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简介：Multiplemyeloma(MM)isamalignancyoftheplasmacellcharacterizedbymigrationandlocalizationtothebonemarrowwherecellsthendisseminateandfacilitatetheformationofbonelesions.Itisassociatedwithaconstellationofdiseasemanifestations,apartfromosteolyticlesions,anemiaandimmuno-suppressionduetolossofnormalhematopoieticstemcellfunction,andcardiacamyloidosisduetomonoclonalimmunoglobulinsecretionaswell[1].Amyloidinfiltrationoftheheartmayfrequentlymasqueradeashypertrophiccardiomyopathy(HCM).HCM,ofwhichunderlyingcauseandpathogenesisarelargelyunknown,ischaracterizedbyleftand/orrightventricularhypertrophy,withpredominantinvolvementoftheinterventricularseptumintheabsenceofothercausesofhypertrophy,suchashypertensionorvalvularheartdiseases[2].Whileexcessivehypertrophyofthemyocardiumismostcommonlyassociatedwithmyocytehypertrophy,infiltrationwithamyloidalwaysneedstobeconsidered.Inthisreportwepresentedtwocasesofmultiplemyelomathatmimickedhypertrophiccardiomyopathysocloselythatitrequiredbonemarroworendomyocardialbiopsytoestablishthediagnosis.

简介：AbstractBone disease is the most common complication in patients with multiple myeloma (MM), and it may lead to skeletal-related events (SREs) such as bone pain, pathological fractures, and spinal cord compression, which impair a patients' quality of life and survival. The pathogenesis of myeloma bone disease (MBD) involves disruption of bone reconstitution balance including excessive activation of osteoclasts, inhibition of osteoblasts, and participation of osteocytes and bone marrow stromal cells. Various factors, such as the receptor activator of nuclear factor-κB ligand (RANKL)/osteoprotegerin (OPG), dickkopf-1 (DKK-1), sclerostin, and activin-A, are involved in the development of MBD. Bisphosphonates and the anti-RANKL antibody denosumab are currently the main treatment options for MBD, delaying the onset of SREs. Denosumab is preferred in patients with MM and renal dysfunction. Although effective drugs have been approved, antimyeloma therapy is the most important method for controlling bone disease.

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简介：AbstractTreatment of multiple myeloma (MM) has advanced dramatically in the past two decades. However, under the conditions of the COVID-19 pandemic, treatment strategies have been modified accordingly. Numerous novel agents, updated trials, and major advances in myeloma have been reported in the American Society of Hematology 2020 annual meeting, either for transplant-eligible or ineligible patients. Hot topics such as the significance of autologous stem cell transplantation (ASCT), development of novel agents, and chimeric antigen receptor-T (CAR-T) cells have been widely discussed. The triplet regimen bortezomib, lenalidomide, and dexamethasone (VRd) is recommended as the standard first-line treatment, and the addition of a fourth drug improves efficacy and survival. The value of ASCT remains undoubtful, even in the era of quadruplet induction. Dual-drug maintenance, including proteasome inhibitors and immunomodulatory drugs, overcomes unfavorable outcomes in high-risk patients. For relapsed/refractory myeloma (RRMM) patients, novel agents such as selinexor and venetoclax are superior. CAR-T cells and other cell-surface-targeted therapies also appear promising.

简介：客观多重骨髓瘤是从B淋巴细胞发源的一种恶意的血浆房间疾病并且分泌monoclonal免疫球蛋白的大数量。它仍然目前是倔强的疾病之一。众多的研究证明在histoneacetylation的不平衡和多重骨髓瘤的occurance之间有一种集中的关系。这里，我们在增长，apoptosis，histoneH3和H4acetylation和histonedeacetylase的表示上调查了triptolide(TPL)的效果8(HDAC8)在vitro，探索它的反骨髓瘤机制。RPMI8226的生长上的triptolide的效果被3-(4,5-Dimethyl-2-thiazolyl)学习的方法-2,5-diphenyl-2H-tetrazolium(MTT)试金。Apoptosis被染色的Hoechst33258检测。acetyl-histoneH3和H4的蛋白质表情被西方的污点决定，并且HDAC8的表示被RT-PCR，西方的污点和共焦的显微镜学估计。结果Triptolide禁止了RPMI8226的增长并且在一个时间依赖者和剂量依赖者举止导致了apoptosis。36hIC50价值是(105.370敢漠?摀畲獧吗？

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简介：Inourpreviousstudies,DAZAP2geneexpressionwasdown-regulatedinuntreatedpatientsofmultiplemyeloma(MM).ForbetterstudyingthestructureandfunctionofDAZAP2,afull-lengthCdnawasisolatedfrommononuclearcellsofanormalhumanbonemarrow,sequencedanddepositedtoGenbank(AY430097).ThissequencehasanidenticalORF(openreadingframe)astheNM_014764fromhumantestisandtheD31767fromhumancelllineKG-1.PhylogeneticanalysisandstructurepredictionrevealthatDAZAP2homologuesarehighlyconservedthroughoutevolutionandshareapolyprolineregionandseveralpotentialSH2/SH3bindingsites.DAZAP2occursasasingle-copygenewithafour-exonorganization.WefurthernoticedthatthefunctionalDAZAP2geneislocatedonChromosome12anditspseudogenegeneisonChromosome2withelectroniclocationofhumanchromosomeinGenbank,thoughnogeneticabnormalitiesofMMhavebeenreportedonChromosome12.TheORFofhumanDAZAP2encodesa17-kDaprotein,whichishighlysimilartomousePrtb.TheDAZAP2proteinismainlylocalizedincytoplasmwithadiscretepatternofpunctuateddistribution.DAZAP2mayassociatewithcarcinogenesisofMMandparticipateinyet-to-beidentifiedsignalingpathwaystoregulateproliferationanddifferentiationofplasmacells.

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简介：目的将在细胞生长，细胞周期和p21wap1/cip1和p27kip1的表情上调查triptolide(TPL)的效果。方法MTT试金被用来在人的多重骨髓瘤RPMI-8226房间在triptolide处理以后决定房间生存能力。房间周期分发上的效果被流动cytometry决定。半量的反向的transcription-PCR被用来检验p21wap1/cip1和p27kip1的mRNA表情。p21wap1/cip1和p27kip1的蛋白质表情被西方的污点决定。改变集中的结果Triptolide以剂量相关、时间相关的时尚导致了房间生存能力抑制并且在RPMI-8226房间引起了G0-G1房间周期前进的阶段拘捕。伴有p21wap1/cip1和p27kip1的表情的起来调整的这些效果。这些结果建议那triptolide的结论经由起来调整的p21wap1/cip1和p27kip1禁止房间增长和房间周期前进，triptolide可以通过这条小径施加它的反癌症活动。