study represents the first detailed anaysis of XBP1 binding sites in different breast cancer cell lines. Examination of XBP1 binding sites in 2 cell types (3 cell lines).
2013-09-26 | E-GEOD-49952 | biostudies-arrayexpress