Plasma cell dyscrasias include monoclonal gammopathy of undermined significance (MGUS), multiple myeloma (MM), plasmacytoma, Waldenström macroglobulinemia (WM), amyloidosis (AL), and POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy monoclonal gammopathy, and skin changes). MGUS, smoldering MM, and symptomatic MM represent a spectrum of the same disease. MGUS is characterized by a serum monoclonal protein <30 g/L, <10% plasma cells in the bone marrow, and absence of end-organ damage (Kyle and Rajkumar, 2009). Smoldering (asymptomatic) MM is characterized by having a serum immunoglobulin (Ig) G or IgA monoclonal protein of 30 g/L or higher and/or 10% or more plasma cells in the . . . [Full Text of this Article]


Plasma cell development
 

Etiology and incidence
 

Molecular pathogenesis
 
Genetic and epigenetic regulation of MM
Epigenetics in MM
Role of the BM microenvironment in MM pathogenesis
Role of adhesion molecules
Role of cytokines in MM
Interleukin-6
Insulin-like growth factor-1
Vascular endothelial growth factor
Role of angiogenesis in MM
Role of chemokines and cell trafficking in MM
Osteoclasts in MM
Osteoblasts in MM
Diagnostic evaluation
Staging/prognostic factors
Survival
Treatment
Initial therapy for patients eligible for SCT
Thalidomide in newly diagnosed transplantation-eligible patients
Bortezomib in newly diagnosed transplantation-eligible patients
Lenalidomide in newly diagnosed transplantation-eligible patients
Combination of these agents in newly diagnosed transplantation-eligible patients
Induction therapy for non–transplantation-eligible patients
Thalidomide
Bortezomib
Lenalidomide
Intensification therapy
Maintenance therapy
Treatment of relapsed and refractory MM
Thalidomide
Bortezomib
Lenalidomide
Supportive care

Plasmacytoma
 

Other plasma cell disorders
 
Amyloidosis
POEMS syndrome
Lymphoplasmacytic lymphoma (WM)

Acknowledgment