Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA393068 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5803080.fastq.gz | Fastqsanger.gz | |||
| SRR5803081.fastq.gz | Fastqsanger.gz | |||
| SRR5803082.fastq.gz | Fastqsanger.gz | |||
| SRR5803083.fastq.gz | Fastqsanger.gz | |||
| SRR5803084.fastq.gz | Fastqsanger.gz |
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Project description:Introduction: The I-SPY 1 TRIAL was designed to evaluate complete pathologic response and tumor volume change, measured by magnetic resonance imaging (MRI), stratified by molecular subtypes and link response to 3-year recurrence free survival (RFS).Methods: Eligible patients had T =3 cm and received neoadjuvant chemotherapy with AC plus optional taxane. Serial MRI, biopsy, and blood draws were conducted over the course of treatment, and a database of multiple molecular profiles was assembled.Results: A total of 221 patients were eligible for analysis: median tumor size was 6.0 cm and median age was 49 years. The I-SPY 1 TRIAL patients had tumors with aggressive biology: 45% were estrogen receptor (ER) negative, 31% Her2+; and 91% high risk by the Netherlands Cancer Institute (NKI) 70-gene profile. After a median of 3.9 years, RFS was 77%. HR/HER2 status improved predictability of RFS with the greatest difference between HR+/HER2- and triple-negative disease (hazard ratio 0.39). Wound healing signature activation, p53 mutation, and Risk of Relapse (ROR) score were highly correlated and also significantly improved the accuracy of RFS predictions when added to stage. The rate of pathologic complete response (pCR) varied considerably from a low of 0-2% (NKI low risk, luminal A) to a high of 43-61% (17q Amplified, HER2 enriched, HR-/HER2+). Both pCR and the more refined residual cancer burden (RCB) were significant predictors of RFS for all patients and even more predictive when analyzed within biomarker subsets. Good risk (NKI low, ROR-S low risk, Wound Healing quiescent, p53 wild type) signatures were associated with significantly higher 3-year RFS than poor risk expression signatures (ROR-S high risk, Wound Healing Activated, p53 mutation, NKI high risk).Conclusion: Importantly, in this set of biologically poor prognosis tumors, pCR predicts for better outcome, especially when analyzed within breast cancer subsets. Keywords: reference x sample reference x sample
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Project description:In this study, we characterize the fusion protein produced by the EPC1-PHF1 translocation in Low Grade Endometrial Stromal Sarcoma (LG-ESS) and Ossifying FibroMyxoid Tumors (OFMT). We express the fusion protein and necessary controls in K562 Cells. The fusion protein assembles a mega-complex harboring both NuA4/TIP60 and PRC2 subunits and enzymatic activities and leads to mislocalization of chromatin marks in the genome, linked to aberrant gene expression.
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Project description:Forkhead box protein A1 (FOXA1) has been shown to have critical functions in prostate and ER alpha positive breast cancer. As a pioneering transcriptional factor, FOXA1 regulates DNA accessibility for the androgen receptor in prostate and the estrogen receptor alpha in ER positive breast cancer, respectively. FOXA1 is also expressed in human epidermal growth factor receptor-2 (HER2/ErbB2) positive breast cancers, but its functions in HER2 positive breast cancer are unclear. The loss of FOXA1 results in a decrease in the viability of HER2 positive and HER2 amplified cell lines suggesting that FOXA1 may have an important role in HER2 positive breast cancers. In this report, we examined patient-derived single-cell RNA sequencing and spatial transcriptomics data and demonstrated that FOXA1 is co-expressed with ErbB2 in HER2 positive breast cancers. Knocking down FOXA1 expression led to the reduction of HER2 expression and signaling. Chromatin Immunoprecipitation Sequencing (ChIP-seq) and Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq) identified FOXA1 binding motifs in the ErbB2 promoter and regulatory element regions, which controlled ErbB2 gene expression. Interestingly, the knockdown of FOXA1 increased Epithelial Mesenchymal Transition (EMT) signaling and inhibited luminal tumor differentiation. Furthermore, FOXA1 and TRPS1 regulated TEAD/YAP-TAZ activity. Taken together, our data demonstrate that FOXA1 is required for HER2 expression and luminal identity in HER2+ breast cancer.
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Project description:Forkhead box protein A1 (FOXA1) has been shown to have critical functions in prostate and ER alpha positive breast cancer. As a pioneering transcriptional factor, FOXA1 regulates DNA accessibility for the androgen receptor in prostate and the estrogen receptor alpha in ER positive breast cancer, respectively. FOXA1 is also expressed in human epidermal growth factor receptor-2 (HER2/ErbB2) positive breast cancers, but its functions in HER2 positive breast cancer are unclear. The loss of FOXA1 results in a decrease in the viability of HER2 positive and HER2 amplified cell lines suggesting that FOXA1 may have an important role in HER2 positive breast cancers. In this report, we examined patient-derived single-cell RNA sequencing and spatial transcriptomics data and demonstrated that FOXA1 is co-expressed with ErbB2 in HER2 positive breast cancers. Knocking down FOXA1 expression led to the reduction of HER2 expression and signaling. Chromatin Immunoprecipitation Sequencing (ChIP-seq) and Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq) identified FOXA1 binding motifs in the ErbB2 promoter and regulatory element regions, which controlled ErbB2 gene expression. Interestingly, the knockdown of FOXA1 increased Epithelial Mesenchymal Transition (EMT) signaling and inhibited luminal tumor differentiation. Furthermore, FOXA1 and TRPS1 regulated TEAD/YAP-TAZ activity. Taken together, our data demonstrate that FOXA1 is required for HER2 expression and luminal identity in HER2+ breast cancer.
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Project description:Forkhead box protein A1 (FOXA1) has been shown to have critical functions in prostate and ER alpha positive breast cancer. As a pioneering transcriptional factor, FOXA1 regulates DNA accessibility for the androgen receptor in prostate and the estrogen receptor alpha in ER positive breast cancer, respectively. FOXA1 is also expressed in human epidermal growth factor receptor-2 (HER2/ErbB2) positive breast cancers, but its functions in HER2 positive breast cancer are unclear. The loss of FOXA1 results in a decrease in the viability of HER2 positive and HER2 amplified cell lines suggesting that FOXA1 may have an important role in HER2 positive breast cancers. In this report, we examined patient-derived single-cell RNA sequencing and spatial transcriptomics data and demonstrated that FOXA1 is co-expressed with ErbB2 in HER2 positive breast cancers. Knocking down FOXA1 expression led to the reduction of HER2 expression and signaling. Chromatin Immunoprecipitation Sequencing (ChIP-seq) and Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq) identified FOXA1 binding motifs in the ErbB2 promoter and regulatory element regions, which controlled ErbB2 gene expression. Interestingly, the knockdown of FOXA1 increased Epithelial Mesenchymal Transition (EMT) signaling and inhibited luminal tumor differentiation. Furthermore, FOXA1 and TRPS1 regulated TEAD/YAP-TAZ activity. Taken together, our data demonstrate that FOXA1 is required for HER2 expression and luminal identity in HER2+ breast cancer.
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Project description:In this study, we characterize the fusion protein produced by the EPC1-PHF1 translocation in Low Grade Endometrial Stromal Sarcoma (LG-ESS) and Ossifying FibroMyxoid Tumors (OFMT). We express the fusion protein and necessary controls in K562 Cells. The fusion protein assembles a mega-complex harboring both NuA4/TIP60 and PRC2 subunits and enzymatic activities and leads to mislocalization of chromatin marks in the genome, linked to aberrant gene expression.
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