Commentary 10.1172/JCI124919

PLK1: a promising and previously unexplored target in double-hit lymphoma

Quais N. Hassan II,1,2 Lapo Alinari,1 and John C. Byrd1

1Department of Internal Medicine, Division of Hematology, Comprehensive Cancer Center, and

2Medical Scientist Training Program, The Ohio State University, Columbus, Ohio, USA.

Address correspondence to: John C. Byrd, Division of Hematology, The Ohio State University, 410 W. 12th Avenue, Columbus, Ohio 43210, USA. Phone: 614.293.8330; Email: john.byrd@osumc.edu.

Find articles by Hassan, Q. in: JCI | PubMed | Google Scholar

1Department of Internal Medicine, Division of Hematology, Comprehensive Cancer Center, and

2Medical Scientist Training Program, The Ohio State University, Columbus, Ohio, USA.

Address correspondence to: John C. Byrd, Division of Hematology, The Ohio State University, 410 W. 12th Avenue, Columbus, Ohio 43210, USA. Phone: 614.293.8330; Email: john.byrd@osumc.edu.

Find articles by Alinari, L. in: JCI | PubMed | Google Scholar

1Department of Internal Medicine, Division of Hematology, Comprehensive Cancer Center, and

2Medical Scientist Training Program, The Ohio State University, Columbus, Ohio, USA.

Address correspondence to: John C. Byrd, Division of Hematology, The Ohio State University, 410 W. 12th Avenue, Columbus, Ohio 43210, USA. Phone: 614.293.8330; Email: john.byrd@osumc.edu.

Find articles by Byrd, J. in: JCI | PubMed | Google Scholar

First published November 5, 2018 - More info

J Clin Invest. https://doi.org/10.1172/JCI124919.
Copyright © 2018, American Society for Clinical Investigation

First published November 5, 2018 - Version history

Inhibitors that target specific kinases or oncoproteins have become popular additions to or replacements for cytotoxic chemotherapies to treat many different types of cancer. However, many tumors lack a discernable target kinase and an amplified oncoprotein and/or rely on several cooperating mechanisms for progression. Thus, combinations of targeted therapies are essential for treating many cancers to avoid the rapid emergence of resistance. In this issue of the JCI, Ren et al. use an elegant kinase activity–profiling method and identify activity of the oncogene polo-like kinase-1 (PLK1) as an important driver of double-hit lymphoma (DHL), an aggressive subgroup of B cell lymphoma characterized by chromosomal translocations involving c-MYC and BCL2 or BCL6. Moreover, PLK1 activity was associated with MYC expression and poor prognosis in DHL patients. PLK1 inhibition with volasertib, alone and in combination with the BCL-2 inhibitor venetoclax, was efficacious in multiple DHL models, including mice harboring DHL patient–derived xenografts. Together, these data support PLK1 as a promising prognostic marker and therapeutic target for DHL.

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