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)

Twelve steroidal platinum(II) complexes were synthesized by reaction of potassium tetrachloroplatinate with steroidal esters of L-methionine and L-histidine. The steroidal esters coordinated as bidentate ligands via S and N donor atoms of L-methionine and via two N donor atoms of L-histidine. Cholesterol, cholestanol, diosgenine, pregnenolone, dehydroepiandrosterone, testosterone, estrone, and estradiol were used as the steroidal compounds. The esters and complexes prepared were characterized by infrared, mass, and (1)H NMR spectroscopy and elemental analysis. Platinum complexes were tested for in vitro cytotoxicity against several cancer cell lines: T-lymphoblastic leukemia CEM, breast carcinoma MCF-7, lung carcinoma A-549, multiple myeloma RPMI 8226, and one normal cell line human fibroblast BJ.
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PMID:Platinum(II) complexes with steroidal esters of L-methionine and L-histidine: synthesis, characterization and cytotoxic activity. 1829 92

TDRD7 is a scaffold protein whose specific function is unknown. It has been identified in complexes with proteins that regulate cytoskeleton dynamics and centrosomal movements, mRNA transport, and protein translation apparatus. Here we report the generation and characterization of monoclonal antibodies against TDRD7 protein. Bacterially expressed His-tagged fragments of TDRD7 were used as antigens. Spleen cells from immunized mice were collected and fused with SP2/0 myeloma cells using PEG 2000. High titer anti-TDRD7 antibody-producing hybridoma cell lines were identified by enzyme-linked immunosorbent assay (ELISA) and then subcloned by limiting dilution. Antibodies produced by E6 clone were further tested for their reactivity with the TDRD7 recombinant proteins. The results obtained clearly indicate that E6 anti-TDRD7 antibodies recognize specifically recombinant 6His-tagged TDRD7 proteins and endogenous TDRD7 in Western blotting, immunoprecipitation, and immunocytochemistry. In summary, these antibodies will be useful for researchers investigating TDRD7 and molecular complexes involving this protein.
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PMID:Generation and characterization of monoclonal antibodies to TDRD7 protein. 1858 16

We present a case of a 76-year-old Japanese man with hypertension and multiple myeloma (MM) presented with syncope and sinus bradycardia. Thalidomide therapy for MM was added to longstanding atenolol therapy one month prior to presentation. His heart rate (HR) was around 70 beats per minute (bpm) before addition of Thalidomide. His HR on presentation was less than 30 bpm. He was treated with intravenous atropine followed by temporary pacemaker and taken off atenolol. His HR returned to around 70 bpm few days after discontinuation of atenolol, even though he was still taking thalidomide, permitting outpatient management without a pacemaker. Both thalidomide and atenolol have been reported to cause bradycardia. Neither agent caused bradycardia when used alone in this patient, but simultaneous use caused symptomatic bradycardia. As thalidomide is prescribed more frequently, clinicians should be aware of the possibility of drug-induced sinus bradycardia due to the interaction of thalidomide and beta-blockers.
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PMID:Syncope and sinus bradycardia from combined use of thalidomide and beta-blocker. 1861 49

We herein report an extremely rare case of a patient with IgD-lambda positive multiple myeloma presenting with myelomatous pleural effusion and ascites. A 58-year-old man visited our hospital with dyspnea as his initial symptom. His chest radiograph findings on admission revealed a left pleural effusion, and later, bilateral involvement. Computed tomography (CT) of the chest showed a paraspinal tumor with extension from the upper mediastinum to the abdomen. The cytological examination demonstrated myeloma cells in the pleural effusion and ascites, and histologically, in the pleura, an abdominal subcutaneous tumor and bone was observed. The pleural effusion was an exudate and slightly bloody. The ADA was 70 IU/L. Pleural effusion accompanying myeloma or primary pleural myeloma is very rare and, furthermore, the extremely rare findings of both myeloma cells in the ascites (although the ascites was mainly caused by liver cirrhosis) and a high ADA activity in the pleural fluid were also observed in this case.
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PMID:Multiple myeloma presenting initially with pleural effusion and a unique paraspinal tumor in the thorax. 1898 37

Hydrocortisone was investigated for its ability todifferentiate human leukemia KU812 cells into maturehematopoietic cells including basophils. Hydrocortisonetreatment increased the amount of intracellular histamine byup-regulation of L-histidine decarboxylase (HDC) mRNA andenhanced cell surface expression of the high affinity IgEreceptor FcepsilonRI. Histamine is catalyzed from L-histidine byHDC, which in blood cell types is only expressed in basophilsand mast cells. Cells, on which the FcepsilonRI expression wasenhanced by hydrocortisone, were shown to release histaminewhen stimulated with anti-IgE antibody after sensitizationwith myeloma IgE, implying that the induced FcepsilonRI moleculeswere able to transduce a signal for degranulation. Theseresults suggest that hydrocortisone promotes differentiationof KU812 cells into functionally mature basophilic cells.
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PMID:Increase in histamine content and enhancement of high affinity IgE receptor FcepsilonRI expression in the human leukemia KU812 cells upon treatment with hydrocortisone. 1900 97

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

Fibroblast growth factor receptor 3 (FGFR3) is a member of the FGFR family of receptor tyrosine kinases, whose function has been implicated in diverse biological processes, including cell proliferation, differentiation, survival, and tumorigenesis. Deregulation of FGFR3 signaling has been implicated with human pathologies, including cancer. Activating mutations in FGFR3 gene are frequently detected in bladder cancer, multiple myeloma, and noninvasive papillary urothelial cell carcinomas, while the overexpression of the receptor is observed in thyroid lymphoma and bladder cancer. The main aim of this study was to generate hybridoma clones producing antibody that could specifically recognize FGFR3/S249C mutant, but not the wild-type FGFR. To achieve this, we used for immunization bacterially expressed fragment of FGFR3 corresponding to loops II-III of the extracellular domain (GST-His/FGFR3/S249C-LII-III), which possesses oncogenic mutation at Ser249 detected in at least 50% of bladder cancers. Primary ELISA screening allowed us to isolate several hybridoma clones that showed specificity towards FGFR3/S249C, but not FGFR3wt protein. Unfortunately, these clones were not stable during single-cell cloning and expansion and lost the ability to recognize specifically FGFR3/S249C. However, this study allowed us to generate several monoclonal antibodies specific towards both FGFR3wt and FGFR3/S249C recombinant proteins. Produced hybridomas secreted MAbs that were specific in Western blotting towards bacterially expressed FGFR3wt and FGFR3/S249C, as well as the full-length receptors ectopically expressed in Sf21 and HEK293 cells. Moreover, transiently expressed wild-type and oncogenic forms of FGFR were efficiently immunoprecipitated with selected antibodies from the lysates of infected Sf21 and transiently transfected HEK293. In summary, generated antibodies should be useful as tools for examining the expression pattern and biological functions of FGFR3 in normal and pathological cells and tissues.
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PMID:Generation of monoclonal antibody targeting fibroblast growth factor receptor 3. 1966 3

Light-Chain Deposition Disease (LCDD) frequently recurs after renal transplantation, displaying a pernicious course. Herein we have described a 39-year-old Caucasian man with a history of immunoglobulin G-kappa multiple myeloma who failed two chemotherapy regimens, but ultimately responded to the combination of thalidomide, bortezomib, and dexamethasone followed by high-dose melphalan and autologous stem cell transplantation 3 years prior to transplantation, during which time he showed no evidence of persistent or recurrent disease. At 3 days following spousal living related renal transplantation, he displayed a rapid deterioration of renal function requiring dialysis therapy. This episode failed to respond to empiric antirejection therapy including anti-thymocyte globulin, plasmapheresis, and anti-CD20 monoclonal antibody. Increasing evidence suggested recurrence of LCDD, including positive immunofluorescence staining of basement membranes and vessels for kappa light chains as well as free kappa light chains in his urine and serum. Following suspension of sirolimus, he was initiated on and responded to bortezomib (1.3 mg/m(2)) with discontinuation of dialysis within 3 weeks and progressively improving renal function. His maintenance therapy, in addition to six 2-week-long cycles of bortezomib separated by 1-week rest periods, includes cyclosporine (50 mg twice daily), prednisone (10 mg daily), and curcumin (9 g daily). In sum, bortezomib rescue therapy salvaged a spousal renal transplant afflicted with recurrent LCDD.
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PMID:Bortezomib successfully reverses early recurrence of light-chain deposition disease in a renal allograft: a case report. 2000 9

A 51-year-old male was diagnosed with an IgA multiple myeloma (MM) after having back pain for several months. His bone marrow showed 30% involvement with plasma cells and his cytogenetics showed t(4:14). His beta2-microglobulin was 6.5 mg/dL at diagnosis and he had multiple lytic lesions, along with a creatinine of 2.3 mg/dL and significant anemia. Induction therapy with lenalidomide, bortezomib and dexamethasone was used, and he was able to achieve complete remission after 4 cycles of therapy. He then went on to receive high-dose chemotherapy with a single autologous stem cell transplant. He tolerated it well and now comes to discuss follow-up treatment plans. He wants to discuss maintenance therapy.
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PMID:ASH evidence-based guidelines: what is the role of maintenance therapy in the treatment of multiple myeloma? 2000 43

A set of mouse IgAs containing amino acids differing amongst the six alpha-chain allotypes was constructed by mutating an S107-IgA plasmid and transfecting it into a non-producer myeloma cell line along with a kappa-chain plasmid. The secreted IgAs were examined for their possession of a covalent bond between alpha- and light (L)-chains and for their ability to bind to three anti-allotypic monoclonal antibodies, HIS-M2, HY-15, and HY-16. IgA of the Igh-2(a) allotype was found to be unique in its total lack of a covalent bond between alpha and L: -chains, formation of which apparently depends on the presence of an "extra" Cys in the hinges of all of the other five allotypes. The allotypic epitopes are associated with identifiable amino acids in the Calpha1 region of the molecule. Binding to HIS-M2 requires Ala 216 whereas binding to HY-15 requires Pro 216 and Asp 222. Binding to Hy-16 requires Arg 183 and either Pro 216 or Ser 216 but not Ala 216. However, binding to HY-16 by all of the IgAs produced by transfectants is impaired by defective glycosylation in the transfected myeloma and is only revealed after deglycosylation.
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PMID:Structural correlates of mouse IgA allotypes. 2001 55


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