Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2006 Oct;34(10):1289-95.
doi: 10.1016/j.exphem.2006.06.017.

Chemokines in multiple myeloma

Rohit Aggarwal  1 , Irene M Ghobrial, G David Roodman
Affiliations
Review

Chemokines in multiple myeloma

Rohit Aggarwal et al. Exp Hematol. 2006 Oct.

Abstract

Objective: In this article we focus on the role that chemokines and chemokine receptors play in the pathogenesis of multiple myeloma and the associated bone destructive process, and consider their utility as novel therapeutic targets for treating this devastating disease.

Methods: Current research on the role that chemokine and chemokine receptors play in the pathogenesis of myeloma is reviewed.

Results: The chemokines, MIP-1alpha, MCP-1, IL-8, and SDF-1, and their receptors play important roles in homing of MM cells, tumor growth, and bone destruction in myeloma. They are attractive therapeutic targets for treating myeloma patients.

Conclusion: Addition of chemokine antagonists to current treatment regimens for myeloma should result in better therapeutic responses because of the loss of both the protective effect of the marrow microenvironment on the MM cells and the induction of osteoclast activity.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Model for the role of chemokines in myeloma tumor progression in bone. MCP-1 and SDF-1 produced by marrow stromal cells/osteoblasts attract myeloma cells to bone. Myeloma cells then bind to marrow stromal cells through VCAM-1 (Step 1). Marrow stromal cells then increase expression of TNF-α, MCP-1, IL-8, and IL-6. Myeloma cells then increase production of MIP-1α and IL-3, which stimulate their growth (Step 2). These cytokines and chemokines enhance myeloma cell survival and growth and increase angiogenesis. The increased expression of RANKL, IL-3, IL-8, MCP-1, IL-6, and MIP-1α induce osteoclast formation and bone destruction (Step 3).
See this image and copyright information in PMC

References

    1. Coleman RE. Skeletal complications of malignancy. Cancer. 1997;80(Suppl):1588–1594. - PubMed
    1. Billadeau D, Ahmann G, Greipp P, Van Ness B. The bone marrow of multiple myeloma patients contains B cell populations at different stages of differentiation that are clonally related to the malignant plasma cell. J Exp Med. 1993;178:1023–1031. - PMC - PubMed
    1. Matsui W, Huff CA, Wang Q, Malehorn MT, Barber J, Tanhehco Y, Smith BD, Civin CI, Jones RJ. Characterization of clonogenic multiple myeloma cells. Blood. 2004;103:2332–2336. - PMC - PubMed
    1. Anderson KC, Shaughnessy JD, Jr, Barlogie B, Harousseau JL, Roodman GD. Multiple myeloma. Hematology (Am Soc Hematol Educ Program) 2002:214–240. - PubMed
    1. Uchiyama H, Barut BA, Mohrbacher AF, Chauhan D, Anderson KC. Adhesion of human myeloma-derived cell lines to bone marrow stromal cells stimulates interleukin-6 secretion. Blood. 1993;82:3712–3720. - PubMed

Publication types