Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA400200 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Breast cancers lacking receptors for estrogen, progesterone or HER2 on their cell surface are called triple-negative breast cancers (TNBCs). TNBCs account for ~15-20% of all invasive breast cancers and do not benefit from anti-hormonal or anti-HER2 treatments. Although patients with TNBC can initially respond to chemotherapy, they do have worse overall prognosis compared to other breast cancer subtypes. Unfortunately, TNBCs lack clear targetable ‘driver’ oncogenes. Thus, there is an unmet need for strategies to improve the therapeutic options for these patients. We used microarrays to assess differences in gene expression in triple-negative breast cancer cells in response to the platinum-based chemotherapeutic agent cisplatin. The purpose was to find drug induced changes in gene expression level that could differentiate cisplatin sensitive from cisplatin resistant TNBC cell lines.
2017-08-26 | GSE103115 | GEO
Project description:DNA repair competency is one determinant of sensitivity to certain chemotherapy drugs, such as cisplatin. Cancer cells with intact DNA repair can avoid the accumulation of genome damage during growth and also can repair platinum-induced DNA damage. We sought genomic signatures indicative of defective DNA repair in cell lines and tumors and correlated these signatures to platinum sensitivity. The number of subchromosomal regions with allelic imbalance extending to the telomere (NtAI) predicted cisplatin sensitivity in vitro and pathologic response to preoperative cisplatin treatment in patients with triple-negative breast cancer (TNBC). In serous ovarian cancer treated with platinum-based chemotherapy, higher levels of NtAI forecast a better initial response. We found an inverse relationship between BRCA1 expression and NtAI in sporadic TNBC and serous ovarian cancers without BRCA1 or BRCA2 mutation. Thus, accumulation of telomeric allelic imbalance is a marker of platinum sensitivity and suggests impaired DNA repair. SNP data from 27 and 40 primary triple negative breast cancer tumor samples from two clinical trials treated with cisplatin and cisplatin + bevacizumab. Labeling, hybridization and data processing was performed by Affymetrix using 70k MIP arrays and 330k MIP arrays. In the cisplatin trial, matched normal samples based on blood from all patients and an additional three samples based on FFPE negative lymph nodes were used as references (30 normal references in total). In the cisplatin+bevacizumab trial, mathed normal samples based on blood from 10 patients were used as references.
2012-03-22 | E-GEOD-28330 | biostudies-arrayexpress
Project description:Gene expression data of human triple-negative breast cancer (TNBC)
| PRJNA594347 | ENA
Project description:This dataset includes mass spectrometry-based proteomic profiles of cisplatin-resistant (cisR) and cisplatin-sensitive (cisS) MDA-MB-231 triple-negative breast cancer (TNBC) cell lines. The study aimed to investigate the molecular alterations contributing to cisplatin resistance using data-independent acquisition (DIA) proteomics. Key findings revealed upregulation of extracellular matrix (ECM) remodeling proteins (e.g., COL6A1, COL6A3), drug efflux transporters (e.g., ABCC4), and membrane-associated resistance proteins (e.g., TIMP1, MMP-14, APP), highlighting their potential roles in chemoresistance. The data provide insights into resistance-associated signaling, metabolic pathways, and potential therapeutic targets in TNBC.
2026-04-07 | PXD062652 | JPOST Repository
Project description:Expression data for triple-negative breast cancer (TNBC) cells following chemotherapy
| PRJNA289375 | ENA
Project description:This dataset presents data-independent acquisition (DIA)-based proteomic profiles generated using a timsTOF Pro mass spectrometer for cisplatin-resistant (cisR) and cisplatin-sensitive (cisS) MDA-MB-231 triple-negative breast cancer (TNBC) cell lines. The objective was to decipher proteomic alterations associated with cisplatin resistance. The analysis uncovered significant upregulation of extracellular matrix (ECM) remodeling proteins (e.g., COL6A1, COL6A2, COL6A3), and invasion-related membrane proteins (e.g., TIMP1, MMP-14, APP) in cisR cells. The dataset offers high-resolution, reproducible proteomic insights into the mechanisms of cisplatin resistance, emphasizing the role of EMT, metabolic reprogramming, and membrane remodeling in TNBC.
2026-04-22 | PXD063175 | JPOST Repository
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:Evidence suggests that BRCA1 mutation associated tumors have increased sensitivity to DNA damaging agents like cisplatin. Sporadic triple negative breast cancers (TNBC) have many phenotypic similarities to BRCA1 tumors and may have a similar sensitivity to cisplatin. We tested the efficacy of cisplatin monotherapy in 28 TNBC patients in a single arm neoadjuvant trial with outcome measured by pathologic treatment response quantified using the Miller-Payne scale. We used microarrays gene expression profiles to determine tumor subtype of each trial tumor sample and to test various expression signatures for association with pathologic response to cisplatin. Pretreatment tumor samples from the clinical trial (N=24 with adequate tissue) were used for RNA extraction, linear amplification, biotin labeling and hybridization to Affymetrix U133 plus 2.0 arrays. A reference set of 51 primary breast tumors representing all subtypes of breast cancer were processed in a similar manner to include linear amplification, and hybridized to Affymetrix arrays.
2009-11-04 | E-GEOD-18864 | biostudies-arrayexpress
Project description:This project aimed to identify key proteins dysregulated by monensin and itssynthetic analog, compound 12, in the triple-negative breast cancer (TNBC) cell line MDA-MB-231. Byanalyzing the molecular changes induced by these compounds, the study sought to elucidate themechanisms underlying their cytotoxic effects on breast cancer cells. Additionally, it explored potentialdifferences in the activity and efficacy of monensin and compound 12, providing critical insights into theirdistinct biological impacts. These findings may contribute to the development of targeted therapeuticstrategies for triple-negative breast cancer, a highly aggressive and treatment-resistant subtype of breastcancer
2026-03-30 | PXD060697 | Pride
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