Plasma Cell Dyscrasias - download pdf or read online

By Aldo M. Roccaro, Irene M. Ghobrial

ISBN-10: 3319403184

ISBN-13: 9783319403182

ISBN-10: 3319403206

ISBN-13: 9783319403205

This e-book presents a concise evaluate of the state-of-the-art within the biology and therapy of plasma cellphone malignancies, a heterogeneous team of ailments essentially characterised by way of the presence of clonal plasma cells in the bone marrow or extramedullary websites. The plasma telephone dyscrasias investigated comprise monoclonal gammopathy of undetermined importance (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 remedy for various sufferer teams, upcoming novel remedies, immunotherapy, and transplantation. The booklet displays the numerous learn advances completed during this box in past times few years, that have greater our realizing of the molecular mechanisms liable for the pathogenesis of plasma phone dyscrasias.

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These translocations lead to significant overexpression of MYC, probably resulting from juxtaposition of super-enhancers surrounding the partner gene to MYC locus. MYC translocations are associated with a poor outcome [25]. Genomic Aberrations in Multiple Myeloma 4 27 Hyperdiploidy Hyperdiploidy (HRD) is defined as a number of chromosomes between 48 and 74. HRD MM are characterized by multiple chromosomal gains, preferentially trisomy of chromosomes 3, 5, 7, 9, 11, 15, 19, and 21 [29]. The mechanism underlying this is not known but one hypothesis suggests that the gain of multiple whole chromosomes occurs during a single catastrophic mitosis rather than through the serial gain of chromosomes over time [30].

Similar to MGUS, miR-21 and the cluster miR-106a-92 were also found to be upregulated in MM, however, in addition, upregulation of miR-32 and the Oncomir-1 cluster miR-17-92 was also present which could indicate a possible role in the progression from MGUS to MM [26]. miR-21 was previously implicated in the oncogenic potential of STAT3 in MM where miR-21 induction by STAT3 represents an important survival stimulus for MM cells [34]. Roccaro et al. further defined the deregulation of miRNAs in MM while also elucidating the functional role of specific miRNAs by investigating their target genes [35].

These translocations can lead to deregulation of cyclins and oncogenes, such as FGFR3, MMSET, and MAF. , TP53, KRAS, NRAS, and FGFR3). Knowledge of the genetic events that underlie disease progression in MM is incomplete. Nevertheless, specific chromosomal abnormalities, such as 17p deletion and 1q amplification are associated with particularly poor prognosis and increased incidence of extramedullary disease. Genetics and epigenetics are inherently linked and in this chapter we will focus on the epigenetics as a mechanism of regulation in this genomically complex disease.

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

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