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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE223025 | GEO | 2024/08/18

REPOSITORIES: GEO

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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.

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

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CSF3R T618I collaborates with RUNX1-RUNX1T1 to expand hematopoietic progenitors and sensitizes to GLI-inhibition

Project description:Activating CSF3R mutations are recurrent in AML with t(8;21) translocation. However, the nature of oncogenic collaboration between alterations of CSF3R and the t(8;21) associated RUNX1-RUNX1T1 fusion remains unclear. In CD34+ hematopoietic stem and progenitor cells from healthy donors, double oncogene expression led to a clonal advantage, increased self-renewal potential, as well as blast-like morphology and distinct immunophenotype. Gene expression profiling revealed hedgehog-signaling as a potential mechanism, with upregulation of GLI2 constituting a putative pharmacological target. Both primary hematopoietic cells and the t(8;21) positive AML cell line SKNO-1 showed increased sensitivity to the GLI-inhibitor GANT61 when expressing CSF3R T618I. Our findings suggest that during leukemogenesis the RUNX1-RUNXT1 fusion and CSF3R mutation act in a synergistic manner to alter hedgehog signaling which can be exploited therapeutically.

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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.

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Human G-MDSCs are Neutrophils at Distinct Maturation Stages that Promote Tumor Growth and Immune Cell Exclusion in Breast Cancer

Project description:Myeloid-derived suppressor cells (MDSC) are known to contribute to immune evasion in cancer. However, the function of the human granulocytic (G)-MDSC subset during tumor progression is largely unknown, and there are no established markers for their identification in human tumor specimens. Using gene expression profiling, mass cytometry and tumor microarrays, we here demonstrate that human G-MDSCs occur as neutrophils at distinct maturation stages, with a disease-specific profile. G-MDSCs derived from patients with metastatic breast cancer (MBC) and malignant melanoma display a unique immature neutrophil profile, that is more similar to healthy donor neutrophils than to G-MDSCs from sepsis patients. Finally, we show that primary G-MDSCs from MBC patients co-transplanted with breast cancer cells, promote tumor growth and affect vessel formation, leading to myeloid immune cell exclusion. Our findings reveal a role for human G-MDSC in tumor progression and have clinical implications also for targeted immunotherapy.

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Mutant-SETBP1 activates transcription of Myc programs to accelerate CSF3R-driven myeloproliferative neoplasms

Project description:Colony stimulating factor 3 receptor (CSF3R) mutations lead to JAK pathway activation and are the molecular hallmark of chronic neutrophilic leukemia (CNL). Approximately half of CNL patients also have mutations in SET binding protein 1 (SETBP1). In this study, we developed models of SETBP1-mutant leukemia to understand the role that SETBP1 plays in CNL. SETBP1 mutations promote self-renewal of CSF3R-mutant hematopoietic progenitors in vitro and prevent cells from undergoing terminal differentiation. In vivo, SETBP1 mutations accelerate leukemia progression, leading to the rapid development of hepatosplenomegaly and granulocytosis. Through transcriptomic and epigenomic profiling, we found that SETBP1 enhances progenitor-associated programs—most strongly upregulating Myc and Myc target genes. In summary, we find that SETBP1 mutations promote aggressive hematopoietic cell expansion when expressed with mutant CSF3R through the upregulation of Myc-associated gene expression programs.

2022-05-11 | GSE189502 | GEO

Tumor Intrinsic Subtype is Reflected in Cancer-Adjacent Benign Tissue

Project description:Introduction: Overall survival of early-stage breast cancer (BC) patients is similar for those who undergo breast conserving therapy (BCT) and mastectomy, however, 10-15% of women undergoing BCT suffer ipsilateral breast tumor recurrence. The risk of recurrence may vary with age or breast cancer subtype. Understanding the gene expression of the cancer-adjacent tissue and/or stromal response to specific tumor subtypes is important for developing clinical strategies to reduce recurrence risk. Methods: We studied gene expression data in cancer-adjacent tissue from 158 BC patients. Complementary in vitro cocultures were used to study cell-cell communication between fibroblasts and specific breast cancer subtypes. Results: Our results suggest that intrinsic tumor subtypes are reflected in histologically normal cancer-adjacent tissue. Gene expression of cancer-adjacent tissues shows that triple negative (Claudin-low or Basal-like tumors) exhibit increased expression of genes involved in inflammation and immune response. While such changes could reflect distinct immune populations present in the microenvironment of different breast cancer subtypes, altered immune response gene expression was also observed in cocultures in the absence of immune cell infiltrates, emphasizing that these inflammatory mediators are secreted by breast-specific cells. In addition, while triple negative BCs are associated with upregulated immune response genes, Luminal breast cancers are more commonly associated with estrogen-response in adjacent tissues. Conclusions: Specific characteristics of BCs are reflected in the surrounding benign tissue. This commonality between tumor and surrounding tissue may underlie second primaries and local recurrences. Biomarkers derived from cancer-adjacent tissue may be helpful in defining personalized surgical strategies or in predicting recurrence risk. reference x sample

2014-04-30 | E-GEOD-50939 | biostudies-arrayexpress

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