Multiple Myeloma Research Consortium (MMRC) Partners With Novartis To Advance Phase II Study Of Deacetylase Inhibitor Main Category: Cancer / Oncology News Article Date: 15 Aug 2007 - 0:00 PDT
The Multiple Myeloma Research Consortium (MMRC) today announced its participation in a Phase II study to determine the efficacy of LBH589 for the treatment of patients with relapsed or refractory multiple myeloma. LBH589 is an orally administered deacetylase inhibitor developed by Novartis Pharmaceuticals.
The MMRC is the only research model of its kind bringing together 13 leading academic institutions to accelerate the development of novel and combination treatments for multiple myeloma, an incurable cancer of the plasma cell. In addition to its most recent partnership with Novartis, the MMRC is facilitating several other clinical trials, including a Phase I study of NPI- 0052, a proteasome inhibitor, in collaboration with Nereus Pharmaceuticals, and a Phase I study of perifosine, lenalidomide (REVLIMID(R)), and dexamethasone in collaboration with Keryx Biopharmaceuticals.
"Deacetylase inhibitors may represent a new treatment options for cancer patients and the MMRC is proud to work with Novartis to advance this important clinical program," said Kathy Giusti, Founder and Chief Executive Officer of the MMRC, as well as a myeloma patient. "This trial and the others the MMRC is facilitating demonstrate the importance of novel collaborations in bringing new treatments to patients."
Named ALPHA-MM, this trial is a single arm, open label, multi-center global study that will enroll 144 patients in the United States, Canada, and Europe. MMRC Member Institutions that will enroll patients are Dana-Farber Cancer Institute, City of Hope National Medical Center, Emory University, Hackensack University Medical Center, Mayo Clinic, H. Lee Moffitt Cancer Center & Research Institute, and Washington University.
This trial is open to patients with relapsed or refractory multiple myeloma who have received at least two lines of therapy, and whose disease progressed on their most recent therapy. Prior therapy must have included bortezomib (VELCADE(R)) or lenalidomide.
LBH589 is part of a promising class of drugs called deacetylase inhibitors or HDAC inhibitors, which may play an important role in helping to slow or stop the growth of multiple myeloma cells. Preclinical laboratory data suggests that LBH589 has significant activity against multiple myeloma cells, including those that are resistant to conventional therapies.
About the Multiple Myeloma Research Consortium (MMRC)
The Multiple Myeloma Research Consortium (MMRC) is a 509(a)3 non-profit organization that integrates leading academic institutions to accelerate drug development in multiple myeloma. It is led from MMRC offices in Norwalk, Conn., and comprises 13 member institutions: City of Hope, Dana-Farber Cancer Institute, Emory University's Winship Cancer Institute, the Cancer Center at Hackensack University Medical Center, H. Lee Moffitt Cancer Center & Research Institute, Mayo Clinic, Ohio State University, Roswell Park Cancer Institute, St. Vincent's Comprehensive Cancer Center of Saint Vincent Catholic Medical Centers of New York, University Health Network (Princess Margaret Hospital), University of Chicago, University of Michigan, and Washington University.
The MMRC was founded in 2004 by Kathy Giusti, a myeloma patient, and with the help of the scientific community. The MMRC is a sister organization to the Multiple Myeloma Research Foundation (MMRF), the world's leading funder of multiple myeloma research. The MMRC is widely recognized as an optimal research model to rapidly address critical challenges in drug development and to explore opportunities in the today's most promising research areas -- genomics, compound validation, and clinical trials. The MMRC is the only consortium to join academic institutions through membership agreements, customized IT systems, and an integrated tissue bank. For more information, please visit http://www.themmrc.org.
Dr. Thomas has been with DNAPrint since 2001. During his time with DNAPrint, Dr. Thomas has been involved with the research and development of a number of projects, including AncestrybyDNA 2.5, EuroDNA, and the forensic versions of those products (DNAWitness, EuroWitness, Retinome). In addition to these products, he has been involved with the pharmaco-genomic research projects undertaken by DNAPrint. Prior to joining DNAPrint, Dr. Thomas was a postdoctoral fellow at H. Lee Moffitt Cancer center where he held a fellowship from the Leukemia and Lymphoma Society of America and was interested in various aspects of cancer research and gene expression. His graduate work was at the Department of Biology and Institute of Molecular Biology at the University of Oregon where he earned his Ph.D. in Biology studying mechanisms of RNA Polymerase II elongation and proofreading. He obtained his B.Sc. in Biological Sciences at University of California, Irvine. Currently Dr. Thomas is a Senior Scientist and Laboratory Manager at DNAPrint.
Molecular Oncology Program, H. Lee Moffitt Cancer Center & Research Institute, University of South Florida, Tampa, FL 33612, USA.
The transcription factor YY1 is a complex protein that is involved in repressing and activating a diverse number of promoters. Numerous studies have attempted to understand how this one factor can act both as a repressor and an activator in such a wide set of different contexts. The fact that YY1 interacts with a number of key regulatory proteins (e.g. TBP, TFIIB, TAFII55, Sp1, and E1A) has suggested that these interactions are important for determining which particular function of YY1 is displayed at a specific promoter. Two groups of proteins, previously known to function as corepressors and coactivators, that now seem likely to modulate YY1's functions, are the histone deacetylases (HDAC) and histone acetyltransferases (HAT). These two groups of enzymes modify histones, and this modification is proposed to alter chromatin structure. Acetylated histones are typically localized to active chromatin while deacetylated histones colocalize with transcriptionally inactive chromatin. When these enzymes are directed to a promoter through a DNA binding factor such as YY1, that promoter can be activated or repressed. This review will discuss the recent work dealing with the different proteins that interact with YY1, with particular emphasis on ones that modify chromatin, and how they could be involved in regulating YY1's activities.
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