@entity33931 and XXXX : recent advances in the treatment of @entity1582 .

@entity1 @entity33931 @entity417 @entity2741 @entity174 @entity8253 @entity2816 @entity1749 @entity16291 @entity1582 @entity177 @entity1583 @entity6985 @entity230
@entity1582 is a @entity1583 characterized by plasma cell clonal expansion as well as end-organ damage due to increased levels of monoclonal proteins in both the plasma and urine. The clinical syndrome is characterized by @entity2741 , @entity177 , @entity417 , and bone involvement that leads to pathologic @entity174 . This progressive disease can result in significant @entity1 morbidity and mortality. Despite advances with treatment options and autologous stem cell transplantation, @entity1582 remains incurable. Current front-line therapies include proteasome inhibitors, immunomodulators, @entity8253 , and @entity230 . Due to the advent of the immunomodulatory agents @entity2816 and @entity6985 , as well as the proteasome inhibitor @entity1749 , overall survival in @entity1 with @entity1582 has improved greatly. However, once @entity1 progress through front-line therapy and have relapsed or refractory disease, treatment options have historically been very limited. @entity33931 , a second-generation proteasome inhibitor, has shown impressive response rates as a single agent in the relapsed and refractory @entity1 setting; this includes @entity1 who are refractory to previous @entity1749 therapy. In addition, a third-generation immunomodulator, @entity16291 , has also shown promising results in a similar @entity1 population, including those @entity1 who have been shown to be refractory to @entity6985 and @entity1749 . Adverse effects of both of these medications have been considered tolerable in the relapsed or refractory population, especially considering the benefits that have been shown. Continuing clinical research will reveal the utility of these agents in combination regimens or in a front-line setting for @entity1 with @entity1582 .
