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Expression data from bone marrow mesenchymal stromal cells obtained from healthy donors and myeloma patients

ABSTRACT: Multiple myeloma (MM) is a B-cell neoplasm characterized by clonal expansion of malignant plasma cells (MM cells) in the bone marrow (BM) compartment, where they acquire resistance to chemotherapy-mediated apoptosis. Natural history of patients include a premalignant stage, the MM diagnosis, the treatment, the remission, and for most of them the relapse. BM mesenchymal stromal cells (MSC) from newly diagnosed MM patients are functionally different from healthy donors (HD) MSC and display a distinct transcriptome. They have been largely involved in MM pathogenesis and chemoresistance acquisition. In order to determine if MM-MSC also participate to relapse, we focused on the characterization of MSC from patients with MM at different stages of the disease. We obtained patient MSC’s samples at diagnosis, at 2 years after intensive treatment without relapse and at the relapse from an intensive treatment. We used MCS from HD as control. All MSC were able to support MM cells growth through released factors, and still multipotent since able to differentiate into osteoblast and adipocyte. A transcriptomic analysis between these groups reveals differences in gene expression between HD and MM MSC whatever stage of the disease, suggesting that the difference in gene expression in MM-MSC persist with time. These data demonstrate an imprinting of MSC as soon as they were in contact with MM cells, which persist even after the disappearance of MM cells. This imprinting is in favour of an easier differentiation towards adipogenesis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE146649 | GEO | 2021/12/30

REPOSITORIES: GEO

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Project description:A rare complication of multiple myeloma is a secondary extramedullary involvement, and the skin is one of the possible sites, due to the physiological homing of plasma cells (PCs) into the skin. The article reports a case of a relapsed refractory MM patient, who developed a cutaneous localization after 16 months from the diagnosis under Bortezomib treatment without a leukemic phase. Patient was refractory to Bortezomib. We analyzed the gene expression profiles, the immunophenotypic and immunohistochemistry profiles of MM cells across the course of the disease at the bone marrow and skin localization. Data obtained were further expanded by an immunohistochemistry analysis on selected molecules in a large cohort of MM patients with cutaneous localization. In particular we focused on the expression of chemokines and chemokine receptors involved in the PC skin homing. The mechanisms behind the extramedullary spread and the formation of localizations outside the BM are not completely understood. Several studies investigated the expression profile of myeloma cells in the extramedullary localization by immunohistochemistry without a prospective molecular and immunohistochemistry study across the progression of the disease and consequently the development of extramedullary localization. This case indicates that the skin homing of MM cells could be related to the high CCR10 expression of at the diagnosis and relapse and the loss of CXCR4 surface expression across the progression of the disease in the contest of Bortezomib resistance. This data was further confirmed in a larger series of patients. Moreover, high expression of CD44, together with the down-regulation of CD54 and the lack of expression of CD56 by MM cells in the BM relapse with the re-acquisition of both antigens during the cutaneous relapse may be the mechanism that drives the escape from BM of PCs and their localization into the skin. Our data have identified a possible mechanism that drives the escape from BM of myeloma cells and their localization into the skin.

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Expression data from bone marrow mesenchymal stromal cells obtained from healthy donors and myeloma patients

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