Format

Send to:

Choose Destination
See comment in PubMed Commons below
Cancer Control. 2003 Sep-Oct;10(5):361-9.

Bortezomib (PS-341): a novel, first-in-class proteasome inhibitor for the treatment of multiple myeloma and other cancers.

Author information

  • 1Jerome Lipper Myeloma Center, Division of Hematologic Oncology, Department of Adult Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA. paul_richardson@dfci.harvard.edu

Abstract

BACKGROUND:

Multiple myeloma (MM) is an incurable malignancy that is diagnosed in approximately 15,000 people in the United States each year. The novel proteasome inhibitor bortezomib has shown antitumor activity in preclinical studies and has entered clinical trials, with encouraging results to date.

METHODS:

We review and summarize preclinical work demonstrating the tumoricidal effects of proteasome inhibition, focusing on the potent and selective proteasome inhibitor bortezomib, the first such agent to progress to clinical trials. We also address the potential for bortezomib as a therapy for MM.

RESULTS:

In preclinical studies bortezomib appears not only to have activity against MM cells, but also to downregulate protective interactions with bone marrow stromal cells and to inhibit blood vessel development. Proteasome inhibition also has been shown to interfere with protective interactions between MM cells and the bone marrow, and to restrict tumor-associated angiogenesis in preclinical models.

CONCLUSIONS:

Proteasome inhibition is a promising new investigational avenue for cancer therapy. Bortezomib is currently available for the treatment of relapsed and refractory MM. Further trials are underway to assess the safety and efficacy of this agent in MM and a range of other cancers.

PMID:
14581890
[PubMed - indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for H. Lee Moffitt Cancer Center & Research Institute
    Loading ...
    Write to the Help Desk