Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA355042 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:For patients with triple negative breast tumours (TNBCs), lacking receptors for oestrogen, progesterone or HER2 on their cell surface, chemotherapy is the main treatment. The taxanes, paclitaxel (PTX) and docetaxel, have become the most commonly-used chemotherapies for these kinds of breast cancer. Although several targeted therapies are currently undergoing clinical trials for TNBC, because of the heterogeneous nature of TNBCs, it is predicted that these may often be used in combination with chemotherapy. Therefore an understanding of the mechanisms of chemotherapy resistance will continue to be important for the treatment of these patients. Given the pleiotropic nature of YB-1, the aim of this study was to understand whether there were mechanisms in addition to those discussed above, by which YB-1 controls response to PTX in TNBCs. We initially followed up two previously studied mechanisms, mediated by ABCB1/MDR1 and DUSP4. We then proceeded to use genomics to identify novel mechanisms by which YB-1 regulates the response of TNBCs to PTX. This analysis identified and experimentally validated EGR1, encoding the early growth response protein 1 (EGR1) as a previously undiscovered mechanism of YB-1-driven PTX resistance.
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Project description:FZD7 Plays a Critical Role in Triple Negative Breast Cancer Proliferation
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Project description:paclitaxel-resistant triple-negative breast cancer cell lines (MDA-MB-231/PTX）transfect BCLIN25-specific si-BCLIN25 to knockdown BCLIN25 and analysis differential paclitaxel-resistantlung adenocarcinoma cell lines（PC9/GR）transfect HUMT-specific shHUMT to knockdown HUMT1 and analysis differential
2021-07-06 | GSE179144 | GEO
Project description:Treatment of triple-negative breast cancer has been challenging and paclitaxel resistance is one of the major obstacles to the better prognosis. Misregulation of alternative splicing (AS) may contribute to tumor progression and chemotherapy resistance. Human AS factor TRA2 has two separate gene paralogs encoding TRA2A and TRA2B proteins. TRA2B is associated with cancer cell survival and therapeutic sensitivity. We used microarrays to detail the global programme of gene expression and alternative splicing events underlying paclitaxel treatment and TRA2A upregulation and identified distinct classes of up-regulated and down-regulate genes as well as alternative splicing genes during this process.
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Project description:Determination of recurrent chromosomal aberrations in Luninal A, Luminal B, HER2-positve, and triple negative breast cancers
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Project description:Gene expression profiling of triple negative breast cancer, normal ductal cells, and normal tissues
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Project description:Immune checkpoint inhibitors combined with chemotherapy represent a promising treatment option in triple-negative breast cancer (TNBC). However, response rates are still relatively low necessitating the design of novel therapeutic strategies to improve clinical outcomes. Here, we describe a triple combination of anti-PDL-1 immune checkpoint blockade, epigenetic modulation thorough BET bromodomain inhibition, and chemotherapy with paclitaxel that effectively inhibits both primary and metastatic tumor growth in two different syngeneic murine breast cancer models. Detailed cellular and molecular profiling of tumors from single and combination treatment arms revealed increased T and B cell infiltration and macrophage reprogramming from M1 to a M2 phenotype in mice treated with triple combination.
2023-08-15 | GSE229426 | GEO
Project description:Immune checkpoint inhibitors combined with chemotherapy represent a promising treatment option in triple-negative breast cancer (TNBC). However, response rates are still relatively low necessitating the design of novel therapeutic strategies to improve clinical outcomes. Here, we describe a triple combination of anti-PDL-1 immune checkpoint blockade, epigenetic modulation thorough BET bromodomain inhibition, and chemotherapy with paclitaxel that effectively inhibits both primary and metastatic tumor growth in two different syngeneic murine breast cancer models. Detailed cellular and molecular profiling of tumors from single and combination treatment arms revealed increased T and B cell infiltration and macrophage reprogramming from M1 to a M2 phenotype in mice treated with triple combination.
2023-08-15 | GSE229422 | GEO
Project description:Triple-negative breast cancer is a heterogeneous disease characterized by poor clinical outcomes and a shortage of targeted treatment options. To discover molecular features of triple-negative breast cancer, we performed quantitative proteomics analysis of twenty human-derived breast cell lines and four primary breast tumors to a depth of more than 12,000 distinct proteins. We used this data to identify breast cancer subtypes at the protein level and demonstrate the precise quantification of biomarkers, signaling proteins, and biological pathways by mass spectrometry. We integrated proteomics data with exome sequence resources to identify genomic aberrations that affect protein expression. We performed a high-throughput drug screen to identify protein markers of drug sensitivity and understand the mechanisms of drug resistance. The genome and proteome provide complementary information that, when combined, yield a powerful engine for therapeutic discovery. This resource is available to the cancer research community to catalyze further analysis and investigation.
2017-12-12 | PXD008222 | Pride
Project description:Standard chemotherapy is the only systemic treatment for triple-negative breast cancer (TNBC). Despite the good initial responses, resistance remains a major therapeutic obstacle. Here, we employed a High-Throughput Screen to identify targeted therapies that overcome chemoresistance in TNBC. We applied short-term paclitaxel treatment and screened 320 small-molecule inhibitors of known targets to identify drugs that preferentially and efficiently target paclitaxel-treated TNBC cells. Among these compounds the SMAC mimetics (BV6, Birinapant) and BH3-mimetics (ABT-737/263) were recognized as potent targeted therapy for multiple paclitaxel-residual TNBC cell lines. However, acquired paclitaxel resistance through repeated paclitaxel pulses result in desensitization to BV6, but not to ABT-263, suggesting that short- and long-term paclitaxel resistance are mediated by distinct mechanisms. Gene expression profiling of paclitaxel-residual, -resistant and naïve MDA-MB-231 cells demonstrated that paclitaxel-residual, as opposed to -resistant cells, were characterized by an apoptotic signature, with downregulation of anti-apoptotic genes (BCL2, BIRC5), activation of apoptosis inducers (IL24, PDCD4), and enrichment of TNFα/NF-κB pathway, including upregulation of TNFSF15, coupled with cell-cycle arrest. BIRC5 and FOXM1 downregulation and IL24 induction was also evident in breast cancer patient datasets following taxane treatment. Exposure of naïve and paclitaxel-resistant cells to supernatants of paclitaxel-residual cells sensitized them to BV6, and treatment with TNFα enhanced the potency of BV6, suggesting that sensitization to BV6 is mediated, at least partially, by secreted factor(s). Our results suggest that administration of SMAC or BH3 mimetics following short-term paclitaxel treatment could be an effective therapeutic strategy for TNBC, while only BH3-mimetics could effectively overcome long-term paclitaxel resistance
2017-01-26 | GSE86839 | GEO