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Related Experiment Video

Updated: Jun 1, 2026

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Published on: May 15, 2019

CCR1 as a target for multiple myeloma.

Sonia Vallet¹, Kenneth C Anderson

¹Massachusetts General Hospital, Harvard Medical School, Department of Hematology Oncology, Boston, MA 02114, USA.

Expert Opinion on Therapeutic Targets

|May 26, 2011

Summary

Chemokines like CCL3 and their receptor CCR1 are key in multiple myeloma (MM) and bone disease. CCR1 antagonists show promise in controlling MM tumor growth and preventing bone loss, paving the way for clinical trials.

Area of Science:

Immunology
Oncology
Hematology

Background:

Chemokines modulate immune responses and are implicated in autoimmune diseases and cancers.
Multiple myeloma (MM) is a hematological malignancy characterized by plasma cell proliferation in the bone marrow.
CCL3 and its receptor CCR1 are central to MM pathogenesis and MM-induced osteolytic bone disease.

Purpose of the Study:

To review the functional role of CCR1 in MM.
To discuss preclinical results of CCR1 antagonists in MM.

Main Methods:

Review of literature on CCR1 function and antagonists in MM.
Analysis of preclinical data from murine and humanized mouse models.

Main Results:

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CCL3 and CCR1 stimulate MM tumor growth directly and indirectly.

These molecules also promote osteolytic bone disease by affecting the osteoclast/osteoblast balance.

Targeting CCR1 or CCL3 reversed these effects, controlling tumor burden and preventing osteolysis in preclinical models.

Conclusions:

Preclinical data support the evaluation of CCR1 inhibitors in clinical trials for MM.
Development of novel antagonists with improved properties is crucial.
Careful patient selection will be important for successful clinical outcomes.