Titlebook: Waldenström’s Macroglobulinemia; Véronique Leblond,Steve Treon,Meletios Dimoploulos Book 2017 Springer International Publishing Switzerlan

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艺术

Genetic and Signaling Abnormalities in Waldenstrom’s Macroglobulinemiaent and bone marrow infiltration at diagnosis. Mutant MYD88 drives critical BTK and HCK signaling and is highly predictive of response to the BTK inhibitor ibrutinib. Additional characteristics of these and other recurrent genomic alterations such as ARID1A and CD79B mutations as well as chromosome 6q deletions are discussed.

Preamble

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Genetic and Signaling Abnormalities in Waldenstrom’s Macroglobulinemiaent and bone marrow infiltration at diagnosis. Mutant MYD88 drives critical BTK and HCK signaling and is highly predictive of response to the BTK inhibitor ibrutinib. Additional characteristics of these and other recurrent genomic alterations such as ARID1A and CD79B mutations as well as chromosome 6q deletions are discussed.

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Molecular Pathways in Growth and Survival: Epigenomicsuch as Waldenstrom’s Macroglobulinemia (WM). Importantly, recent evidences have suggested that WM cells present with an aberrant histone acetylation status, and this may be due to deregulated microRNA profiling within the WM tumor clone, thus providing the preclinical support for using miRNA-based therapies in this disease.

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Hyperviscosity Syndrome, Cold Agglutinin Hemolytic Anemia, and Cryoglobulinemiatial presentation. Prompt recognition and therapy are keys to effective management. Urgent plasmapheresis is indicated for symptomatic hyperviscosity syndrome (HVS). Proper collection of blood specimens is essential for accurate interpretation in cold agglutinin and cryoglobulinemia patients.