Quantification of number of CD38 sites on bone marrow plasma cells in patients with light chain amyloidosis and smoldering multiple myeloma

Kriegsmann, Katharina; Dittrich, Tobias; Neuber, Brigitte; Awwad, Mohamed H.S.; Hegenbart, Ute; Goldschmidt, Hartmut; Hillengaß, Jens; Hose, Dirk; Seckinger, Anja; Müller‐Tidow, Carsten; Ho, Anthony D.; Schönland, Stefan; Hundemer, Michael

doi:10.1002/cyto.b.21636

Cited by 13 publications

(14 citation statements)

References 33 publications

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“…First, these antibodies possess classic Fc-dependent immune effector mechanisms for cancer cell lysis and removal, typically antibody-dependent cellular cytotoxicity (ADCC) (Frerichs et al, 2018;van de Donk et al, 2018). The effectiveness of the isatuximab-mediated ADCC correlates with cell-surface CD38 levels (Kriegsmann et al, 2018). Notably, since CD38 is highly expressed on multiple myeloma cells, with relatively low expression on normal myeloid or lymphoid cells (Chini et al, 2018;Krejcik et al, 2016), multiple myeloma cells are specifically susceptible to CD38 depletion.…”

Section: Cd38-cd38mentioning

confidence: 99%

Subcellular compartmentalization of NAD+ and its role in cancer: A sereNADe of metabolic melodies

Zhu

Liu

Park

et al. 2019

Pharmacology & Therapeutics

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Nicotinamide adenine dinucleotide (NAD +) is an essential biomolecule involved in many critical processes. Its role as both a driver of energy production and a signaling molecule underscores its importance in health and disease. NAD + signaling impacts multiple processes that are dysregulated in cancer, including DNA repair, cell proliferation, differentiation, redoxregulation, and oxidative stress. Distribution of NAD + is highly compartmentalized, with each subcellular NAD + pool differentially regulated and preferentially involved in distinct NAD +-dependent signaling or metabolic events. Emerging evidence suggests that targeting NAD + metabolism is likely to repress many specific mechanisms underlying tumor development and progression, including proliferation, survival, metabolic adaptations, invasive capabilities, heterotypic interactions with the tumor microenvironment, and stress response including notably DNA maintenance and repair. Here we provide a comprehensive overview of how compartmentalized NAD + metabolism in mitochondria, nucleus, cytosol, and extracellular space impacts cancer formation and progression, along with a discussion of the therapeutic potential of NAD +-targeting drugs in cancer.

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Section: Cd38-cd38mentioning

confidence: 99%

Subcellular compartmentalization of NAD+ and its role in cancer: A sereNADe of metabolic melodies

Zhu

Liu

Park

et al. 2019

Pharmacology & Therapeutics

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“…CD38 is a transmembrane glycoprotein molecule that plays an important role in cell adhesion and is heavily present in clonal PCs [ 98 ]. Daratumumab is a humanized monoclonal antibody against CD38 that can initiate antibody-mediated cellular toxicity along with complement-mediated cytotoxicity [ 99 ]. After achieving a satisfactory outcome in treating MM, daratumumab has been used in clinical trials of AL amyloidosis treatment recently, mainly for relapsed/refractory disease.…”

Section: Monoclonal Antibodies Targeting Cd38mentioning

confidence: 99%

Current Updates on the Management of AL Amyloidosis

El‐Sayed¹,

Usher²,

Habib³

et al. 2021

J Hematol

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Systemic immunoglobulin light chain (AL) amyloidosis is a rare but fatal disease. It results from clonal proliferation of plasma cells with excessive production of insoluble misfolded proteins that aggregate in the extracellular matrix, causing damage to the normal architecture and function of various organs. For decades, treatment for AL amyloidosis was based mainly on therapeutic agents previously studied for its more common counterpart, multiple myeloma. As the prevalence and incidence of AL amyloidosis have increased, ongoing research has been conducted with treatments typically used in myeloma with varying success. In this review, we focus on current treatment strategies and updates to clinical guidelines and therapeutics for AL amyloidosis.

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“…Daratumumab, a monoclonal CD38 antibody, has also shown promise outcome in t(11;14)-positive patients as a salvage therapeutic modality, demonstrating a longer hemEFS [ 30 ]. This may be explained by the higher CD38 expression level in patients with t(11;14) [ 45 ], which can promote the antibody-dependent cytotoxicity effect of daratumumab [ 46 ].…”

Section: Immunoglobulin Heavy Chain Translocationmentioning

confidence: 99%

Genetic pathogenesis of immunoglobulin light chain amyloidosis: basic characteristics and clinical applications

2021

Exp Hematol Oncol

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Immunoglobulin light chain amyloidosis (AL) is an indolent plasma cell disorder characterized by free immunoglobulin light chain (FLC) misfolding and amyloid fibril deposition. The cytogenetic pattern of AL shows profound similarity with that of other plasma cell disorders but harbors distinct features. AL can be classified into two primary subtypes: non-hyperdiploidy and hyperdiploidy. Non-hyperdiploidy usually involves immunoglobulin heavy chain translocations, and t(11;14) is the hallmark of this disease. T(11;14) is associated with low plasma cell count but high FLC level and displays distinct response outcomes to different treatment modalities. Hyperdiploidy is associated with plasmacytosis and subclone formation, and it generally confers a neutral or inferior prognostic outcome. Other chromosome abnormalities and driver gene mutations are considered as secondary cytogenetic aberrations that occur during disease evolution. These genetic aberrations contribute to the proliferation of plasma cells, which secrete excess FLC for amyloid deposition. Other genetic factors, such as specific usage of immunoglobulin light chain germline genes and light chain somatic mutations, also play an essential role in amyloid fibril deposition in AL. This paper will propose a framework of AL classification based on genetic aberrations and discuss the amyloid formation of AL from a genetic aspect.

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Quantification of number of CD38 sites on bone marrow plasma cells in patients with light chain amyloidosis and smoldering multiple myeloma

Cited by 13 publications

References 33 publications

Subcellular compartmentalization of NAD+ and its role in cancer: A sereNADe of metabolic melodies

Subcellular compartmentalization of NAD+ and its role in cancer: A sereNADe of metabolic melodies

Current Updates on the Management of AL Amyloidosis

Genetic pathogenesis of immunoglobulin light chain amyloidosis: basic characteristics and clinical applications

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