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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 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 Citation Map 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. Related Collections Neoplasia Apoptosis Signal Transduction Gene Expression Genomics Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 March 2003, Vol. 101, No. 6, pp. 2377-2380 NEOPLASIA Brief report 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 From the Jerome Lipper Multiple Myeloma Center, Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston MA; Department of Medicine, Harvard Medical School, Boston, MA; Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA; Beth Israel Deaconess Medical Center (BIDMC) Genomics Center, BIDMC, Harvard Institutes of Medicine, Boston, MA; Boston VA Health Care System, Boston, MA. The proteasome inhibitor PS-341 inhibits nuclear factor-B (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 proapoptotic effects, down-regulates the expression of several effectors involved in the cellular response to genotoxic stress. These data suggest that, in addition to down-regulating 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. © 2003 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Baritaki, K. Yeung, M. Palladino, J. Berenson, and B. 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