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Awakening and Eliminating Dormant Cancer Cells: A Foundation for Resistance Removal and Recurrence-Free Recovery [ChIP-seq]

ABSTRACT: Awakening and Eliminating Dormant Cancer Cells: A Foundation for Resistance Removal and Recurrence-Free Recovery [ChIP-seq]

PROVIDER: PRJNA690627 | ENA |

REPOSITORIES: ENA

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Awakening and Eliminating Dormant Cancer Cells: A Foundation for Resistance Removal and Recurrence-Free Recovery

Project description:Awakening and Eliminating Dormant Cancer Cells: A Foundation for Resistance Removal and Recurrence-Free Recovery

| PRJNA690604 | ENA

Awakening and Eliminating Dormant Cancer Cells: A Foundation for Resistance Removal and Recurrence-Free Recovery [ATAC-seq]

Project description:Awakening and Eliminating Dormant Cancer Cells: A Foundation for Resistance Removal and Recurrence-Free Recovery [ATAC-seq]

| PRJNA690628 | ENA

Awakening and Eliminating Dormant Cancer Cells: A Foundation for Resistance Removal and Recurrence-Free Recovery [RNA-seq]

Project description:Awakening and Eliminating Dormant Cancer Cells: A Foundation for Resistance Removal and Recurrence-Free Recovery [RNA-seq]

| PRJNA690630 | ENA

Awakening and Eliminating Dormant Cancer Cells: A Foundation for Resistance Removal and Recurrence-Free Recovery [ChIP-seq]

Project description:Tumor therapy mainly targets the tumor bulk, but tends to fail to eradicate the small resistant population of dormant cancer cells (DCCs) that enable relapse and/or metastasis beyond therapy. Using chemoradiotherapy resistant assay and SETD4 expression of a histone lysine methyltransferase, DCCs with high capacity of tumor-initiation and tumorsphere formation were isolated from three types of breast tumors. Exogenous DEK, a nuclear protein, activated the DCCs by binding to open chromatin which decreased SETD4, up-regulated the MYC and down-regulated the P53 signaling pathways. DEK-containing exosomes in blood highly correlate with tumor progress and exosomal DEK promotes tumor relapse and metastasis beyond chemoradiotherapy. Beyond activation, these formerly dormant cancer cells lost their chemoradiotherapy resistance. In treatment of DEK-containing exosomes plus chemoradiotherapy in mice, three types of breast tumors were eliminated without recurrence. Prior DCCs reactivation, as triggered by exogenous DEK may provide treatment options that eliminate both metastasis and recurrence potential.

2024-01-07 | GSE164427 | GEO

Awakening and Eliminating Dormant Cancer Cells: A Foundation for Resistance Removal and Recurrence-Free Recovery [ATAC-seq]

2024-01-07 | GSE164426 | GEO

Awakening and Eliminating Dormant Cancer Cells: A Foundation for Resistance Removal and Recurrence-Free Recovery [RNA-seq]

2024-01-07 | GSE164428 | GEO

Awakening and Eliminating Dormant Cancer Cells: A Foundation for Resistance Removal and Recurrence-Free Recovery

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-01-07 | GSE164429 | GEO

Comparative transcriptome of proliferative cells, dormant cells and awaken cells throught a DDR1 depletion

Project description:The goal of this study is to compare the trancriptome of proliferative THEP3 cells to their dormant counterpart DHEP3 and an awaken version through DDR1 receptor depletion (shRNA control verus shRNA DDR1) to identify target genes involved in the dormancy state and the awakening process from where metatsiss will arise.

2021-10-20 | GSE182890 | GEO

Unperturbed dormancy recording reveals stochastic awakening strategies in endocrine treated breast cancer cells

Project description:Hormone dependent breast cancer (HDBC) is the most commonly diagnosed tumor type in women. Adjuvant endocrine therapies (ET) have been the cornerstone in the clinical management of HDBC patients for over forty years. A vast proportion of HDBC patients incur long periods of clinical dormancy following ET, with tumour awakening appearing at a steady pace for up to 25 years (Pan et al., 2017). Extensive genomic studies have demonstrated that 15-30% of clinical relapses develop recurrent genomic changes which contribute to drug resistance (i.e. ESR1 activating mutations) (Bertucci et al., 2019; Magnani et al., 2017; Razavi et al., 2018). However, even in these cases, there is no conclusive evidence around the pre-existence vs. de novo nature of these events. Here, we analyzed histone PTMs in dormant and awakened breast cancer cells treated with endocrine therapy.

2024-05-23 | PXD038030 | Pride

Awakening dormant glycosyltransferases in CHO cells with CRISPRa.

Project description:Chinese hamster ovary (CHO) cells are the preferred workhorse for the biopharmaceutical industry, and CRISPR/Cas9 has proven powerful for generating targeted gene perturbations in CHO cells. Here, we expand the CRISPR engineering toolbox with CRISPR activation (CRISPRa) to increase transcription of endogenous genes. We successfully increased transcription of Mgat3 and St6gal1, and verified their activity on a functional level by subsequently detecting that the appropriate glycan structures were produced. This study demonstrates that CRISPRa can make targeted alterations of CHO cells for desired phenotypes.

| S-EPMC7261405 | biostudies-literature

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