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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE124438 | GEO | 2019/02/26

REPOSITORIES: GEO

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

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.

2019-02-26 | GSE124437 | GEO

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

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

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

Phenotypic and genomic analysis of multiple myeloma minimal residual disease clonal plasma cells: a new model to understand chemoresistance

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

2016-01-28 | GSE70399 | GEO

Phenotypic and genomic analysis of multiple myeloma minimal residual disease clonal plasma cells: a new model to understand chemoresistance

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-01-28 | E-GEOD-70399 | biostudies-arrayexpress

Phenotypic and genomic analysis of multiple myeloma minimal residual disease clonal plasma cells: a new model to understand chemoresistance [HuGene-1_0 Expression]

Project description:Persistence of chemoresistant minimal residual disease (MRD) plasma cells (PCs) relates to inferior survival in multiple myeloma (MM). MRD PCs are therefore a minor clone able to recapitulate the initial tumor burden at relapse and accordingly, its characterization may represent a unique model to understand chemoresistance; unfortunately, the MRD clone has never been biologically investigated. Here, we compared the antigenic profile of MRD vs. diagnostic clonal PCs in 40 elderly MM patients enrolled in the GEM2010MAS65 study, and showed that the MRD clone is enriched by cells over-expressing integrins (CD11a/CD11c/CD29/CD49d/CD49e), chemokine receptors (CXCR4) and adhesion molecules (CD44/CD54). Genetic profiling of MRD vs. diagnostic PCs showed identical copy number alterations (CNAs) in 3/8 cases, 2 patients with linear acquisition of additional CNAs in MRD clonal PCs, and 3 cases with variable acquisition and loss of CNAs over time. The MRD clone showed significant downregulation of genes particularly related to protein processing in endoplasmic reticulum, as well as novel deregulated genes such as ALCAM that is prognostically relevant in MM and identifies chemoresistant PCs in vitro. Together, we show that therapy-induced clonal selection is already present at the MRD stage, in which chemoresistant PCs show a specific phenotypic signature that may result from the persistence of clones with different genetic and gene expression profiles.

2016-01-28 | GSE70398 | GEO

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