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)

The expressed immunoglobulin gamma 2b (IgG2b) heavy-chain gene of 4T001 was cloned into the shuttle vector pSV2-gpt and transfected into myeloma J558L and lymphoma A20.2J. Northern blots indicated that the transfected gamma 2b gene was processed in a manner similar to the endogenous heavy chain in both lymphoma and myeloma cells. To identify sequences important for immunoglobulin mRNA processing, we constructed deletions around the secretion-specific polyadenylation site and introduced the deleted genes into J558L cells. The BAL deletion lacked 670 base pairs of intervening sequence between secreted and membrane regions; the Kpn deletion lacked 830 base pairs in this region. J558L cells transfected with either the entire gamma 2b gene or the delta BAL vector produced predominantly secretion-specific gamma 2b mRNA and protein. J558L cells transfected with the delta Kpn vector produced approximately equimolar amounts of secretion-specific and membrane-specific gamma 2b mRNA. Both 55,000-dalton secreted and 62,000-dalton putative surface IgG2b proteins were detected in the delta Kpn transfectants. We conclude that sequences absent in the Kpn deletion but present in the BAL deletion exert an important role in the production of secretion-specific mRNA. The Kpn deletion removes the normal site of cleavage and poly(A) addition, and it is possible that it is the absence of this site which changes the processing pattern. Alternatively, it is possible that sequences absent in the Kpn deletion but present in the BAL deletion function in regulating the production of predominantly secretion-specific mRNA in myeloma cells. The possible role of a highly conserved sequence found in this region is discussed.
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PMID:Sequences near the 3' secretion-specific polyadenylation site influence levels of secretion-specific and membrane-specific IgG2b mRNA in myeloma cells. 287 62

T cell-replacing factor (TRF)/IL-5 is a glycosylated polypeptide that acts as a key factor for B cell growth and differentiation. Since IL-5 action is probably mediated by specific cell surface receptor(s), we have characterized the binding of IL-5 to cells using biosynthetically [35S]methionine-labeled IL-5 and 125I-IL-5 that had been prepared using Bolton-Hunter reagent. The radiolabeled IL-5 binds specifically to BCL1-B20 (in vitro line) (a murine chronic B cell leukemic cell line previously shown to differentiate into IgM-secreting cells in response to IL-5) within 10 min at 37 degrees C. There are two classes of binding sites with high affinity (Kd = 66 pM) and low affinity (Kd = 12 nM) for IL-5 and an average number of binding sites for high affinity and for low affinity were 400 and 7,500 per cell, respectively. The specificity of binding of radiolabeled IL-5 has been confirmed by demonstrating that only unlabeled IL-5 and anti-IL-5 mAb but not by IL-1, IL-2, IL-3, IFN-gamma, and GM-CSF inhibit radiolabeled IL-5 binding to BCL1-B20 cells. Treatment of surface-bound radiolabeled IL-5 with bivalent crosslinkers identified a membrane polypeptide of Mr 46,500 to which IL-5 is crosslinked. A variety of cell types have been surveyed for the capacity to bind specifically radiolabeled IL-5 with high affinity. BCL1 cells MOPC104E (murine myeloma cell line) expressed IL-5-R, whereas BAL. 17 and L10 A (B cell lymphoma) did not. T cell line, mastocytoma cell line, or macrophage tumor cell line did not display detectable levels of IL-5-R. were hardly detectable on normal resting B cells but were expressed on LPS-activated B cells, fitting the function of IL-5 that acts on activated B cells for their differentiation into Ig-secreting cells. Intriguingly, early B cell lines (J-87 and T-88) that grow in the presence of IL-5 expressed significant but low numbers of high-affinity binding sites for IL-5. The biological effects of IL-5 were mediated by high-affinity binding sites. The identification and characterization of IL-5-R should provide new insight into the apparent diverse biological activities of IL-5.
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PMID:Receptors for T cell-replacing factor/interleukin 5. Specificity, quantitation, and its implication. 326 7

The lack of apoptosis or programmed cell death in human tumor cells has been suggested to be one factor allowing uncontrolled growth of neoplasms. We have developed a mouse monoclonal antibody (MAb) that induces programmed cell death in a human acute leukemia cell line (KM-3) of the pre B-cell type. Stable, antibody-producing hybridomas were produced by fusing mouse myeloma cells to spleen cells from mice immunized with viable KM-3 cells. Incubation of KM-3 cells with the MAb (designated anti-BAL) resulted in growth inhibition and subsequent cell death within 2-3 days. Anti-BAL required cross-linking with a rabbit anti-mouse antibody to induce DNA fragmentation typical of apoptosis. Immunoblotting experiments with anti-BAL identified a 37-kDa protein, apparently different from any previously described apoptosis-related surface antigen. Strongest expression of the antigen was generally found on cells of lymphoid or myeloid origin. However, several other cell types such as fibroblasts and endothelial cells were also stained by anti-BAL in flow cytometry but less intensively. Despite the apparent presence of this cell surface-bound 37-kDa antigen on several normal and malignant cell types, anti-BAL induced cell death only in human malignant cell lines expressing a more immature phenotype.
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PMID:A cell surface antigen (BAL) defined by a mouse monoclonal antibody inducing apoptosis in a human lymphocytic leukemia cell line. 818 58

Six hybridoma cell lines secretion monoclonal antibodies(MAbs) against broad bean wilt virus(BBWV) were produced by fusing mouse myeloma cells(SP 2/0) with spleen cells from BAL B/c immunized by the BBWV particles. The hybridoma cell lines secreted MAbs stably after cultured in vitro for 3 months or stored in liquid nitrogen and then revived for several times. The titres of ascitic fluids of six MAbs ranged from 1:256,000 to 1:640,000 when measured by indirect ELISA. In agarose gel immunodiffusion test, it showed that the six MAbs represented the same isotype of murine antibodies, IgG1. Six MAbs could detect 4 tested BBWV isolates, but didn't crossreact with other 5 plant viruses. The result of Western blot showed that all the six MAbs can react with the 44.7 kD large coat protein subunit of BBWV. This is the first report of production of MAbs against BBWV.
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PMID:[Production of monoclonal antibodies to broad bean wilt virus and application in virus detection]. 1254 40

Four hybridoma cell lines secreting monoclonal antibodies(MAbs) against Tomato mosaic virus(ToMV) were produced by fusing mouse myeloma cells(SP2/0) with spleen cells from BAL B/c immunized by the ToMV particle. The four MAbs could specifically react with ToMV, and the MAbs from two cell lines can react with ToMV and TMV simultaneously. The titres of ascitic fluids of four MAbs ranged from 1:32,000 to 1:1,024,000 with ELISA, and the sensitivity for detection virus from the plant sap reached over 1:2000 dilution. The MAbs didn't crossreact with other plant viruses. The result of Western-blot showed that two MAbs can react with the 17.6 kD ToMV coat protein submit specifically, while the other two MAbs can not react with it, they are supposed to against conformational determinants of ToMV CP.
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PMID:[Production of monoclonal antibodies to tomato mosaic virus and application in virus detection]. 1255 52

Lenalidomide is an immunomodulatory agent approved for use in patients with myelodysplastic syndrome, and in combination with dexamethasone for refractory or relapsed multiple myeloma. Pulmonary toxicity is believed to be uncommon. In this report, we describe a patient receiving lenalidomide in whom dyspnea, fever, hypoxia, and diffuse pulmonary infiltrates developed. BAL demonstrated a significant lymphocytic alveolitis typical for hypersensitivity pneumonitis. Extensive workup for other causes, including infections, was negative. Finally, the patient had improvement in symptoms and oxygenation after withdrawing lenalidomide and recurrence of symptoms when the drug was restarted. Thus, the patient's clinical course and workup strongly support a diagnosis of lenalidomide-induced hypersensitivity pneumonitis-like syndrome. Physicians should be cognizant of this potential complication in patients receiving thalidomide or thalidomide-like drugs who present with fever and pulmonary infiltrates and fail to improve despite treatment with broad-spectrum antibiotics.
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PMID:Hypersensitivity pneumonitis-like syndrome associated with the use of lenalidomide. 1749 8

A 68-year-old man with multiple myeloma was admitted to our hospital complaining of slight fever and dyspnea on effort 4 months after treatment with thalidomide. Chest HRCT findings showed diffuse ground-glass attenuation, small nodules, and interlobular septal thickening in bilateral lungs. BAL showed marked lymphocytosis, and TBLB revealed alveolitis with exudative change, consistent with drug-induced interstitial pneumonitis. His thalidomide treatment was withdrawn and his symptoms and HRCT findings improved. Therefore, we diagnosed thalidomide-induced interstitial pneumonitis. Thalidomide-induced interstitial pneumonitis is rare, and only 4 cases have been reported in the literature. We concluded that we should consider thalidomide-induced interstitial pneumonitis in cases with multiple myeloma following thalidomide treatment.
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PMID:[Case of thalidomide-induced interstitial pneumonia]. 1951 9

Pulmonary involvement with multiple myeloma is rare. We report the case of a 61-year-old man with past medical history of chronic respiratory failure with emphysema, and a known multiple myeloma (Durie and Salmon stage III B and t(4;14) translocation). Six months after diagnosis and first line of treatment, he presented acute dyspnea with interstitial lung disease. Computed tomography showed severe bullous emphysema and diffuse, patchy, multifocal infiltrations bilaterally with nodular character, small bilateral pleural effusions, mediastinal lymphadenopathy, and a known lytic lesion of the 12th vertebra. He was treated with piperacillin-tazobactam, amikacin, oseltamivir, and methylprednisolone. Finally, outcome was unfavourable. Postmortem analysis revealed diffuse and nodular infracentimetric infiltration of the lung parenchyma by neoplastic plasma cells. Physicians should be aware that acute respiratory distress syndrome not responding to treatment of common causes could be a manifestation of the disease, even with negative BAL or biopsy and could be promptly treated with salvage therapy.
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PMID:Lung postmortem autopsy revealing extramedullary involvement in multiple myeloma causing acute respiratory distress syndrome. 2516 87