Transcriptomic profiling of 62 breast cancer cell lines and PDX models
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE152908 | GEO | 2020/06/21
REPOSITORIES: GEO
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Project description:RNA-seq was performed on breast cancer cell lines and primary tumors RNA-seq was performed on 28 breast cancer cell lines, 42 Triple Negative Breast Cancer (TNBC) primary tumors, and 42 Estrogen Receptor Positive (ER+) and HER2 Negative Breast Cancer primary tumors, 30 uninovlved breast tissue samples that were adjacent to ER+ primary tumors, 5 breast tissue samples from reduction mammoplasty procedures performed on patients with no known cancer, and 21 uninvolved breast tissue samples that were adjacent to TNBC primary tumors.
2014-06-11 | E-GEOD-58135 | biostudies-arrayexpress
Project description:Breast cancer, categorised into hormone receptor-positive (HR+), HER2-positive (HER2+), and triple-negative (TNBC) subtypes, exhibits varied outcomes based on the number of tumour-infiltrating lymphocytes (TILs). Increased TIL levels are associated with better outcomes in HER2+ and TNBC, while HR+ individuals with high TIL levels show shorter survival but greater neoadjuvant chemotherapy response. To explore the divergent roles of TIL levels across various subtypes and their effect on immune cell composition, we employed single-cell RNA sequencing on 31 patients with breast cancer. HR+ breast cancer with high TIL levels (TIL-high) revealed increased SPP1+ macrophages, increased SPP1 expression in other monocytes/macrophages (mono/macro) subgroups, and enriched pathways associated with extracellular matrix (ECM) remodelling in mono/macro. Moreover, cell–cell interaction analyses revealed enhanced SPP1, MIF, and FN1 signalling in the interaction between SPP1+ macrophages and T-cells in TIL-high HR+ breast cancer. Spatial transcriptomics data highlighted the close proximity of SPP1+ macrophages, CD8+ T-cells, and CD4+ T-cells in TIL-high HR+ breast cancer. Our findings unveil the novel influence of SPP1+ macrophages on T-cells in TIL-high HR+ breast cancer, potentially explaining the poor prognosis and offering insights for targeted interventions.
2024-10-09 | GSE261774 | GEO
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
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:Transcriptomic profiling of 62 breast cancer cell lines and PDX models
| PRJNA640820 | ENA
Project description:The clinical relevance of tumor infiltrating lymphocytes (TILs) in breast cancer (BC) is not firmly established. We aimed to validate previous prognostic findings in triple negative breast cancer (TNBC) and investigate predictive associations with trastuzumab benefit in HER2 overexpressing disease (HER2+).
2022-07-16 | GSE47994 | GEO
Project description:Eribulin prolongs overall survival in patients with pre-treated advanced breast cancer. However, no biomarker exists to prospectively select patients who will benefit the most from this drug. SOLTI-1007-NeoEribulin is a phase II, open-label, two cohort, exploratory pharmacogenomic study in patients with clinical stage I-II HER2-negative breast cancer receiving neoadjuvant eribulin monotherapy treatment. Primary objective was to explore the association of baseline tumor gene expression with pathological complete response in the breast (pCRB) at surgery. Key secondary objectives were pCRB rates in all patients and according to HR status, gene expression changes during treatment and safety. 101 hormonal receptor-positive (HR+) and 73 triple negative breast cancer (TNBC) patients were recruited. The pCRB rates were 6.4% in all patients, 4.9% in HR+ disease and 8.2% in TNBC. The TNBC cohort was interrupted due to a progression disease rate of 30.1%. The pCRB rates differed according to intrinsic subtypes: 28.6% in HER2-E, 11.1% in Normal-like, 7.9% in Luminal B, 5.9% in Basal-like and 0% in Luminal A (HER2-E vs. others odds ratio=7.05, 95% CI 1.80-42.14; p-value = 0.032). Intrinsic subtype changes at surgery occurred in 33.3% of cases, mostly (49.0%) Luminal B converting to Luminal A or Basal-likes converting to Normal-like. Baseline tumor infiltrating lymphocytes (TILs) were significantly associated with pCR. Eribulin showed a good safety profile with a low response and pCRB rates. Patients with HER2-negative disease with a HER2-enriched profile may benefit the most from eribulin. In addition, significant biological activity of eribulin is observed in Luminal B and Basal-like subtypes.
2021-12-10 | GSE186102 | GEO
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: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
Project description:Hormone receptor-positive (HR+)/human epidermal growth factor receptor 2-negative (HER2-) breast cancer, the most common type of breast cancer, is facing challenges such as endocrine therapy resistance and distant relapse. Immunotherapy has shown progress in treating triple-negative breast cancer, but immunological research on HR+/HER2- breast cancer is still in its early stages. Here, we performed a multi-omics analysis of a large cohort of HR+/HER2- breast cancer patients (n = 351) and revealed that HR+/HER2- breast cancer possessed a highly heterogeneous tumor immune microenvironment. Notably, the immunological heterogeneity of HR+/HER2- breast cancer was related to MAP3K1 mutation and we validated experimentally that MAP3K1 mutation could attenuate CD8+ T cell-mediated antitumor immunity. Mechanistically, MAP3K1 mutation suppressed MHC-I-mediated tumor antigen presentation through promoting the degradation of antigen peptide transporter 1/2 (TAP1/2) mRNAs, thereby driving tumor immune escape. In preclinical models, the postbiotics tyramine could reverse the MAP3K1 mutation-induced MHC-I reduction, thereby augmenting the efficacy of immunotherapy.
2024-12-20 | GSE276527 | GEO