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Increase of blood CSF3R+ myeloid-derived suppressor cell predicts breast cancer recurrence [Myeloid]

ABSTRACT: Increase of blood CSF3R+ myeloid-derived suppressor cell predicts breast cancer recurrence [Myeloid]

PROVIDER: PRJNA924729 | ENA |

REPOSITORIES: ENA

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Increase of blood CSF3R+ myeloid-derived suppressor cell predicts breast cancer recurrence

Project description:Increase of blood CSF3R+ myeloid-derived suppressor cell predicts breast cancer recurrence

| PRJNA924714 | ENA

Increase of blood CSF3R+ myeloid-derived suppressor cell predicts breast cancer recurrence [Immune]

Project description:Increase of blood CSF3R+ myeloid-derived suppressor cell predicts breast cancer recurrence [Immune]

| PRJNA924726 | ENA

Increase of blood CSF3R+ myeloid-derived suppressor cell predicts breast cancer recurrence [Myeloid]

Project description:Early detection of recurrence by using specific biomarkers is still a clinically unmet need although methodologies for monitoring tumor markers, cell-free DNA and circulating tumor cells have been established for decades. Because recurrence is developed from metastatic or dormant cancer cells that are under immune surveillance, alteration in the population and function of immune cells may promote recurrence. In this study, we utilized an animal model to imitate breast tumor recurrence after surgical resection and investigated the abundance and gene expression profile of immune cells by using two NanoString Panels. Our results showed that myeloid-derived-suppressor cells (MDSC) were significantly increased during recurrence. Comparison of our NanoString data with a single-cell RNA sequencing dataset of MDSC in another spontaneous breast cancer model identified colony-stimulating factor 3 receptor (Csf3r)-positive MDSC as a potential marker to predict tumor recurrence. In vitro experiments demonstrated that Csf3R+ MDSC exhibited enhanced ROS levels and stronger T cell suppression ability. Furthermore, these findings were validated in two published PBMC databases.

2024-08-18 | GSE223028 | GEO

Increase of blood CSF3R+ myeloid-derived suppressor cell predicts breast cancer recurrence [Immune]

2024-08-18 | GSE223025 | GEO

Increase of blood CSF3R+ myeloid-derived suppressor cell predicts breast cancer recurrence

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

2024-08-18 | GSE223029 | GEO

RUNX1-ETO translocations must proceed CSF3R mutations to promote acute myeloid leukemia development

Project description:Acute myeloid leukemia (AML) is a deadly blood cancer character by an overproduction of immature myeloid cells. AML has a high degree of genetic diversity, and the presence or absence of particular genetic alterations can greatly impact prognosis. In AML, patients with CSF3R mutations exhibit high relapse rates and poor overall survival. A recent study found that 90.5% of patients with CSF3R mutations had cooccurring RUNX1-ETO (8;21), CBFB-MYH11, or CEBPA mutations7. The RUNX1-ETO and CBFB-MYH11 translocations disrupt the core binding factor complex, an important transcriptional regulator in myeloid development. In this study, we evaluated how RUNX1-ETO modifies CSF3RT618I-driven transcriptional changes to promote the production of myeloblasts in AML. We find that RUNX1-ETO accelerates CSF3R-driven oncogenesis both in vitro and in vivo. Furthermore, RUNX1-ETO impairs the ability of CSF3R to drive myeloid differentiation associated transcriptional programs resulting in the production of immature myeloblasts which characterize this disease.

2023-10-11 | GSE218829 | GEO

CEBPA Dysfunction Intiates CSF3R Mutant Acute Myeloid Leukemia Through Disruption of Myeloid Lineage Enhancers (Microarray)

Project description:Acute Myeloid Leukemia (AML) develops due to the acquisition of mutations from multiple functional classes. Here, we demonstrate that activating mutations in the granulocyte colony stimulating factor receptor (CSF3R), cooperate with loss of function mutations in the transcription factor CEBPA to promote acute leukemia development. Terminal myeloid differentiation in response to granulocyte colony-stimulating factor signaling requires wild type CEBPA and is blocked by mutations in CEBPA. Inhibition of the histone demethylase LSD1, restores differentiation and in combination with JAK/STAT blockade, produces significant disease response in vivo. Mutant CEBPA blocks myeloid differentiation by preventing the activation of differentiation-associated enhancers. As enhancer activation precedes promoter activation, CEBPA mutations must occur prior to CSF3R mutations to effectively block differentiation and promote leukemia formation in vivo. This study demonstrates that order-dependent oncogene interaction is a fundamental process in AML. Dissecting this process is critical for understanding disease evolution to enable the development of effective therapeutics.

2019-12-02 | GSE122161 | GEO

CEBPA Dysfunction Intiates CSF3R Mutant Acute Myeloid Leukemia Through Disruption of Myeloid Lineage Enhancers (ChIP-seq)

2019-12-02 | GSE122162 | GEO

Transcription profiling of human colon cancer patients metastasis gene expression profile predicts recurrence and death in colon cancer patients

Project description:This SuperSeries is composed of the following subset Series:; GSE17536: Metastasis Gene Expression Profile Predicts Recurrence and Death in Colon Cancer Patients (Moffitt Samples); GSE17537: Metastasis Gene Expression Profile Predicts Recurrence and Death in Colon Cancer Patients (VMC Samples) Experiment Overall Design: Refer to individual Series

2009-11-23 | E-GEOD-17538 | biostudies-arrayexpress

CEBPA Dysfunction Intiates CSF3R Mutant Acute Myeloid Leukemia Through Disruption of Myeloid Lineage Enhancers (RNA-seq - simultaneous)

2019-12-02 | GSE122164 | GEO