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Aberrant extrafollicular B cells, immune dysfunction and myeloid inflammation precede malignancy in Waldenstrom macroglobulinemia

ABSTRACT: Aberrant extrafollicular B cells, immune dysfunction and myeloid inflammation precede malignancy in Waldenstrom macroglobulinemia

PROVIDER: PRJNA742751 | ENA |

REPOSITORIES: ENA

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Aberrant extrafollicular B cells, immune dysfunction and myeloid inflammation precede malignancy in Waldenstrom macroglobulinemia

Project description:Waldenstrom macroglobulinemia (WM) and its precursor IgM gammopathy are distinct disorders characterized by the growth of mature IgM-expressing B cell clone predominantly in the bone marrow. Here we show that these disorders originate in the setting of expansion of genomically aberrant extrafollicular B cells, immune dysfunction and myeloid inflammation that begins before the expansion of the malignant clone. Host response to these early lesions involves the induction of tumor-specific T cell immunity that may include MYD88 mutation-specific responses. Hematopoietic progenitors carry the oncogenic MYD88 mutations characteristic of the malignant WM clone. These data provide an example of how oncogenic mutations in earlier progenitors may create the milieu promoting the evolution of malignant phenotype in differentiated cells.

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Aberrant Extrafollicular B Cells, Immune Dysfunction, Myeloid Inflammation, and MyD88-Mutant Progenitors Precede Waldenstrom Macroglobulinemia.

Project description:Waldenstrom macroglobulinemia (WM) and its precursor IgM gammopathy are distinct disorders characterized by clonal mature IgM-expressing B-cell outgrowth in the bone marrow. Here, we show by high-dimensional single-cell immunogenomic profiling of patient samples that these disorders originate in the setting of global B-cell compartment alterations, characterized by expansion of genomically aberrant extrafollicular B cells of the nonmalignant clonotype. Alterations in the immune microenvironment preceding malignant clonal expansion include myeloid inflammation and naïve B- and T-cell depletion. Host response to these early lesions involves clone-specific T-cell immunity that may include MYD88 mutation-specific responses. Hematopoietic progenitors carry the oncogenic MYD88 mutations characteristic of the malignant WM clone. These data support a model for WM pathogenesis wherein oncogenic alterations and signaling in progenitors, myeloid inflammation, and global alterations in extrafollicular B cells create the milieu promoting extranodal pattern of growth in differentiated malignant cells.SignificanceThese data provide evidence that growth of the malignant clone in WM is preceded by expansion of extrafollicular B cells, myeloid inflammation, and immune dysfunction in the preneoplastic phase. These changes may be related in part to MYD88 oncogenic signaling in pre-B progenitor cells and suggest a novel model for WM pathogenesis. This article is highlighted in the In This Issue feature, p. 549.

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Project description:microRNA-155 acts as an oncogenic miRNA in B-cell lymphoproliferative disorders including Waldenstrom Macroglobulinemia (WM) and Chronic Lymphocytic Leukemia (CLL). we used an 8-mer LNA (locked nucleic acid) phosphorothioate oligonucleotide targeting the seed region of miR-155 to effectively antagonize in vitro tumor growth in WM.

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