Published online Jan 26, 2015. doi: 10.4252/wjsc.v7.i1.84
Peer-review started: July 30, 2014
First decision: September 28, 2014
Revised: October 14, 2014
Accepted: October 28, 2014
Article in press: December 16, 2014
Published online: January 26, 2015
Processing time: 169 Days and 11.5 Hours
Multiple myeloma (MM) is a hematologic malignancy of monoclonal plasma cells which remains incurable despite recent advances in therapies. The presence of cancer stem cells (CSCs) has been demonstrated in many solid and hematologic tumors, so the idea of CSCs has been proposed for MM, even if MM CSCs have not been define yet. The existence of myeloma CSCs with clonotypic B and clonotypic non B cells was postulated by many groups. This review aims to focus on these distinct clonotypic subpopulations and on their ability to develop and sustain MM. The bone marrow microenvironment provides to MM CSCs self-renewal, survival and drug resistance thanks to the presence of normal and cancer stem cell niches. The niches and CSCs interact each other through adhesion molecules and the interplay between ligands and receptors activates stemness signaling (Hedgehog, Wnt and Notch pathways). MM CSCs are also supposed to be responsible for drug resistance that happens in three steps from the initial cancer cell homing microenvironment-mediated to development of microenvironment-independent drug resistance. In this review, we will underline all these aspects of MM CSCs.
Core tip: Multiple myeloma is a still incurable malignancy. Several study about multiple myeloma cancer stem cells showed their ability of self-renewal, survival and drug resistance. Besides, these cells are able to initiate and develop tumor when transferred into mice recipients. So understanding multiple myeloma cancer stem cells mechanisms becomes important to design new efficient targeting strategies for multiple myeloma. The aim of this review is to elucidate the state of art about multiple myeloma cancer stem cells and their critical role in maintenance of disease.