By Esteban Braggio Ph.D., Rafael Fonseca M.D. (auth.), Nikhil C. Munshi, Kenneth C. Anderson (eds.)
Despite the advances in traditional, novel agent and excessive dose chemotherapy a number of myeloma (MM) continues to be incurable. with a view to triumph over resistance to present treatments and increase sufferer final result, novel biologically-based remedy methods are being constructed. present translational learn in MM concentrating on the improvement of molecularly-based mix remedies has nice promise to accomplish excessive frequency and sturdy responses within the majority of sufferers. significant advances are making this target attainable. First, contemporary advances in genomics and proteomics in MM have allowed for elevated realizing of sickness pathogenesis, pointed out novel healing ambitions, allowed for molecular class, and supplied the medical motive for combining distinctive remedies to extend tumor telephone cytotoxicity and abrogate drug resistance. moment, there's now an elevated knowing of ways adhesion of MM cells in bone marrow (BM) extra affects gene expression in MM cells, in addition to in BM stromal cells (BMSCs). due to those advances in oncogenomics at the one hand and elevated figuring out of the position of the BM within the pathogenesis of MM at the different, a brand new remedy paradigm concentrating on the tumor phone and its BM microenvironment to beat drug resistance and increase sufferer consequence has now been built. Thalidomide, lenalidomide, and Bortezomib are 3 brokers which objective the tumor mobile in its microenvironment in either laboratory and animal types and that have speedily translated from the bench to the bedside. Ongoing efforts are utilizing oncogenomics and phone signaling reviews to spot subsequent iteration of cures in MM at the one hand, and to notify the layout of blend trials at the different. This new paradigm for overcoming drug resistance and enhancing sufferer final result in MM has nice promise not just to alter the ordinary background of MM, but additionally to function a version for detailed therapeutics directed to enhance final result of sufferers with MM.
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Additional resources for Advances in Biology and Therapy of Multiple Myeloma: Volume 1: Basic Science
D. Shaughnessy, Jr. C. C. 1007/978-1-4614-4666-8_3, © Springer Science+Business Media New York 2013 41 42 S. Usmani et al. exclusive and speciﬁc to each malignancy. This hypothesis was difﬁcult to test, however, until the completion of the human genome project [2, 3] and the development of high-throughput tools capable of analyzing the activities of all genes simultaneously . It is now believed that the human genome consists of ~25,000 mRNA-encoding genes, and this complexity is increased by posttranscriptional modiﬁcations, such as alternative splicing.
The translocation disrupts the MMSET gene within the ﬁrst introns, leading to the generation of a novel chimeric IGH-MMSET gene. So far, neither the physiological function of MMSET (it could be involved in the regulation of chromatin remodeling), nor the consequences of its deregulation by the translocation are known. However, this chimeric gene is constantly present in the t(4;14) cases, and MMSET may represent the primary target of the t(4;14). Several studies did show that the t(4;14) is associated with a poor prognosis (Fig.
In contrast to translocations involving the 14q32 region, they are thought to be secondary events and can be acquired during evolution. J. Corre and H. 5 Abnormalities of the 1q Region More recently, the Arkansas group did report on the prognostic value of 1q gains . In cytogenetic studies, extracopies of the long arm of chromosome 1 have been described in about one-third of the patients . Actually, this abnormality is not restricted to myeloma and has been reported in many tumor types, both in hematological neoplasms and in solid tumors.
Advances in Biology and Therapy of Multiple Myeloma: Volume 1: Basic Science by Esteban Braggio Ph.D., Rafael Fonseca M.D. (auth.), Nikhil C. Munshi, Kenneth C. Anderson (eds.)