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Original Articles

The contribution of MYC and PLK1 expression to proliferative capacity in diffuse large B-cell lymphoma

ORCID Icon, , , , , , ORCID Icon, , , , , , , , , & ORCID Icon show all
Pages 3214-3224 | Received 16 Feb 2019, Accepted 11 Jun 2019, Published online: 01 Jul 2019
 

Abstract

Polo-like kinase-1 (PLK1) regulates the MYC-dependent kinome in aggressive B-cell lymphoma. However, the role of PLK1 and MYC toward proliferation in diffuse large B-cell lymphoma (DLBCL) is unknown. We use multiplexed fluorescent immunohistochemistry (fIHC) to evaluate the co-localization of MYC, PLK1 and Ki67 to study their association with proliferation in DLBCL. The majority (98%, 95% CI 95–100%) of MYC/PLK1-double positive tumor cells expressed Ki67, underscoring the key role of the MYC/PLK1 circuit in proliferation. However, only 38% (95% CI 23–40%) and 51% (95% CI 46–51%) of Ki67-positive cells expressed MYC and PLK1, respectively. Notably, 40% (95% CI 26–43%) of Ki67-positive cells are MYC- and PLK-negative. A stronger correlation exists between PLK1 and Ki67 expression (R = 0.74, p < .001) than with MYC and Ki67 expression (R = 0.52, p < .001). Overall, the results indicate that PLK1 has a higher association than MYC in DLBCL proliferation and there are mechanisms besides MYC and PLK1 influencing DLBCL proliferation.

Acknowledgments

SBN is supported by the National Medical Research Council, Clinician Scientist Award [WBS R-179-000-063-213]

Author contributions

SBN and ADJ conceptualized the study design. MH analyzed the data. HMP performed the multiplex fIHC staining. SF and SBN scored the IHC. MLO, MH and SBN wrote the manuscript. The rest of the authors collected and reviewed cases, and contributed to the writing of the manuscript.

Potential conflict of interest

Disclosure forms provided by the authors are available with the full text of this article online at https://doi.org/10.1080/10428194.2019.1633629.

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