Disease relevance of Multiple Myeloma

• Deep venous thrombosis and thalidomide therapy for multiple myeloma [1].
• IL-6 has been shown to be a plasmacytoma growth factor in mice and is believed to play a key role in the development of human multiple myeloma [2].
• The antiserum reacted at a lower titer with the Jijoye and EB-3 lines of Burkitt's lymphoma, the RPMI 4098 cell line of normal human lymphocytes, and culture lines of human melanoma and osteogenic sarcoma than with the RPMI 8226 cells or bone marrow from certain patients having multiple myeloma [3].
• In advanced forms of plasma cell malignancies, such as cases of multiple myeloma in stages II and III and of plasma cell leukemia, some cells of lymphoid morphology expressed common acute lymphoblastic leukemia antigen (CALLA, CD10) and HLA-DR, but contained no detectable terminal deoxynucleotidyl transferase enzyme [4].
• TBG t1/2 was 2.5 days in a patient with multiple myeloma and 3.6 days in two patients with thyrotoxicosis [5].

Psychiatry related information on Multiple Myeloma

• Because IL-6 has been implicated in the etiopathology of different human diseases including multiple myeloma, rheumatoid arthritis, multiple sclerosis, acquired immunodeficiency syndrome dementia complex, and Alzheimer's disease, its inhibition may be of therapeutic interest [6].
• This report is presented as a possible case of steroid-induced catatonia in a 62-year-old woman following treatment with melphalan, prednisone, and cimetidine for multiple myeloma of the IgA class with associated mild hypercalcemia [7].
• Reversible dementia due to thalidomide therapy for multiple myeloma [8].

High impact information on Multiple Myeloma

• Deregulation of MUM1/IRF4 by chromosomal translocation in multiple myeloma [9].
• Efficacy of pamidronate in reducing skeletal events in patients with advanced multiple myeloma. Myeloma Aredia Study Group [10].
• Erythropoietin treatment of anemia associated with multiple myeloma [11].
• Multiple hematopoietic-cell lineages in multiple myeloma [12].
• Twenty-nine patients with advanced refractory multiple myeloma were treated with intermittent high-dose dexamethasone in combination with four-day infusions of vincristine and doxorubicin [13].

Chemical compound and disease context of Multiple Myeloma

• Thalidomide in multiple myeloma [14].
• Dichloromethylene diphosphonate (Cl2MDP), an inhibitor of oestoclast activity, was evaluated for its ability to decrease the excessive mobilization of skeletal calcium that complicates multiple myeloma [15].
• Effects of dichloromethylene diphosphonate on skeletal mobilization of calcium in multiple myeloma [15].
• A randomized double-blind study was carried out in 26 patients with multiple myeloma to compare the therapeutic effect of sodium fluoride (50 mg twice daily) plus calcium carbonate (1 g four times daily) and placebo [16].
• We have identified a circulating, heparin-like anticoagulant in a patient with multiple myeloma (IgG4 lambda) who had serious clinically evident bleeding that contributed to his death [17].
• 7. SDX-308 effectively suppressed TNF-alpha-induced IKK-gamma and IkappaB-alpha phosphorylation and degradation and subsequent NF-kappaB activation in human multiple myeloma cells [18].
• In this article, we review the role of the phosphatidylinositol 3-kinase/Akt pathway in the pathogenesis of multiple myeloma and the potential therapeutic implications of targeting this pathway in the treatment of multiple myeloma [19].

Biological context of Multiple Myeloma

• Using flow cytometry, we searched for evidence of the expression of genes specific for different hematopoietic lineages by tumor cells in bone marrow aspirates from 27 patients with aneuploid multiple myeloma [20].
• These findings provide evidence that constitutively activated Stat3 signaling contributes to the pathogenesis of multiple myeloma by preventing apoptosis [21].
• 2-Methoxyestradiol overcomes drug resistance in multiple myeloma cells [22].
• SOCS-1, a negative regulator of cytokine signaling, is frequently silenced by methylation in multiple myeloma [23].
• Identification of a second transforming gene, rasn, in a human multiple myeloma line with a rearranged c-myc allele [24].

Anatomical context of Multiple Myeloma

• Interleukin 6 (IL-6) is a major growth factor for tumor plasma cells involved in human multiple myeloma (MM) [25].
• CONCLUSION: Alpha radiation may account for the increased risk of tumors of the liver, gallbladder, and peritoneum as well as leukemia and multiple myeloma, whereas confounding factors most probably contribute to the increased risks at other sites [26].
• Mortality was significantly elevated for accidents and cancers of the lymphatic and hematopoietic systems, particularly from lymphosarcoma and reticulum cell sarcoma, other neoplasms of lymphoid tissue (i.e., giant follicular lymphoma and other primary malignant neoplasms of lymphoid tissue), and multiple myeloma [27].
• Although we have previously shown that HGF/MET signaling controls survival and proliferation of multiple myeloma (MM), its role in the pathogenesis of other B-cell malignancies has remained largely unexplored [28].
• Enrichment of functional CD8 memory T cells specific for MUC1 in bone marrow of patients with multiple myeloma [29].

Gene context of Multiple Myeloma

• We report that one STAT family member, Stat3, is constitutively activated in bone marrow mononuclear cells from patients with multiple myeloma and in the IL-6-dependent human myeloma cell line U266 [21].
• Transcriptional inactivation of STAT3 by PPARgamma suppresses IL-6-responsive multiple myeloma cells [30].
• Oncostatin M (OSM) is a 28-kD glycoprotein recently identified as a growth factor for human multiple myeloma cells [31].
• Oncostatin M induces association of Grb2 with Janus kinase JAK2 in multiple myeloma cells [31].
• Cyclin D dysregulation: an early and unifying pathogenic event in multiple myeloma [32].

Analytical, diagnostic and therapeutic context of Multiple Myeloma

• Carcinoma of the breast. Occurence after treatment with melphalan for multiple myeloma [33].
• Bone marrow cells of 82 patients with multiple myeloma were subjected to flow cytometric analysis of DNA and cytoplasmic immunoglobulin (CIg) content using propidium iodide and direct immunofluorescence assays [34].
• We studied 21 patients with multiple myeloma; disease had progressed during primary chemotherapy in 6 and was resistant to VAD (vincristine, doxorubicin, dexamethasone) in 15 [35].
• High-dose melphalan with autologous bone marrow transplantation for multiple myeloma [36].
• Combination chemotherapy with intermittent 1-3-bis(2-chloroethyl)1-nitrosourea (BCNU), cyclophosphamide, and prednisone for multiple myeloma [37].

References