ライフサイエンスコーパス: multiple myeloma

1 f high bone turnover (eg, bone metastases or multiple myeloma).

2 are key components of treatment regimens for multiple myeloma.

3 rial in patients with relapsed or refractory multiple myeloma.

4 patients with B-cell malignancies, including multiple myeloma.

5 ls in a xenograft mouse model of established multiple myeloma.

6 nt in determining Bcl-2 family dependence in multiple myeloma.

7 lupus erythematosis and relapsed/refractory multiple myeloma.

8 nts newly diagnosed with biclonal gammopathy multiple myeloma.

9 8 years, only 1 (2.5%) patient progressed to multiple myeloma.

10 nts with relapsed or refractory lymphoma and multiple myeloma.

11 and dexamethasone in relapsed or refractory multiple myeloma.

12 nce their efficacy in relapsed or refractory multiple myeloma.

13 tors in patients with relapsed or refractory multiple myeloma.

14 hhorn syndrome and is overexpressed in human multiple myeloma.

15 of DEPTOR specifically occurs in a model of multiple myeloma.

16 treatment option for relapsed or refractory multiple myeloma.

17 to extended survival in xenograft models of multiple myeloma.

18 and prolonged survival in a murine model of multiple myeloma.

19 , 20.6, and 21.3 in matched controls without multiple myeloma.

20 ng those with DLBCL, Hodgkin's lymphoma, and multiple myeloma.

21 rexpressed in a number of cancers, including multiple myeloma.

22 has been approved in clinical treatment for multiple myeloma.

23 represent a promising treatment strategy in multiple myeloma.

24 ation, especially for patients with advanced multiple myeloma.

25 tolerated regimen for patients with relapsed multiple myeloma.

26 clonal antibody, in patients with refractory multiple myeloma.

27 the benefit of KRd in patients with relapsed multiple myeloma.

28 o prevent dissemination and overt relapse in multiple myeloma.

29 lonal antibody approved for the treatment of multiple myeloma.

30 support system for therapeutic management of multiple myeloma.

31 have an impact on the pathogenesis of human multiple myeloma.

32 family dependence is highly heterogeneous in multiple myeloma.

33 vestigation as a target for immunotherapy in multiple myeloma.

34 as such as chronic lymphocytic leukemia, and multiple myeloma.

35 roving patient outcomes for the treatment of Multiple Myeloma.

36 myeloma-specific T cells in a mouse model of multiple myeloma.

37 ents with breast cancer, prostate cancer, or multiple myeloma.

38 lymphoma but also acute myeloid leukemia and multiple myeloma.

39 ncer, 689 with prostate cancer, and 278 with multiple myeloma), 795 completed the study at 2 years.

40 , we recruited patients with newly diagnosed multiple myeloma aged 18 years and older from participat

41 Serum sclerostin level is elevated in multiple myeloma, an osteolytic malignancy, where it mig

42 Proteasome inhibitors benefit patients with multiple myeloma and B cell-dependent autoimmune disorde

43 nciple of STAT3-driven cancer development in multiple myeloma and beyond.

44 of immune activation that is upregulated in multiple myeloma and is a critical component of the immu

45 neoplastic disease, in particular refractory multiple myeloma and mantle cell lymphoma.

46 ndent manner and induces tumor cell death in multiple myeloma and neuroblastoma cells as well as othe

47 nically established targets overexpressed in multiple myeloma and non-Hodgkin lymphoma, respectively.

48 ignaling including IL6 that is implicated in multiple myeloma and other hematopoietic malignancies.

49 yglucose ((18)F-FDG) PET/CT in patients with multiple myeloma and other plasma cell disorders, includ

50 orubicin were observed in vitro against both multiple myeloma and ovarian cancer cells.

51 is the main cause of acute kidney injury in multiple myeloma and persistent reduction in kidney func

52 Mechanistic studies revealed that multiple myeloma and proliferating endothelial cells can

53 ll therapy as an effective treatment against multiple myeloma and provide novel insights into the con

54 plasma cell disorders, including smouldering multiple myeloma and solitary plasmacytoma.

55 8 years or older, had relapsed or refractory multiple myeloma, and had received between one and three

56 diagnosis of bone involvement by metastases, multiple myeloma, and lymphoma, and evaluation of treatm

57 ding immunoglobulin light-chain amyloidosis, multiple myeloma, and Waldenstrom macroglobulinemia.

58 ance; 15 multiple myelomas; seven smoldering multiple myelomas; and three other neoplasms.

59 w that, in patients with biclonal gammopathy multiple myeloma, anti-multiple myeloma therapies exert

60 nts with relapsed or refractory lymphoma and multiple myeloma are limited.

61 t seek to identify, with biclonal gammopathy multiple myeloma as an investigative model, the genetic

62 for the Treatment of Patients With Relapsed Multiple Myeloma (ASPIRE) trial.

63 n of re-induction treatment in patients with multiple myeloma at first relapse after a first ASCT.

64 us updates the definition for high-risk (HR) multiple myeloma based on cytogenetics Several cytogenet

65 h newly diagnosed and relapsed or refractory multiple myeloma because it assesses bone damage with re

66 interest from a therapeutic perspective for multiple myeloma because we have shown that targeting Ra

67 e inhibitors have revolutionized outcomes in multiple myeloma, but they are used empirically, and pri

68 identified patients with biclonal gammopathy multiple myeloma by central laboratory analysis of 6399

69 ne marrow (BM) infiltration in patients with multiple myeloma by using a virtual noncalcium (VNCa) te

70 For patients with relapsed or refractory multiple myeloma, carfilzomib with dexamethasone could b

71 -diagnosed peripheral blood samples from 624 multiple myeloma cases and 1,246 individually matched co

72 ated depletion of endogenous FAM46C enhanced multiple myeloma cell growth, decreased Ig light chain a

73 sion, particularly Notch3 and 4, stimulating multiple myeloma cell growth.

74 esults define CD166 as a pivotal director in multiple myeloma cell homing to the bone marrow and mult

75 disease, suggesting that targeting osteocyte-multiple myeloma cell interactions through specific Notc

76 iption 3 (STAT3) facilitates survival in the multiple myeloma cell line INA-6 and therefore represent

77 hich we discovered to be highly expressed in multiple myeloma cell lines and primary bone marrow cell

78 As a substantial number of multiple myeloma cell lines and primary samples were fou

79 CD166 deficiency in multiple myeloma cell lines or CD138(+) bone marrow cell

80 ines therapeutic susceptibility across human multiple myeloma cell lines to a gamut of standard-of-ca

81 a S2R+ cell line and several NSCLC and human multiple myeloma cell lines to identify conserved intera

82 In vitro cytotoxicity against multiple myeloma cell lines was directly correlated with

83 complex and triggers necrotic cell death in multiple myeloma cell lines.

84 ing mTORC1 in the critical role of DEPTOR in multiple myeloma cell viability.

85 ed that osteocyte apoptosis was initiated by multiple myeloma cell-mediated activation of Notch signa

86 Notch signaling and was further amplified by multiple myeloma cell-secreted TNF.

87 inhibition, CCF642 caused acute ER stress in multiple myeloma cells accompanied by apoptosis-inducing

88 mTORC1 paralysis protects multiple myeloma cells against DEPTOR silencing, implica

89 ssess the ex vivo drug sensitivity of single multiple myeloma cells based on measuring their mass acc

90 CD166 silencing in multiple myeloma cells enabled longer survival, a smalle

91 CD166(+) multiple myeloma cells homed more efficiently than CD166

92 Its silencing in multiple myeloma cells is sufficient to induce cytotoxic

93 Conversely, CD166 expression in multiple myeloma cells promoted osteoclastogenesis by ac

94 antly, direct contact between osteocytes and multiple myeloma cells reciprocally activated Notch sign

95 Although normal plasma cells and most multiple myeloma cells require Mcl-1 for survival, a sub

96 Multiple myeloma cells secrete more disulfide bond-rich

97 Exposure of multiple myeloma cells to VLX1570 resulted in thermostab

98 Treatment of multiple myeloma cells with VLX1570 induced the accumula

99 Sdc1 suppresses ASK1-dependent apoptosis in multiple myeloma cells.

100 roporation of siRNA reduced the viability of multiple myeloma cells.

101 id leukemia (AML), non-Hodgkin lymphoma, and multiple myeloma cells.

102 pression induces substantial cytotoxicity in multiple myeloma cells.

103 haracterised by the coexistence of an active multiple myeloma clone and a benign MGUS clone, and thus

104 rols from seven cohorts participating in the Multiple Myeloma Cohort Consortium.

105 raphy-adjusted incidence ratios of ESRD from multiple myeloma decreased between 2001-2002 and 2009-20

106 ce to date that adiponectin protects against multiple myeloma development, particularly among overwei

107 a cells and have been shown to contribute to multiple myeloma development; yet, little is known of th

108 alysis of 6399 newly diagnosed patients with multiple myeloma enrolled in three UK clinical trials (M

109 ising target for antibody-based treatment of multiple myeloma, especially in patients with gain of ch

110 th previously treated relapsed or refractory multiple myeloma from five cancer centres in the USA.

111 teoblast activity, but their contribution to multiple myeloma growth and bone disease is unknown.

112 Although transcriptome profiles in multiple myeloma has been described, landscape of expres

113 The standard treatment of relapsed multiple myeloma has been either lenalidomide-dexamethas

114 Although management of multiple myeloma has changed substantially in the last d

115 is unknown whether the burden of ESRD due to multiple myeloma has changed, or whether survival of pat

116 nical success of bortezomib, particularly in multiple myeloma, has established the validity of the pr

117 For the management of RI in patients with multiple myeloma, high fluid intake is indicated along w

118 one of the most recurrently mutated genes in multiple myeloma; however its role in disease pathogenes

119 o distinguish between smouldering and active multiple myeloma, if whole-body X-ray (WBXR) is negative

120 ammopathy of renal significance in 30 (60%), multiple myeloma in 17 (34%), and chronic lymphocytic le

121 n the standard treatment for newly diagnosed multiple myeloma in adults up to 65 years of age.

122 These data suggest the incidence of RRT from multiple myeloma in the United States has decreased in t

123 y B-cell leukemia, mantle cell lymphoma, and multiple myeloma in vitro.

124 erogeneity and the evolutionary processes in multiple myeloma.In multiple myeloma, malignant cells ex

125 Survivors of multiple myeloma (incidence rate ratio [IRR], 1.70; P <

126 d Drug Administration (FDA) for treatment of multiple myeloma, induces HbF production by decreasing l

127 Multiple myeloma is a plasma cell malignancy characteriz

128 Biclonal gammopathy multiple myeloma is characterised by the coexistence of

129 The treatment of multiple myeloma is considered a continuously evolving p

130 Multiple myeloma is consistently preceded by monoclonal

131 Disease progression and relapse in multiple myeloma is dependent on the ability of the mult

132 However, an imbalanced distribution of multiple myeloma is frequently observed in medical imagi

133 Multiple myeloma is highly dependent on the bone marrow

134 oma; Hodgkin lymphoma; non-Hodgkin lymphoma; multiple myeloma; leukemia; and all other cancers combin

135 ic for a variety of human cancer cell lines, multiple myeloma lines consistently exhibiting high sens

136 therapy on MGUS (which we defined as M2) and multiple myeloma (M1) clones-overall, within patients, a

137 In multiple myeloma malignant plasma cells expand within th

138 volutionary processes in multiple myeloma.In multiple myeloma, malignant cells expand within bone mar

139 In an analysis of >800 primary multiple myelomas, MAX alterations occurred at a frequen

140 have been implicated as efficacy targets in multiple myeloma (MM) and 5q deletion associated myelody

141 oximately 30% of de novo and 70% of relapsed multiple myeloma (MM) and is correlated with disease pro

142 To gain insight into the clonal dynamics of multiple myeloma (MM) and its possible influence on pati

143 vestigated the sources of IL-8 production in multiple myeloma (MM) and its potential roles in MM path

144 ibe a new PRIT approach for the treatment of multiple myeloma (MM) and other B-cell malignancies, for

145 atory drug (IMiDs) with clinical efficacy in multiple myeloma (MM) and other late B-cell neoplasms.

146 patterns in the bone marrow of patients with multiple myeloma (MM) and to determine a threshold ADC t

147 All cases of multiple myeloma (MM) are preceded by precursor states t

148 Our results from applying GISPA to human multiple myeloma (MM) cell lines contained genes of know

149 oid cell leukemia sequence 1 (MCL-1) promote multiple myeloma (MM) cell survival.

150 importance of glutamine (Gln) metabolism in multiple myeloma (MM) cells and its potential role as a

151 Interactions between multiple myeloma (MM) cells and the BM microenvironment

152 We found that treatment of human multiple myeloma (MM) cells with the small-molecular inh

153 CD38 is highly and uniformly expressed on multiple myeloma (MM) cells, and at relatively low level

154 e BCL-2 inhibitor that induces cell death in multiple myeloma (MM) cells, particularly in those harbo

155 rapamycin complex1) activity in ER-stressed multiple myeloma (MM) cells.

156 Notably, multiple myeloma (MM) expresses high levels of ADK, and

157 Multiple myeloma (MM) has benefited from significant adv

158 Multiple myeloma (MM) is a hematological cancer for whic

159 Multiple myeloma (MM) is a nearly always incurable malig

160 Multiple myeloma (MM) is a plasma B-cell hematologic can

161 Multiple myeloma (MM) is a plasma cell cancer that devel

162 Multiple myeloma (MM) is a plasma cell malignancy that i

163 Multiple myeloma (MM) is a plasma cell malignancy with a

164 ments that can circumvent chemoresistance in Multiple Myeloma (MM) is a priority.

165 Multiple myeloma (MM) is an age-related hematologic mali

166 Multiple myeloma (MM) is characterized by the expansion

167 Multiple myeloma (MM) is characterized by wide variabili

168 Multiple myeloma (MM) is the second most common hematolo

169 Despite novel therapies, relapse of multiple myeloma (MM) is virtually inevitable.

170 e expression profiles (GEP) from a cohort of multiple myeloma (MM) patients and normal individuals us

171 Primed CD56bright cells from multiple myeloma (MM) patients displayed superior respon

172 Guidelines for monitoring multiple myeloma (MM) patients expressing light chains o

173 For decades, the main imaging tool in multiple myeloma (MM) patients was plain radiography.

174 The prognosis of multiple myeloma (MM) patients who become refractory to

175 asome inhibition is an effective therapy for multiple myeloma (MM) patients; however, the emergence o

176 t-derived AL PCs, in comparison with primary multiple myeloma (MM) PCs, the prototypical PI-responsiv

177 ociation between the number of patients with multiple myeloma (MM) treated annually at a treatment fa

178 rption into microfluidic devices by treating multiple myeloma (MM) tumor cells with two MM drugs (bor

179 the B cell lineage marker FcRH5 expressed in multiple myeloma (MM) tumor cells.

180 cific miRNAs are aberrantly overexpressed in multiple myeloma (MM) tumor plasma cells compared to the

181 Survival following a diagnosis of multiple myeloma (MM) varies between patients and some o

182 ma/chronic lymphocytic leukemia (NHL/CLL) or multiple myeloma (MM) with autologous T cells geneticall

183 esent challenges for effective management of multiple myeloma (MM), a plasma cell cancer.

184 In multiple myeloma (MM), a plasma cell malignancy, most tu

185 in diverse forms of malignancies, including multiple myeloma (MM), and thus represent potential ther

186 (BCMA) is a promising therapeutic target for multiple myeloma (MM), but expression is variable, and e

187 croRNA (miRNA) in several cancers, including multiple myeloma (MM), by controlling the expression of

188 available for the treatment of patients with multiple myeloma (MM), including alkylators, steroids, i

189 A novel approach for sorting exosomes from multiple myeloma (MM), monoclonal gammopathy of undeterm

190 IAP2 are recurrently homozygously deleted in multiple myeloma (MM), resulting in constitutive activat

191 In both AL and multiple myeloma (MM), soluble immunoglobulin light chai

192 mopathy of undetermined significance (MGUS), multiple myeloma (MM), Waldenstrom macroglobulinemia (WM

193 ded for patients with relapsed or refractory multiple myeloma (MM).

194 e first demonstration of a role for CARM1 in multiple myeloma (MM).

195 ligand (PD-L1) facilitate immune evasion in multiple myeloma (MM).

196 n many hematological malignancies, including multiple myeloma (MM).

197 uation of malignant plasma cell (PC) disease multiple myeloma (MM).

198 ociated with several cancer types, including multiple myeloma (MM).

199 imal residual disease (MRD) in patients with multiple myeloma (MM).

200 f circulating exosomal microRNAs (miRNAs) in multiple myeloma (MM).

201 utic target for pharmacological treatment of multiple myeloma (MM).

202 n heavily pretreated relapsed and refractory multiple myeloma (MM).

203 PCs) is associated with inferior survival in multiple myeloma (MM).

204 nal antibody, has activity as monotherapy in multiple myeloma (MM).

205 own to have a negative impact on survival in multiple myeloma (MM).

206 th novel mechanisms of action are needed for multiple myeloma (MM).

207 n multiple types of human cancers, including multiple myeloma (MM).

208 xamethasone (KRd) for relapsed or refractory multiple myeloma (MM).

209 o adversely impact outcomes in patients with multiple myeloma (MM).

210 (PET-CT) are important imaging techniques in multiple myeloma (MM).

211 tients with relapsed lenalidomide-refractory multiple myeloma (MM).

212 pact of depth of response in newly diagnosed multiple myeloma (MM).

213 1,842), Hodgkin lymphoma (HL, N = 1,465) and multiple myeloma (MM, N = 3,790).

214 ials (RCTs) of patients with newly diagnosed multiple myeloma (NDMM).

215 s from a cohort of patients with lymphoma or multiple myeloma (non-leukaemia cohort).

216 yeloid leukemia, acute lymphocytic leukemia, multiple myeloma, non-Hodgkin lymphoma, Hodgkin lymphoma

217 hanged, or whether survival of patients with multiple myeloma on RRT has improved.

218 bi-specific antibodies for the treatment of multiple myeloma: one targets FcRH5 expressed on B cells

219 spective study, 34 consecutive patients with multiple myeloma or monoclonal gammopathy of unknown sig

220 that 70% of Mef(-/-)Rad50(s/s) mice die from multiple myeloma or other plasma cell neoplasms.

221 ancies and may serve as a key determinant of multiple myeloma pathophysiology.

222 colinostat and venetoclax, in a cohort of 19 multiple myeloma patient samples, yielded consistent res

223 In contrast, FAM46C mutations found in multiple myeloma patients abrogate this cytotoxicity, in

224 Samples from multiple myeloma patients also revealed a decreased copy

225 sphonates have benefits in breast cancer and multiple myeloma patients and have been used with adopti

226 distribution of CgA-derived polypeptides in multiple myeloma patients and the subsequent implication

227 conferred poor prognosis in newly diagnosed multiple myeloma patients and was associated with an inc

228 ell lines or CD138(+) bone marrow cells from multiple myeloma patients compromised their ability to i

229 Moreover, multiple myeloma patients treated with pomalidomide demo

230 55 newly diagnosed and homogeneously treated multiple myeloma patients with long follow-up.

231 designed to predict therapeutic response in multiple myeloma patients within a clinically actionable

232 ty of chemosensitivity of primary cells from multiple myeloma patients, allowing us to predict clinic

233 From a cohort of 52 multiple myeloma patients, EMMA correctly classified 96%

234 e we demonstrate that HIF-2alpha upregulates multiple myeloma PC CXCL12 expression, decreasing migrat

235 CCR1 activation potently induces multiple myeloma PC migration toward CCL3 while abrogati

236 C migration toward CCL3 while abrogating the multiple myeloma PC migratory response to CXCL12.

237 In addition, increased CCR1 expression by multiple myeloma PCs conferred poor prognosis in newly d

238 d CCR1 upregulation in driving the egress of multiple myeloma PCs from the bone marrow.

239 s associated with an increase in circulating multiple myeloma PCs in these patients.

240 s associated with increased recirculation of multiple myeloma PCs.

241 ed CXCL12, thereby enabling dissemination of multiple myeloma PCs.

242 expression of the chemokine receptor CCR1 in multiple myeloma PCs.

243 However, studies comparing how MGUS and multiple myeloma plasma cell clones respond to these the

244 We aimed to identify how MGUS and multiple myeloma plasma cell clones responded to anti-mu

245 es exert a greater depth of response against multiple myeloma plasma cell clones than MGUS plasma cel

246 e myeloma is dependent on the ability of the multiple myeloma plasma cells (PC) to reenter the circul

247 sts that the underlying features that render multiple myeloma plasma cells susceptible to therapy are

248 lective CDK4/6 inhibitors has been modest in multiple myeloma, potentially because of incomplete targ

249 ing antiproliferative activity of VLX1570 in multiple myeloma, primarily associated with inhibition o

250 heterogeneity, providing novel insight into multiple myeloma progression and evolution.

251 The results support a model for multiple myeloma progression with clonal sweeps in the e

252 e myeloma cell homing to the bone marrow and multiple myeloma progression, rationalizing its further

253 ome available for relapsed and/or refractory multiple myeloma (R/R MM) after a long period in which d

254 actory B-cell lymphoma, T-cell lymphoma, and multiple myeloma received the anti-PD-1 monoclonal antib

255 Eligible patients with multiple myeloma relapsing after a previous ASCT were re

256 ndations for the diagnosis and management of multiple myeloma-related renal impairment (RI).

257 Multiple myeloma remains treatable but incurable.

258 To prospectively evaluate multiple myeloma risk in relation to adiponectin levels

259 Patients with relapsed and/or refractory multiple myeloma (RRMM) have poor prognosis.

260 e 2 study, patients with relapsed/refractory multiple myeloma (RRMM) received elotuzumab with bortezo

261 tment of relapsed or relapsed and refractory multiple myeloma (RRMM).

262 g (QW), in patients with relapsed/refractory multiple myeloma (RRMM).

263 Among adults with multiple myeloma, RVD therapy plus transplantation was a

264 ctivation of histone methyltransferase (HMT) multiple myeloma SET domain (MMSET) in mouse B cells and

265 Overexpression of the multiple myeloma set domain (MMSET) Wolf-Hirschhorn synd

266 lonal gammopathies of renal significance; 15 multiple myelomas; seven smoldering multiple myelomas; a

267 eutic trials targeting BCMA in patients with multiple myeloma should consider possible effects on pDC

268 ve currently in clinical trials for relapsed multiple myeloma, significantly inhibited in vivo tumor

269 es due to breast cancer, prostate cancer, or multiple myeloma, the use of zoledronic acid every 12 we

270 h biclonal gammopathy multiple myeloma, anti-multiple myeloma therapies exert a greater depth of resp

271 ch is usually only treated by a form of anti-multiple myeloma therapy if it is causing substantial di

272 myeloma plasma cell clones responded to anti-multiple myeloma therapy in patients newly diagnosed wit

273 as difference in response achieved with anti-multiple myeloma therapy on MGUS (which we defined as M2

274 esponses of separate clones to the same anti-multiple myeloma therapy, in the same patient, at the sa

275 US plasma cell clones are responsive to anti-multiple myeloma therapy.

276 nts with relapsed or relapsed and refractory multiple myeloma to receive bortezomib (1.3 mg per squar

277 We randomly assigned 700 patients with multiple myeloma to receive induction therapy with three

278 psed, refractory, or relapsed and refractory multiple myeloma to receive ixazomib plus lenalidomide-d

279 knowledge, carfilzomib is the first and only multiple myeloma treatment that extends overall survival

280 study as a candidate therapeutic target for multiple myeloma treatment.

281 nduce programmed cell death (PCD) of CD38(+) multiple myeloma tumor cell lines when cross-linked in v

282 an experimental therapeutic to dually attack multiple myeloma tumor cell survival and tumor angiogene

283 d extensive extramedullary manifestations of multiple myeloma undergoing CXCR4-directed endoradiother

284 Diagnosis of multiple myeloma was based on the presence of an immunog

285 Following hospital admission, multiple myeloma was diagnosed and confirmed by bone mar

286 Using the Vk*MYC mouse model of multiple myeloma, we further demonstrate that exogenousl

287 isms underlying relapse from chemotherapy in multiple myeloma, we performed a longitudinal study of 3

288 d suggest new mechanisms of tumorigenesis in multiple myeloma, we performed RNA sequencing in a cohor

289 model has prognostic value in patients with multiple myeloma who are treated with IMiDs.

290 reast cancer, metastatic prostate cancer, or multiple myeloma who had at least 1 site of bone involve

291 and dexamethasone for patients with relapsed multiple myeloma who have received two or more previous

292 rates in patients with previously untreated multiple myeloma who were not planned for immediate auto

293 and the USA, patients (age >/=18 years) with multiple myeloma who were previously treated with at lea

294 patients (aged >/=18 years) with lymphoma or multiple myeloma who were refractory to or had relapsed

295 th newly diagnosed or relapsed or refractory multiple myeloma who were treated in clinical trials wit

296 aluated in patients with relapsed/refractory multiple myeloma with >/=2 prior lines of therapy who we

297 44 patients with biclonal gammopathy multiple myeloma with IgG or IgA MGUS clones were subseq

298 r assessing BM infiltration in patients with multiple myeloma with precision comparable to that of MR

299 us in a mouse xenograft model (KMS-12 BM) of multiple myeloma, with 93% tumor growth inhibition at 50

300 some have been validated in the treatment of multiple myeloma, with several FDA-approved therapeutics