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) is still incurable. with a view to conquer resistance to present treatments and increase sufferer end result, novel biologically-based therapy techniques are being constructed. present translational examine in MM concentrating on the advance of molecularly-based blend treatments has nice promise to accomplish excessive frequency and sturdy responses within the majority of sufferers. significant advances are making this objective attainable. First, fresh advances in genomics and proteomics in MM have allowed for elevated figuring out of sickness pathogenesis, pointed out novel healing goals, allowed for molecular type, and supplied the clinical cause for combining distinctive remedies to extend tumor mobilephone cytotoxicity and abrogate drug resistance. moment, there's now an elevated knowing of the way adhesion of MM cells in bone marrow (BM) additional affects gene expression in MM cells, in addition to in BM stromal cells (BMSCs). because of those advances in oncogenomics at the one hand and elevated realizing of the position of the BM within the pathogenesis of MM at the different, a brand new remedy paradigm concentrating on the tumor telephone and its BM microenvironment to beat drug resistance and enhance sufferer consequence has now been built. Thalidomide, lenalidomide, and Bortezomib are 3 brokers which goal the tumor cellphone in its microenvironment in either laboratory and animal versions and that have swiftly translated from the bench to the bedside. Ongoing efforts are utilizing oncogenomics and mobile signaling reviews to spot subsequent iteration of remedies 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 end result in MM has nice promise not just to alter the ordinary historical past of MM, but in addition to function a version for certain therapeutics directed to enhance end result of sufferers with MM.
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Additional resources for Advances in Biology and Therapy of Multiple Myeloma: Volume 1: Basic Science
Shaughnessy J, Tian E, Sawyer J et al (2003) Prognostic impact of cytogenetic and interphase ﬂuorescence in situ hybridization-deﬁned chromosome 13 deletion in multiple myeloma: early results of total therapy II. Br J Haematol 120:44–52 28. Chiecchio L, Protheroe RK, Ibrahim AH et al (2006) Deletion of chromosome 13 detected by conventional cytogenetics is a critical prognostic factor in myeloma. Leukemia 20: 1610–1617 29. Laï JL, Michaux L, Dastugue N et al (1998) Cytogenetics in multiple myeloma: a multicenter study of 24 patients with t(11;14)(q13;q32) or its variant.
Myeloma plasma cells can be clearly distinguished from those of healthy donors based on expression of ~120 of 6,800 genes analyzed. Unsupervised clustering of these early global gene-expression data showed that MM could be divided into four distinct molecular subgroups, MM1–MM4, with MM1 being more like MGUS and MM4 being related to myeloma cell lines. The MM4 group also had a higher incidence of cytogenetic abnormalities (CAs) and high serum levels of beta-2-microglobulin, clinical features historically linked to poor prognosis.
Finally, almost 20% of the patients display a 14q32 translocation with other multiple chromosomal partners. The role of these nonrecurrent translocations is totally unknown. In contrast to the recurrent 14q32 translocations described above, these ones are mostly observed in patients with hyperdiploid karyotypes. They may reﬂect a genetic instability, especially focused on the 14q32 region and the IGH gene, which is physiologically rearranged at several stages of the B-cell differentiation. , del(17p), has been described in about 10% of the patients with myeloma [53, 54].
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.)