Magic year for multiple myeloma therapeutics: Key takeaways from the ASH 2015 annual meeting

Kejie Zhang, Aakash Desai, Dongfeng Zeng, Tiejun Gong, Peihua Lu and Michael Wang _

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Oncotarget. 2017; 8:10748-10759. https://doi.org/10.18632/oncotarget.13314

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Kejie Zhang1,*, Aakash Desai2,3,*, Dongfeng Zeng4, Tiejun Gong5, Peihua Lu6 and Michael Wang7

1 Department of Hematology, Zhongshan Hospital, Xiamen University, Fujian Medical University Clinic Teaching Hospital, Xiamen, China

2 Department of Lymphoma/Myeloma, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA

3 University of Texas Health Science Center, Houston, Texas, USA

4 Department of Hematology, Xinqiao hospital, Third Military Medical University, Chongqing, China

5 Institute of Hematology and Oncology, Harbin first Hospital, Harbin, China

6 Department of Hematology, Hebei Yanda Ludaopei Hospital, Beijing, China

7 Department of Lymphoma/Myeloma, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA

* These authors have equal contribution to this work

Correspondence to:

Michael Wang, email:

Keywords: multiple myeloma, Ixazomib, elotuzumab, daratumumab

Received: March 25, 2016 Accepted: October 19, 2016 Published: November 11, 2016


Despite the availability of various anticancer agents, Multiple Myeloma (MM) remains incurable in most cases, along with high relapse rate in the patients treated with these agents. The year 2015 saw major advancements in our battle against multiple myeloma. In 2015, the U.S. Food and Drug Administration (FDA) approved three new therapies for multiple myeloma, namely Ixazomib (an oral proteasome inhibitor), Daratumumab and Elotuzumab (monoclonal antibodies against CD38 and SLAMF7 respectively). The purpose of this review is to provide a detailed analysis of these aforementioned breakthrough therapies and two other newer agents, Filanesib (kinesis spindle inhibitor) and selinexor (SINE inhibitor), presented at the 2015 annual meeting of American Society of Hematology (ASH). We also describe the role of agents targeting PD-1 axis and chimeric antigen receptor T (CAR-T) cells in the treatment of MM.

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