Download Plasma Cell Dyscrasias by Aldo M. Roccaro, Irene M. Ghobrial PDF

By Aldo M. Roccaro, Irene M. Ghobrial

This ebook offers a concise assessment of the cutting-edge within the biology and therapy of plasma telephone malignancies, a heterogeneous workforce of ailments basically characterised via the presence of clonal plasma cells in the bone marrow or extramedullary websites. The plasma mobilephone dyscrasias investigated comprise monoclonal gammopathy of undetermined value (MGUS), a number of myeloma, plasmacytoma, immunoglobulin deposition illnesses (primary amyloidosis and systemic gentle and heavy chain deposition diseases), and Waldenström’s macroglobulinemia. on the subject of a number of myeloma, the insurance levels from genomic aberrations and microRNAs to therapy for various sufferer teams, upcoming novel cures, immunotherapy, and transplantation. The publication displays the numerous learn advances accomplished during this box in the past few years, that have superior our figuring out of the molecular mechanisms answerable for the pathogenesis of plasma phone dyscrasias.

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Fonseca R, Debes-Marun CS, Picken EB et al (2003) The recurrent IgH translocations are highly associated with nonhyperdiploid variant multiple myeloma. Blood 102(7):2562–2567 32. Pawlyn C, Melchor L, Murison A et al (2015) Coexistent hyperdiploidy does not abrogate poor prognosis in myeloma with adverse cytogenetics and may precede IGH translocations. Blood 125(5):831–840 33. Chng WJ, Kumar S, Vanwier S et al (2007) Molecular dissection of hyperdiploid multiple myeloma by gene expression profiling.

Leukemia 22(5):1044–1052 55. Lode L, Eveillard M, Trichet V et al (2010) Mutations in TP53 are exclusively associated with del(17p) in multiple myeloma. Haematologica 95(11):1973–1976 56. Drach J, Ackermann J, Fritz E et al (1998) Presence of a p53 gene deletion in patients with multiple myeloma predicts for short survival after conventional-dose chemotherapy. Blood 92 (3):802–809 57. Lawrence MS, Stojanov P, Polak P et al (2013) Mutational heterogeneity in cancer and the search for new cancer-associated genes.

16. Walker BA, Wardell CP, Johnson DC et al (2013) Characterization of IGH locus breakpoints in multiple myeloma indicates a subset of translocations appear to occur in pregerminal center B cells. Blood 121(17):3413–3419 17. Santra M, Zhan F, Tian E, Barlogie B, Shaughnessy J Jr (2003) A subset of multiple myeloma harboring the t(4;14)(p16;q32) translocation lacks FGFR3 expression but maintains an IGH/MMSET fusion transcript. Blood 101(6):2374–2376 18. Keats JJ, Maxwell CA, Taylor BJ et al (2005) Overexpression of transcripts originating from the MMSET locus characterizes all t(4;14)(p16;q32)-positive multiple myeloma patients.

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