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Transcriptomic Profiling of Circulating Tumor Cells in Multiple Myeloma: A New Model to Understand Disease Dissemination II

ABSTRACT: Transcriptomic Profiling of Circulating Tumor Cells in Multiple Myeloma: A New Model to Understand Disease Dissemination II

PROVIDER: PRJNA512011 | ENA |

REPOSITORIES: ENA

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Transcriptomic Profiling of Circulating Tumor Cells in Multiple Myeloma: A New Model to Understand Disease Dissemination II

Project description:The number of peripheral blood (PB) circulating tumor cells (CTCs) predicts risk of transformation in smoldering multiple myeloma (MM) and survival in active MM. Growing evidence suggests that as the tumor progresses and the microenvironment becomes hypoxic, clonal plasma cells (PCs) constantly invade new regions of the bone marrow (BM) through induced systemic recirculation. Of note, the frequency of CTCs is typically low and thus, it could be hypothesized that the dissemination of MM is made by few tumor cells with unique features that induce them to egress the BM and spread the disease through PB. This hypothesis has not been demonstrated because the molecular profile of CTCs in MM has not been investigated. We used gene expression profiling (GEP) arrays to identify gene regulatory networks related to disease dissemination by comparing the molecular profile of CTCs with patient-matched BM clonal PCs.

2019-02-26 | GSE124436 | GEO

Transcriptomic Profiling of Circulating Tumor Cells in Multiple Myeloma: A New Model to Understand Disease Dissemination I

2019-02-26 | GSE124435 | GEO

Transcriptomic Profiling of Circulating Tumor Cells in Multiple Myeloma: A New Model to Understand Disease Dissemination III

2019-02-26 | GSE124437 | GEO

Transcriptomic Profiling of Circulating Tumor Cells in Multiple Myeloma: A New Model to Understand Disease Dissemination

Project description:Transcriptomic Profiling of Circulating Tumor Cells in Multiple Myeloma: A New Model to Understand Disease Dissemination

| PRJNA512008 | ENA

Transcriptomic Profiling of Circulating Tumor Cells in Multiple Myeloma: A New Model to Understand Disease Dissemination III

Project description:Transcriptomic Profiling of Circulating Tumor Cells in Multiple Myeloma: A New Model to Understand Disease Dissemination III

| PRJNA512009 | ENA

Transcriptomic Profiling of Circulating Tumor Cells in Multiple Myeloma: A New Model to Understand Disease Dissemination I

Project description:Transcriptomic Profiling of Circulating Tumor Cells in Multiple Myeloma: A New Model to Understand Disease Dissemination I

| PRJNA512010 | ENA

Transcriptomic Profiling of Circulating Tumor Cells in Multiple Myeloma: A New Model to Understand Disease Dissemination II

Project description:Transcriptomic Profiling of Circulating Tumor Cells in Multiple Myeloma: A New Model to Understand Disease Dissemination II

| PRJNA512011 | ENA

Tissue-resident macrophages promote multiple myeloma early dissemination and progression via IL-6 and TNFa

Project description:Multiple myeloma (MM) is a plasma cell malignancy characterized by the presence of multiple foci in the skeleton. These distinct tumor foci indicate cycles of tumor growth and dissemination that seed new clusters and drives disease progression. Utilizing an intra-tibial Vk*MYC murine myeloma, we found that CD169 + radiation-resistant, tissue-resident macrophages (MPs) were critical for myeloma early dissemination and disease progression. While depletion of these MPs had no effect on tumor proliferation, it reduced myeloma BM egress and spreading to other bones, which improved overall survival as a single therapy and in combination with BM transplantation. Myeloma dissemination correlated with an increased inflammatory signature in BM MPs, as well as production of IL-6 and TNFα by tumor-associated MPs (TAMs). Exogenous i.v. IL-6 and TNFa could trigger myeloma intravasation in the BM by increasing vascular leakiness in the BM, and by enhancing myeloma motility by reducing CD138 adhesion. Moreover, mice lacking IL-6 had defects in myeloma dissemination as in MP-depleted recipients. While in TNFa or TNFaR deficient mice had defects in MM dissemination, engraftment was also impaired. These effects on myeloma dissemination required production of cytokines in the radiation-resistant compartment, containing these radiation-resistant BM MPs. Taken together, we propose BM egress of myeloma cells is regulated by localized inflammation in foci, driven in part by CD169 + MPs.

2021-06-09 | GSE176385 | GEO

Transcriptomic Profiling of Circulating Tumor Cells in Multiple Myeloma: A New Model to Understand Disease Dissemination

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

2019-02-26 | GSE124438 | GEO

Deciphering clonal evolution and dissemination of Multiple Myeloma cells in vivo

Project description:Deciphering clonal evolution and dissemination of Multiple Myeloma cells in vivo

| PRJNA495356 | ENA