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BET Bromodomain Inhibition as a Therapeutic Strategy to Target c-Myc
Efficacy of JQ1 in three murine models of multiple myeloma establishes the therapeutic rationale for BET bromodomain inhibition in this disease and other malignancies characterized by pathologic activation of c-Myc.
Biological properties of extracellular vesicles and their physiological functions
- M. Yáñez-Mó, P. Siljander, +57 authors O. De Wever
- Biology, MedicineJournal of extracellular vesicles
- 1 January 2015
A comprehensive overview of the current understanding of the physiological roles of EVs is provided, drawing on the unique EV expertise of academia-based scientists, clinicians and industry based in 27 European countries, the United States and Australia.
Ibrutinib in previously treated Waldenström's macroglobulinemia.
Ibrutinib was highly active, associated with durable responses, and safe in pretreated patients with Waldenström's macroglobulinemia, and the effect of MYD88 and CXCR4 mutations on outcomes was investigated.
Phase II trial of single-agent temsirolimus (CCI-779) for relapsed mantle cell lymphoma.
- T. Witzig, S. Geyer, +10 authors S. Kaufmann
- MedicineJournal of clinical oncology : official journal…
- 10 August 2005
It is demonstrated that agents that selectively target cellular pathways dysregulated in MCL cells can produce therapeutic benefit and single-agent temsirolimus has substantial antitumor activity in relapsed MCL.
Mechanisms of regulation of CXCR4/SDF-1 (CXCL12)-dependent migration and homing in multiple myeloma.
It is demonstrated that SDF-1/CXCR4 is a critical regulator of MM homing and that it provides the framework for inhibitors of this pathway to be used in future clinical trials to abrogate MM trafficking.
Lenalidomide, bortezomib, and dexamethasone combination therapy in patients with newly diagnosed multiple myeloma.
Lenalidomide-bortezomib-dexamethasone demonstrates favorable tolerability and is highly effective in the treatment of newly diagnosed myeloma.
BM mesenchymal stromal cell-derived exosomes facilitate multiple myeloma progression.
- A. Roccaro, A. Sacco, +10 authors I. Ghobrial
- MedicineThe Journal of clinical investigation
- 1 April 2013
In vitro and in vivo studies demonstrated that exosome transfer from BM-MSCs to clonal plasma cells represents a previously undescribed and unique mechanism that highlights the contribution of BM- MSCs to MM disease progression.
MicroRNAs 15a and 16 regulate tumor proliferation in multiple myeloma.
MicroRNA expression profiling of bone marrow derived CD138(+) MM cells versus their normal cellular counterparts and validated data by qRT-PCR indicate that microRNAs play a pivotal role in the biology of MM and represent important targets for novel therapies in MM.
Genomic complexity of multiple myeloma and its clinical implications
- S. Manier, K. Salem, Jihye Park, D. Landau, G. Getz, I. Ghobrial
- Biology, MedicineNature Reviews Clinical Oncology
- 1 February 2017
This Review describes the 'driver' gene alterations involved in the development and progression of MM, with a focus on the sequential acquisition of the main genomic aberrations and provides valuable insight into the clonal heterogeneity and clonal evolution of the disease.
Bone Marrow Microenvironment in Multiple Myeloma Progression
- S. Manier, A. Sacco, X. Leleu, I. Ghobrial, A. Roccaro
- Biology, MedicineJournal of biomedicine & biotechnology
- 3 October 2012
How the interaction between the malignant plasma cell and the BM microenvironment allowed myeloma progression through cell homing and the new concept of premetastatic niche is discussed.