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Prepublished online as a Blood First Edition Paper on November 7, 2002; DOI 10.1182/blood-2002-06-1768. This Article Full Text (PDF) All Versions of this Article: 2002-06-1768v1 101/6/2377    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Mitsiades, N. Articles by Anderson, K. C Search for Related Content PubMed PubMed Citation Articles by Mitsiades, N. Articles by Anderson, K. C Social Bookmarking                   What's this? Submitted June 14, 2002 Accepted October 17, 2002 The proteasome inhibitor PS-341 potentiates sensitivity of multiple myeloma cells to conventional chemotherapeutic agents: therapeutic applications Nicholas Mitsiades, Constantine S Mitsiades, Paul G Richardson, Vassiliki Poulaki, Yu-Tzu Tai, Dharminder Chauhan, Galinos Fanourakis, Xuesong Gu, Charles Bailey, Marie Joseph, Towia A Libermann, Robert Schlossman, Nikhil C Munshi, Teru Hideshima, and Kenneth C Anderson* Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, MA, USA Massachusetts Eye and Ear Infirmary, Boston, MA, USA BIDMC Genomics Center, Beth Israel Deaconess Medical Center, Boston, MA, USA * Corresponding author; email: kenneth_anderson{at}dfci.harvard.edu. The proteasome inhibitor PS-341 inhibits NF-B activation, induces apoptosis in cancer cells including multiple myeloma (MM) cells, and has marked clinical activity as a monotherapy for MM. In this study, we found that subtoxic concentrations of PS-341 potently sensitized MM cell lines and patient cells to DNA-damaging chemotherapeutic agents such as doxorubicin and melphalan, including cells resistant to these drugs and those isolated from a patient who had relapsed after PS-341 monotherapy. Moreover, PS-341 abolished cell adhesion-mediated drug resistance. Using gene expression profiling and proteomic analysis, we demonstrate that PS-341, among its other pro-apoptotic effects, downregulates the expression of several effectors involved in the cellular response to genotoxic stress. These data suggest that, in addition to downregulating the expression of apoptosis inhibitors, PS-341 inhibits genotoxic stress response pathways and thereby restores sensitivity to DNA-damaging chemotherapeutic agents. These studies therefore provide the framework for clinical use of this agent in combination with conventional chemotherapy. 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