ライフサイエンスコーパス: plasma cell

1 nd 8 white blood cells, including 1 atypical plasma cell.

2 antigen is expressed by normal and malignant plasma cells.

3 expressed in patient MM cells than in normal plasma cells.

4 ntial for the tumorigenesis of the malignant plasma cells.

5 ependent plasmablasts and T-cell-independent plasma cells.

6 r Blimp-1 is necessary for the generation of plasma cells.

7 or T cell-independent B220(-)CD138(+) IgM(+) plasma cells.

8 used by immunoglobulin LC produced by clonal plasma cells.

9 IgA, rectal memory B cells, and total rectal plasma cells.

10 activated B cells and antibody production in plasma cells.

11 3(-)CD25(+)CD71(+) BR1 cells and a subset of plasma cells.

12 mory based upon intrinsic longevity of human plasma cells.

13 of B cells into isotype-switched B cells and plasma cells.

14 ents have normal numbers of B cells but lack plasma cells.

15 ed the differentiation of B lymphocytes into plasma cells.

16 (TFH) cell responses and reduced numbers of plasma cells.

17 specific, or PspC-specific memory B cells or plasma cells.

18 with differentiation into memory B cells or plasma cells.

19 gulate IgG4 antibodies on differentiation to plasma cells.

20 expansion, T cell activation, and increased plasma cells.

21 oma is an aggressive hematopoietic cancer of plasma cells.

22 , including depleting autoantibody-producing plasma cells.

23 creased antibody titers and lower numbers of plasma cells.

24 prevented differentiation of GC B cells and plasma cells.

25 ing B cells, macrophages, and CD138-positive plasma cells.

26 s the B cell maturation antigen expressed on plasma cells.

27 Ag-specific memory B cells and Ab-secreting plasma cells.

28 ding to the generation of memory B cells and plasma cells.

29 chromosomal/genetic changes present in tumor plasma cells.

30 rmation of GCs, and increasing the number of plasma cells.

31 e we show that antigen-specific, induced IgM plasma cells also persist for a lifetime.

32 h cells and mount defective T-cell-dependent plasma cell and germinal centre responses.

33 D4 antigen; they are important in supporting plasma cell and germinal centre responses.

34 duction was detected in cultures of CD138(+) plasma cells and CD138(-) cells isolated from bone marro

35 o specifically target antibody production by plasma cells and determine the impact on atherosclerotic

36 ite-specific survival of bone marrow-derived plasma cells and durable antibody responses to multiple

37 these humoral responses generate long-lived plasma cells and generate Abs capable of neutralizing va

38 files which has a greater impact on changing plasma cells and germinal center B cell populations in f

39 1 (XBP1) drive B-cell differentiation toward plasma cells and have been shown to contribute to multip

40 are not affected, both differentiation into plasma cells and IgM production are impaired in Stat1(-/

41 Increased frequency of antigen-specific plasma cells and long-lived bone marrow plasma cells was

42 d developed fewer spleen and bone marrow IgG plasma cells and memory B cells, compared with controls.

43 al expansion, and differentiation to produce plasma cells and memory B cells.

44 Although normal plasma cells and most multiple myeloma cells require Mcl

45 The anti-FcRH5/CD3 TDB kills human plasma cells and patient-derived myeloma cells at picomo

46 As key antibody producers, plasma cells and plasmablasts are critical components of

47 , alterations existed in the distribution of plasma cells and plasmablasts between macaques that exhi

48 emia and unvaccinated macaques had increased plasma cells and plasmablasts compared to vaccinated ani

49 nsitional stage 2-like B cells, and CD138(+) plasma cells and plasmablasts.

50 -existing antibodies expressed by long-lived plasma cells and rapidly reactive memory B cells (MBC).

51 present precursors of autoantibody-secreting plasma cells and suggests a role for these autoreactive

52 ysis of human tonsillar tissue revealed that plasma cells and their precursors in the GC expressed hi

53 ed CD8(+) T cells, terminally differentiated plasma cells, and activated epithelial cells, pointing t

54 main IRF4(hi) subsets of interest: CD138(+) plasma cells, and CD138(-) plasmablasts.

55 ntre cells are transient, most IgE cells are plasma cells, and high affinity IgE is produced by the s

56 g class-switched B cells, antibody-secreting plasma cells, and memory B cells.

57 oliferation, differentiation of B cells into plasma cells, and robust antibody secretion after a few

58 Long-lived plasma cells are critical to humoral immunity as a lifel

59 lin gene retrieval analysis shows that these plasma cells are derived from a germ line repertoire of

60 c processes that regulate antibody-secreting plasma cells are not well understood.

61 entres and then home to the bone marrow, IgM plasma cells are primarily retained within the spleen an

62 However, these IgM plasma cells are probably not antigen-selected, as repla

63 luorescence in situ hybridization (iFISH) of plasma cells are routinely evaluated as prognostic marke

64 Plasma cells are the major producers of antibodies durin

65 Hence, many essential functions of plasma cells are under the control of Blimp-1.

66 Because recent studies have identified plasma cells as a relevant source of the immunosuppressi

67 It highlights the importance of plasma cells as regulatory cells in allergic inflammatio

68 After treatment, bone marrow plasma cells became undetectable by flow cytometry, and

69 responding patients with < 1% of circulating plasma cells before HDM/ASCT.

70 We review here aspects of plasma cell biology with an emphasis on recent studies a

71 of significance for normal PCD and malignant plasma cell biology.

72 26; melphalan-resistant LR5) and bone marrow plasma cells (BMPCs) from MM patients who responded (n =

73 We show that LGR4 is expressed by MM plasma cells, but not by normal plasma cells or B cells.

74 lin light chains (LC) are produced by clonal plasma cells, but only in AL do they form amyloid deposi

75 ed with decreased IgG-expressing B cells and plasma cells, but unchanged numbers and functions of mye

76 ofiled the reactivities of single murine IgA plasma cells by cloning and characterizing large numbers

77 s with important functions in GC B cells and plasma cells by inducing and maintaining DNase I hyperse

78 Multiple myeloma (MM) is a plasma cell cancer that develops in the skeleton causing

79 ctive management of multiple myeloma (MM), a plasma cell cancer.

80 ent isotype, and a terminally differentiated plasma cell cannot contribute to the memory pool.

81 ffinity maturation of the B cells to produce plasma cells capable of secreting high-affinity antibody

82 hematologic malignancy of clonal bone marrow plasma cells characterized by destructive bone lesions a

83 g developed that might be combined with anti-plasma cell chemotherapy.

84 AL) amyloidosis is caused by a usually small plasma cell clone producing a misfolded light chain that

85 are linking specific characteristics of the plasma cell clone to response to different types of trea

86 genetic alterations that affect whether MGUS plasma cell clones are responsive to anti-multiple myelo

87 dies comparing how MGUS and multiple myeloma plasma cell clones respond to these therapies are scarce

88 ed to identify how MGUS and multiple myeloma plasma cell clones responded to anti-multiple myeloma th

89 r depth of response against multiple myeloma plasma cell clones than MGUS plasma cell clones.

90 ble to therapy are present in only some MGUS plasma cell clones.

91 ultiple myeloma plasma cell clones than MGUS plasma cell clones.

92 e also report the persistence of numerous BM plasma cell clonotypes ( approximately 2%) identifiable

93 Inhibition of DNA methylation enhanced plasma cell commitment in a cell-division-dependent mann

94 overexpressed in multiple myeloma (MM) tumor plasma cells compared to their normal counterpart, sugge

95 d by neutrophils and infiltrating submucosal plasma cells consisting primarily of T cells.

96 Of note, treatment-resistant plasma cells contained a substantial proportion of CD19(

97 ow levels similar to their normal B-cell and plasma cell counterparts.

98 bone marrow samples, the microfluidic-based plasma cell counts exhibited excellent correlation with

99 ls, permits quantitation of rare circulating plasma cells (CPCs) in blood and subsequent fluorescence

100 h autoreactive memory B cell development and plasma cell-derived autoantibody production.

101 Molecular signatures of B and plasma cells detected in PBMCs were highly correlated wi

102 Provision of sIgM rescued plasma cell development from mus(-/-) but not Fcmr(-/-)

103 2 controlled germinal center (GC) B cell and plasma cell development.

104 is indicates that high affinity IgE and IgG1 plasma cells differentiate from rare CD80(+)CD73(+) high

105 ysis of miRNAs and mRNAs during human normal plasma cell differentiation (PCD).

106 revealed that MYSM1 intrinsically represses plasma cell differentiation and antibody production.

107 and disease progression via perturbation in plasma cell differentiation and endoplasmic reticulum ho

108 is known about the role of mTOR signaling in plasma cell differentiation and function.

109 stance in MM and retinoid signaling promotes plasma cell differentiation and Ig production, we invest

110 RA within the BM microenvironment prevented plasma cell differentiation and promoted a B cell-like,

111 T follicular helper cells, TPH cells induce plasma cell differentiation in vitro through IL-21 secre

112 Finally, plasma cell differentiation of sorted LPS-stimulated MZ

113 Here, analysis of plasma cell differentiation revealed DNA hypomethylation

114 maturation, class switch recombination, and plasma cell differentiation within the germinal center.

115 elves controls the germinal center reaction, plasma cell differentiation, and specific Ab production

116 eptors (TLR), despite paradoxically enhanced plasma cell differentiation.

117 d3 and E-protein activity govern both GC and plasma cell differentiation.

118 ly and late phases of antibody responses and plasma cell differentiation.

119 iptional network that controls GC B cell and plasma cell differentiation.

120 ed genes essential for B-cell activation and plasma cell differentiation.

121 ation reflects the cis-regulatory history of plasma cell differentiation.

122 ly demonstrated a critical role for Cdc42 in plasma cell differentiation.

123 class switch recombination and memory B and plasma cell differentiation.

124 candidates for clinical trials testing novel plasma cell-directed chemotherapy beyond first line may

125 cance (MGUS) is an asymptomatic premalignant plasma cell disorder.

126 in patients with multiple myeloma and other plasma cell disorders, including smouldering multiple my

127 trate that Zbtb32(-/-) secondary bone marrow plasma cells display elevated expression of genes that p

128 Plasma cell dyscrasias, including monoclonal gammopathy

129 In multiple myeloma malignant plasma cells expand within the bone marrow.

130 rious hematological and solid tissues, while plasma cells express particularly high levels of CD38.

131 of (a) terminally differentiated B-1-derived plasma cells expressing the transcriptional regulator of

132 ion of high affinity memory B cells into the plasma cell fate, our findings provide fundamental insig

133 ctor neutralization significantly diminished plasma cell formation, directly linking EG with the humo

134 rity of patients with mCRPC, the analysis of plasma cell-free DNA (cfDNA) has recently emerged as a m

135 ps between circulating tumor cells (CTCs) or plasma cell-free DNA (cfDNA) on one side and a comprehen

136 n addition, immature granulocyte (IG) count, plasma cell-free DNA (cfDNA), and plasma citrullinated h

137 To characterize plasma cell-free eccDNAs, we performed sequencing analys

138 In this study, we found that plasma cell-free RNA was significantly increased followi

139 Env-specific memory B cell, plasmablast, or plasma cell frequencies in the three compartments.

140 if the same macaques maintained high mucosal plasma cell frequencies postinfection and if this transl

141 virus (SIV) exposure correlated with rectal plasma cell frequency in vaccinated female rhesus macaqu

142 In rectal tissue, plasma cell frequency positively correlated with plasma

143 In contrast, sclerostin was not expressed by plasma cells from 630 patients with myeloma or 54 myelom

144 LCs are secreted from clonally expanded plasma cells, generally as disulfide-linked dimers, with

145 ll-activating factor that highly accelerated plasma cell generation and antigen-specific antibody pro

146 on of germinal center (GC) B cell phenotype, plasma cell generation, and virus-specific Ab responses.

147 g B cell proliferation, differentiation, and plasma cell generation.

148 During differentiation of primary B cells to plasma cells, hnRNPLL mediates a genome-wide switch of R

149 ividual across 6.5 years to show that the BM plasma cell immunoglobulin heavy chain repertoire is rem

150 evelopment and differentiation of long-lived plasma cells in a multilayered process that is tightly c

151 tigen-specific memory B cells in spleens and plasma cells in bone marrow despite their lower levels o

152 omplete depletion of B cells and bone marrow plasma cells in cynomolgus monkeys.

153 Plasma cells in human bone marrow (BM) are thought to be

154 tion of GCs, and increased the population of plasma cells in immunized mice.

155 ngivalis, greater IL-12 expression, and more plasma cells in lymph nodes following oral inoculation a

156 as a common feature of normal and neoplastic plasma cells in mice, and IL-10 levels increased with my

157 rogated the generation of antibody-secreting plasma cells in mice.

158 The contribution of autoantibody-producing plasma cells in multiple sclerosis (MS) remains unclear.

159 te response, germinal centers in the spleen, plasma cells in popliteal lymphoid nodes, bone marrow ce

160 high-level expression of SLAMF7 on malignant plasma cells in previously untreated and in relapsed/ref

161 6 (IL-6) only regulates B cells committed to plasma cells in response to T-dependent (TD) antigens wi

162 rized by abnormal proliferation of malignant plasma cells in the bone marrow (BM).

163 characterized by the expansion of malignant plasma cells in the bone marrow (BM).

164 iple myeloma, an overabundance of monoclonal plasma cells in the bone marrow induces localized osteol

165 rminal centres and persist as long-lived IgG plasma cells in the bone marrow.

166 ed with the frequency of treatment-resistant plasma cells in the bone marrow.

167 rategies led to the ablation of newly formed plasma cells in the spleen and bone marrow while also ob

168 e glycoprotein trimeric gp41; 2) produced by plasma cells in the submucosa and ectopic tertiary lymph

169 Fibrosis and accumulation of IgG4(+) plasma cells in tissue are hallmarks of the disease, and

170 plasmablasts ex vivo and antibody-secreting plasma cells in vivo.

171 ory B cells decreased and the number of 6BPS plasma cells increased postinoculation.

172 atures of human MM, including bone malignant plasma cell infiltration, a monoclonal immunoglobulin pe

173 and confirmed by the findings of bone marrow plasma cell infiltration, with t(11;14) chromosomal abno

174 n vivo differentiation to antibody-secreting plasma cells is blocked.

175 ation/differentiation of memory B cells into plasma cells is required to sustain long-term antibody p

176 ewer T follicular helper cells, B cells, and plasma cells, leading to decreased production of anti-ds

177 Primary plasma cell leukemia (pPCL) is a rare and aggressive mal

178 A woman in her 40s with a history of plasma cell leukemia presented with 1 month of intermitt

179 extramedullary stages of the disease such as plasma cell leukemia.

180 Dual-infected cells displayed a plasma cell-like gene expression pattern similar to PELs

181 induce high levels of bone marrow long-lived plasma cell (LLPC) antibody production.

182 accines induced antigen-specific, long-lived plasma cells (LLPCs), which persisted in the bone marrow

183 tion of memory B cells (MBCs) and long-lived plasma cells (LLPCs).

184 ation or infection is mediated by long-lived plasma cells (LLPCs).

185 unoglobulin-secreting activity of long-lived plasma cells (LLPCs).

186 Multiple myeloma is a plasma cell malignancy characterized by recurrent IgH tr

187 Multiple myeloma (MM) is a plasma cell malignancy leading to significant life-expec

188 Multiple myeloma (MM) is a plasma cell malignancy that is largely incurable due to

189 Multiple myeloma (MM) is a plasma cell malignancy with a significant heritable basi

190 In multiple myeloma (MM), a plasma cell malignancy, most tumors display hallmarks of

191 d increased Ig production--both hallmarks of plasma-cell maturation.

192 ination/BrdU administration, indicating that plasma cells may persist for a prolonged period of time

193 Immunizations that maximize these plasma cell metabolic properties might thus provide endu

194 Moreover, BrdU(+) cells with plasma cell morphology can be detected for 10 years afte

195 To maintain Ab titers, individual plasma cells must survive for extended periods, perhaps

196 to investigate the entire spectrum of human plasma cell neoplasia and illustrate the utility of huma

197 the context of various immune disorders and plasma cell neoplasia.

198 N in the allograft and clinically detectable plasma cell neoplasm 9 years after the first renal manif

199 Multiple myeloma is a fatal plasma cell neoplasm accounting for over 10,000 deaths i

200 Multiple myeloma is a plasma cell neoplasm with an extremely variable clinical

201 whole exome sequencing, the pathogenesis of plasma cell neoplasms in these mice is not linked to act

202 tulates the systemic manifestations of human plasma cell neoplasms, and implicates cooperativity betw

203 e observed for acute lymphoblastic leukemia, plasma cell neoplasms, or diffuse large B-cell lymphoma.

204 s/s) mice die from multiple myeloma or other plasma cell neoplasms.

205 sis of proteins involved in establishment of plasma cell niches in sorted bone marrow and rectal cell

206 ge immediately elicits striking increases in plasma cells not only in the female reproductive tract b

207 a panel of anti-TG2 mAbs generated from gut plasma cells of celiac patients and identified four epit

208 dentified epitopes targeted by antibodies of plasma cells of the disease lesion.

209 It is commonly postulated that plasma cells only gain access to these signals within sp

210 ressed by MM plasma cells, but not by normal plasma cells or B cells.

211 plexes by antibody generated from GC-derived plasma cell output will gradually reduce the availabilit

212 he fate choice made by B cells, favoring the plasma cell over memory cell fate without significantly

213 s elevated levels of factors associated with plasma cell (PC) differentiation.

214 Unexpectedly, such DeltaV-kappaLCs inhibit plasma cell (PC) differentiation.

215 d XBP1, transcriptional master regulators of plasma cell (PC) differentiation.

216 ng modalities in the evaluation of malignant plasma cell (PC) disease multiple myeloma (MM).

217 Blimp-1 is essential for efficient plasma cell (PC) generation, and although CD40 signaling

218 their mediators enhance memory responses and plasma cell (PC) survival, suggesting that they directly

219 ndent on the ability of the multiple myeloma plasma cells (PC) to reenter the circulation and dissemi

220 nvestigated frequencies of serotype-specific plasma cells (PCs) and memory B-cells (Bmems) as potenti

221 The number of monotypic plasma cells (PCs) and the polytypic PCs/bone marrow PCs

222 Plasma cells (PCs) as effectors of humoral immunity prod

223 We newly identified mucosal IgA-producing plasma cells (PCs) as one major iNOS(+) cell population

224 hat SpA altered the fate of plasmablasts and plasma cells (PCs) by enhancing the short-lived extrafol

225 Studies in mice indicate that plasma cells (PCs) can survive up to a lifetime, even in

226 Plasma cells (PCs) derived from germinal centers (GCs) s

227 emory B cells (Bmem) in the draining LNs and plasma cells (PCs) in the bone marrow (BM) for up to 360

228 hemoresistant minimal residual disease (MRD) plasma cells (PCs) is associated with inferior survival

229 Survival of antibody-secreting plasma cells (PCs) is vital for sustained antibody produ

230 myeloma (EMM) is defined by the presence of plasma cells (PCs) outside the bone marrow in a patient

231 Long-lived human plasma cells (PCs) play central roles in immunity and au

232 Plasma cells (PCs) produce antibodies that mediate immun

233 IgE-expressing (IgE(+) ) plasma cells (PCs) provide a continuous source of allerg

234 follicular pathway gives rise to short-lived plasma cells (PCs) that can rapidly secrete protective a

235 We found that gut IgM(+) plasma cells (PCs) were more abundant in humans than mic

236 tributed conventionally to long-lived IgE(+) plasma cells (PCs), this has not been directly and compr

237 ell high-throughput sequencing on gut lesion plasma cells (PCs), we have analyzed the transglutaminas

238 is known about the biology of amyloidogenic plasma cells (PCs).

239 nvolve the same cellular compartment: clonal plasma cells (PCs).

240 ollected 248 liquid biopsy samples including plasma, cell pellet (UCP) and supernatant (USN) from spu

241 ed that a maximum number of 30 IgG4-positive plasma cells per high-power field in the orbital tissue

242 se was made based on identification of a few plasma cells per high-power field that were positive for

243 CD138 antigen, which is highly expressed on plasma cells, permits quantitation of rare circulating p

244 Plasmacytosis (ie, an expansion of plasma cell populations to much greater than the homeost

245 B-lineage cells (B lymphocytes and plasma cells) predominate in the inflammatory infiltrate

246 igh-throughput B cell receptor sequencing of plasma cells produced following AS03-adjuvanted and non-

247 bodies during and after infections, and each plasma cell produces some thousands of antibody molecule

248 contribute to the generation of B cells and plasma cells producing somatically mutated gut antigen-s

249 germinal center formation, and autoreactive plasma cell production.

250 These mice initially show an abnormal plasma cell proliferation and monoclonal protein product

251 We have identified TJP1 as a determinant of plasma cell proteasome inhibitor susceptibility.

252 Finally, antibodies from long-lived IgM plasma cells provide protective host immunity against a

253 was previously shown to be a major player in plasma-cell regulation, emphasizing the role of non-H2O2

254 es, which led to increased expression of the plasma cell regulator IRF4 and proteins involved in immu

255 survival advantage of Zbtb32(-/-) secondary plasma cells relative to wild-type counterparts.

256 On the basis of these results, long-lived plasma cells represent a key cell population responsible

257 to the germinal centre and induce memory and plasma cell responses.

258 IgG antibodies, germinal center B cells, and plasma cells secreting antigen-specific antibodies, as w

259 xplain why generation of epitope 1-targeting plasma cells seems to be favored in celiac patients.

260 tometric evaluation of normal and neoplastic plasma cells, since the therapeutic antibody can affect

261 Cs took up more glucose than did short-lived plasma cells (SLPCs) in vivo, and this glucose was essen

262 ) is a nearly always incurable malignancy of plasma cells, so new approaches to treatment are needed.

263 These data suggested that CD19(+)CD20(-) plasma cells spared by anti-CD20 therapy likely contribu

264 from newly formed B cells until the ultimate plasma cell stage.

265 (MM) microenvironment that support malignant plasma cell survival and resistance to therapy.

266 ith the rescue of B cell class switching and plasma cell survival by enforced NF-kappaB activation, i

267 secrete a variety of cytokines that promote plasma cell survival by regulating antiapoptotic members

268 l-1 dependence through the production of the plasma cell survival cytokine interleukin-6 (IL-6).

269 current concepts and information surrounding plasma cell survival niches, and consider two opposing m

270 Although it is clear that plasma cell survival requires cell extrinsic signals, th

271 rlying features that render multiple myeloma plasma cells susceptible to therapy are present in only

272 proliferation, and generation of short-lived plasma cells that reside in extrafollicular foci.

273 ed a significant proportion of IgA-producing plasma cells that shared phenotypic and functional attri

274 equired for the development of IgE-producing plasma cells, the source of IL-4 and cellular requiremen

275 f recognized early and treated with targeted plasma cell therapy, can be managed very effectively.

276 cells to proliferate and differentiate into plasma cells thereby leading to antibody production.

277 A) are constitutively secreted by intestinal plasma cells to coat and contain the commensal microbiot

278 on with that of bone marrow plasmablasts and plasma cells to control viremia during chronic infection

279 ntrast the potential contribution of mucosal plasma cells to mediate protection at sites of infection

280 of primary human preneoplastic and malignant plasma cells together with non-malignant cells in vivo.

281 The high levels of immunoglobulin and plasma cell transcripts is consistent with the anti-MAP

282 itiating myelomagenic mutations that promote plasma cell transformation.

283 pecially broad and high expression levels in plasma cell tumors such as multiple myeloma (MM).

284 ific plasma cells and long-lived bone marrow plasma cells was detected in the MNP boosted group as we

285 CD138(+)/B220(+) plasma cells were detected, suggesting the retinal lymph

286 The CD138-expressing plasma cells were distinctly localized as a dense infilt

287 Indeed, B cells and plasma cells were inherently sensitive to Rab7 gene knoc

288 ration/survival of B cells and generation of plasma cells were not affected.

289 kedly decreased early B-cell precursors, but plasma cells were present.

290 is was minimal, T cells outnumbered B cells, plasma cells were prominent, and mild fibrosis was prese

291 r DNA, frequencies of long-lived bone marrow plasma cells were unaffected.

292 tient received CAR-BCMA T cells, bone marrow plasma cells were undetectable by flow cytometry, and th

293 is, are characterized by clonal expansion of plasma cells which produce a vast amount of an immunoglo

294 Unlike long-lived IgG plasma cells, which develop in germinal centres and then

295 d a substantial proportion of CD19(+)CD20(-) plasma cells, which would have otherwise been targeted b

296 extramedullary sites of proliferating clonal plasma cells while providing important prognostic inform

297 on and the development of memory B cells and plasma cells, while regulatory CD4(+) (Treg) cells inclu

298 filtrations of lymphocytes, macrophages, and plasma cells with some horses displaying subclinical sig

299 vailable GEP data from patients' bone marrow plasma cells, with long-term follow-up and clinicopathol

300 wed that bortezomib (BTZ) partially depletes plasma cells, yet has limited efficacy for desensitizati