Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two monoclonal antibodies, DA7 and DC10, were obtained from fusions of mouse myeloma cells with splenic lymphocytes from mice immunized with human breast cancer cells of PMC 42 line. The indirect immunofluorescence studies performed on established tumor cell lines together with immunoperoxidase staining of normal human tissues showed that the components reacting with the antibodies were cytokeratins. Positive reaction was noted in all epithelia derived cultured cells and in all simple epithelial tissues known to express keratin 18. Immunoblotting performed on various cytoskeletal preparations demonstrated strong staining of a single band with a mobility corresponding to that of cytokeratin 18 (45 kD). The negative immunoperoxidase reaction found in different epithelial tissues of seven animal species suggests that both antibodies are specific for human keratin 18. It was shown that DA7 and DC10 antibodies exhibited strong reaction in paraffin embedded tissues fixed in either methacarn or standard formalin. These characteristics predetermine both antibodies as suitable reagents for the specialized histopathological work.
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PMID:Novel monoclonal antibodies defining epitope of human cytokeratin 18 molecule. 246 1

Despite the advances in our knowledge of myeloma cell biology, our understanding of myeloma pathogenesis is still incomplete. In this review, we present a summary of the cellular and molecular aspects of B-cell development and immunoglobulin (lg) gene rearrangement which have been important in defining the characteristics of the myeloma plasma cell (MPC). The PMC has undergone variable gene recombination, somatic hypermutation and isotype switching, and is therefore at a postgerminal center stage of development. The finding of preswitch clonal cells and isotype variants have raised interesting questions about the cell of origin of myeloma, for which no conclusive data is as yet available. However much information has been obtained about the chromosomal and genetic aberrations in myeloma, including monosomy 13, Ig heavy chain (IgH) switch region translocations, numerical abnormalities and a multitude of heterogeneous changes. A variety of techniques have been developed to overcome the insensitivity of conventional karyotyping, utilizing molecular cytogenetic strategies ranging from the delineation of precise loci by fluorescent in situ hybridization, a more "global" assessment of the genome by multicolor spectral karyotyping, to the quantitation of chromosomal material of specific origin by comparative genomic hybridization. Whether the abnormalities detected represent oncogenic insults, are involved in disease progression or are simply "by-products" of genetic instability is still unclear. For IgH translocations, the role of candidate genes such as Cyclin D1 and FGFR3 has been studied extensively by quantitating their expression and assessment of their oncogenicity (e.g. for FGFR3) in animal models. The significance of other aberrations such as c-myc, ras and p53 has also been investigated. With the advent of oligonucleotide microarrays, the expression of thousands of genes can be efficiently examined. So far, this approach seems promising in defining subgroups of different disease behavior, and may highlight specific genes and molecular mechanisms which are important in myeloma pathogenesis.
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PMID:The biology and cytogenetics of multiple myeloma. 1261 99

Background: Multiple myeloma (MM) is a heterogeneous disease characterized by chromosomal translocation, deletion, and amplification in plasma cells, resulting in a huge heterogeneity in its outcomes. Of all these cytogenetic abnormalities, Amp1q21 is most commonly detected, which is always associated with significantly shorter progression-free survival (PFS) and overall survival (OS) than normal 1q copy number status. In the era of novel agents such as bortezomib, ixazomib, lenalidomide, a head-to-head comparison of all these agents is still absent, especially in the patients with Amp1q21 alone. So, aiming to explore the optimum therapy to the patients with Amp1q21 only, we conduct this study. Patients and Methods: We searched the PubMed, the Cochrane Library, PMC and the Embase databases, and we selected all the randomized controlled trials (RCTs) in English about MM with Amp1q21 up to April, 2019. A total of 72 papers were full screened and finally 2 literatures can be included in our study. Results: Of the two studies, the one is about IRd (ixazomib, lenalidomide, dexamethasone) vs. placebo-Rd (HR, 0.781; 95% CI, 0.492-1.240), another is about VAD (vincristine, adriamycin, dexamethasone) vs. PAD (bortezomib, adriamycin, dexamethasone) (3-year survival rate: 59% vs. 83%, p=0.016). Conclusion: From this review, MM patients with Amp1q21 may somewhat benefit from ixazomib but the evidence is still stuffless. What's more, a head-to-head comparison between ixazomib and other agents among MM patients with Amp1q21 is also absent. So, we sincerely expect this review can attract some attention for the therapy of this special part of patients. This study was registered in https://www.crd.york.ac.uk/prospero/#recordDetails.
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PMID:Prognostic Value and Efficacy Evaluation of Novel Drugs for Multiple Myeloma Patients with 1q21 Amplification (Amp1q21) Only: A Systematic Review of Randomized Controlled Trials. 3220 34