ABSTRACT
Multiple myeloma (MM) is still considered an incurable disease. However, drugs with different mechanisms of action that can improve the efficiency of treatment offer hope. Still, there are concerns about an unacceptable increase in toxicity with such regimens. The results of recently published clinical studies of elotuzumab in combination with lenalidomide/dexamethasone or pomalidomide/dexamethasone confirm previous hopes to improve the effect of that treatment. Humanized monoclonal antibodies aimed at SLAMF7 stimulate natural killer cells to fight against MM cells. Elotuzumab used in combination with lenalidomide/dexamethasone or with pomalidomide/dexamethasone is approved by the US FDA to treat patients with relapsed and/or refractory MM. The article is a summary of the recent knowledge about the possibility of using elotuzumab in the treatment of relapsed and/or refractory MM and shows its potential uses in the future.
Subject(s)
Antibodies, Monoclonal, Humanized/therapeutic use , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Multiple Myeloma/drug therapy , Neoplasm Recurrence, Local/drug therapy , Antibodies, Monoclonal, Humanized/pharmacology , Antineoplastic Combined Chemotherapy Protocols/pharmacology , Bortezomib/pharmacology , Bortezomib/therapeutic use , Cell Line, Tumor , Clinical Trials as Topic , Dexamethasone/pharmacology , Dexamethasone/therapeutic use , Drug Resistance, Neoplasm/drug effects , Drug Resistance, Neoplasm/immunology , Humans , Killer Cells, Natural/drug effects , Killer Cells, Natural/immunology , Lenalidomide/pharmacology , Lenalidomide/therapeutic use , Mesenchymal Stem Cells/drug effects , Mesenchymal Stem Cells/immunology , Multiple Myeloma/immunology , Multiple Myeloma/mortality , Multiple Myeloma/pathology , Neoplasm Recurrence, Local/immunology , Neoplasm Recurrence, Local/mortality , Neoplasm Recurrence, Local/pathology , Progression-Free Survival , Thalidomide/analogs & derivatives , Thalidomide/pharmacology , Thalidomide/therapeutic useABSTRACT
INTRODUCTION: Autophagy is a highly conservative self-degradative process. It aims at elimination-impaired proteins and cellular organelles. Previous research confirmed the autophagy role in cancer pathogenesis. AREAS COVERED: This article discusses the role of autophagy in the development of AML. Autophagy seems to be a 'double-sword' mechanism, hence, either its suppression or induction could promote neoplasm growth. This mechanism could also be the aim of the 'molecular targeted therapy.' Chemo- and radiotherapy induce cellular stress in neoplasm cells with subsequent autophagy suppression. Simultaneously, it is claimed that the autophagy suppression increases chemosensitivity 'in neoplastic cells. Some agents, like bortezomib, in turn could promote autophagy process, e.g. in AML (acute myeloid leukemia). However, currently there are not many studies focusing on the role of autophagy in patients suffering for AML. In this review, we summarize the research done so far on the role of autophagy in the development of AML. EXPERT OPINION: The analysis of autophagy genes expression profiling in AML could be a relevant factor in the diagnostic process and treatment 'individualization.' Autophagy modulation seems to be a relevant target in the oncological therapy - it could limit disease progression and increase the effectiveness of treatment.