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Original Article: Clinical

Strong immunoexpression of dickkopf-1 is associated with response to bortezomib in multiple myeloma

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Pages 2670-2678 | Received 27 Oct 2017, Accepted 11 Feb 2018, Published online: 27 Mar 2018
 

Abstract

The predictive significance of osteolysis-related proteins was evaluated in bortezomib-treated multiple myeloma. The clinicopathological characteristics were collected retrospectively. Immunohistochemistry was performed for analyzing receptor activator of NF-κB ligand (RANKL), osteoprotegerin (OPG), macrophage inflammatory protein 1 alpha (MIP1α), and dickkopf-1 (DKK1) expression. Among clinicopatholgical characteristics, osteolytic lesion was associated with higher response to bortezomib treatment (79% vs. 46%). High DKK1 expression was significantly correlated with osteolytic lesion (p = .003), whereas RANKL, OPG, and MIP1α were not. In high DKK1 expression, higher response to bortezomib was observed (84% vs. 44%). In multivariate analysis, high DKK1 expression was associated with better response to bortezomib (p = .005). Patients with high DKK1 expression had longer median progression-free survival (PFS) and overall survival (OS) after bortezomib treatment. In multivariate analysis, high DKK1 expression was an independent prognostic factor of favorable PFS (p = .027) and OS (p = .035). In multiple myeloma treated with bortezomib, expression status of DKK1 may be a useful predictive marker.

Potential conflict of interest

Disclosure forms provided by the authors are available with the full text of this article online at https://doi.org/10.1080/10428194.2018.1443331.

Additional information

Funding

This work was supported by grants from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare [HI14C1967] to Yong Won Choi. The funder did not have any role in the design and conduct of the study, the analysis and interpretation of the data, decision to publish, and preparation of the manuscript.

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