ライフサイエンスコーパス: myeloma cell

1 reased in TRAF3-reconstituted human multiple myeloma cells.

2 ble to the B-cell immune system in untreated myeloma cells.

3 -T) that appears to be specific for multiple myeloma cells.

4 l adhesion-dependent alterations in multiple myeloma cells.

5 redirects T cells to lyse malignant multiple myeloma cells.

6 f these transcription factors kills multiple myeloma cells.

7 he regulation of drug resistance in multiple myeloma cells.

8 monstrated on BCR-ABL-positive H929 multiple myeloma cells.

9 tutively localized on the plasma membrane of myeloma cells.

10 at impairs T-cell recognition and killing of myeloma cells.

11 zomib) resistant and drug-sensitive multiple myeloma cells.

12 experiment is an in vitro system of multiple myeloma cells.

13 and in primary human bone marrow (BM) CD1381 myeloma cells.

14 apoptosis of both MM cell lines and patient myeloma cells.

15 yeloma is associated with CRBN expression in myeloma cells.

16 hibitor, which induces apoptosis in multiple myeloma cells.

17 ed by autologous dendritic cells, but not by myeloma cells.

18 with CD38-targeted imaging of OPM2 multiple myeloma cells.

19 loid leukemia, B cell lymphoma, and multiple myeloma cells.

20 ma-dependent and stroma-independent multiple myeloma cells.

21 ein is aberrantly expressed in most multiple myeloma cells.

22 ay underline specific weaknesses of multiple myeloma cells.

23 ainst both MM cell lines and primary patient myeloma cells.

24 expression of this protein protects multiple myeloma cells.

25 ple myeloma cells including primary multiple myeloma cells.

26 mediated late apoptosis/necrosis of multiple myeloma cells.

27 ets CD38, an antigen expressed on nearly all myeloma cells.

28 y, free light chains, renal fibroblasts, and myeloma cells.

29 rs also induced cell death in multiple human myeloma cells.

30 potential drug targets to eradicate dormant myeloma cells.

31 r cell lines and in patient-derived multiple myeloma cells.

32 d is dependent on surface CD38 expression on myeloma cells.

33 ia (AML), non-Hodgkin lymphoma, and multiple myeloma cells.

34 t hemocyanin, were fused with P3/NS1/1-Ag4-1 myeloma cells.

35 induces substantial cytotoxicity in multiple myeloma cells.

36 producing mouse B-lymphocytes by fusion with myeloma cells.

37 presses ASK1-dependent apoptosis in multiple myeloma cells.

38 n of siRNA reduced the viability of multiple myeloma cells.

39 n, CCF642 caused acute ER stress in multiple myeloma cells accompanied by apoptosis-inducing calcium

40 fibronectin-mediated binding of exosomes to myeloma cells activated p38 and pERK signaling and expre

41 ratios, but lacked CD49d and showed enhanced myeloma cell adhesion molecule (MCAM) expression.

42 odels of multiple myeloma and in vitro using myeloma cell-adipocyte cocultures.

43 More importantly, autocrine SHH protected myeloma cells against chemotherapy-induced apoptosis in

44 mTORC1 paralysis protects multiple myeloma cells against DEPTOR silencing, implicating mTOR

45 In contrast, inoculation of myeloma cells alone did not result in myeloma.

46 Furthermore, CD166 deficiency in multiple myeloma cells also reduced the formation of osteolytic d

47 In addition, multiple myeloma cells altered adipocyte gene expression and cyto

48 Coinoculation of myeloma cells and a BMSC line, isolated from myeloma-per

49 TSP1 binds to human myeloma cells and activates TGF-beta produced by culture

50 ase gene marking of patient-derived multiple myeloma cells and bioluminescent imaging, we were able t

51 iprocal interactions and cross-regulation of myeloma cells and BMAds play a role in multiple myeloma

52 in small cohorts of samples as expressed by myeloma cells and cells of the BM microenvironment.

53 te that JNK2 is required for the survival of myeloma cells and constitutively suppresses JNK1-mediate

54 and optimization of mAb production in murine myeloma cells and in the quality control of mAbs for ind

55 olytically shed from the surface of multiple myeloma cells and is abundant in the bone marrow microen

56 transmembrane glycoprotein overexpressed in myeloma cells and is implicated in MM cell signaling.

57 e prevailing GSL produced by patient-derived myeloma cells and MM cell lines, and exogenous addition

58 ecular components of the interaction between myeloma cells and the bone marrow microenvironment, poin

59 RANKL was observed exclusively with multiple myeloma cells and was strongly influenced by posttranscr

60 RF4, which is essential for the viability of myeloma cells, and the concomitant repression of the IRF

61 F4, on myeloma cell lines as well as primary myeloma cells, and we show that inhibition of c-MYC acti

62 LI1/BCL-2 axis, leading to the inhibition of myeloma cell apoptosis.

63 Our results provide further evidence that myeloma cells are addicted to c-MYC activity and that c-

64 These findings indicate that multiple myeloma cells are dependent on MUC1-C and TIGAR for main

65 Thus, myeloma cells are exceptionally sensitive to increased t

66 The growth and survival of myeloma cells are greatly affected by their surrounding

67 Dormant myeloma cells are resistant to chemotherapy that targets

68 Myeloma cells are sensitive to TRAIL through the two dea

69 e confirmed on bortezomib-resistant multiple myeloma cells as well as on bone marrow-derived primary

70 kills human plasma cells and patient-derived myeloma cells at picomolar concentrations and results in

71 ex vivo drug sensitivity of single multiple myeloma cells based on measuring their mass accumulation

72 lecule library using a multilayered multiple myeloma cell-based cytotoxicity assay that modeled disea

73 Dickkopf-1 (DKK1), broadly expressed in myeloma cells but highly restricted in normal tissues, t

74 strate that SHH was mainly secreted by human myeloma cells but not by stromal cells in MM bone marrow

75 ases the proteasome inhibitor sensitivity of myeloma cells by altering the cellular proteasome capaci

76 PARP14 was found to promote the survival of myeloma cells by binding and inhibiting JNK1.

77 , heat shock may also be especially toxic to myeloma cells by causing protein unfolding, increasing f

78 red the growth and dissemination of multiple myeloma cells by inducing mitochondrial oxidative stress

79 )(p16.3;q32) were assessed in CD138-purified myeloma cells by interphase fluorescent in situ hybridiz

80 In this study, we track individual myeloma cells by intravital imaging as they colonize the

81 Blocking of CEACAM-6 on the surface of myeloma cells by specific monoclonal antibodies or CEACA

82 orted that elevation of heparanase levels in myeloma cells causes a dramatic reduction in the amount

83 transferred to secondary recipients and was myeloma cell clone specific.

84 In a model of macrophage-myeloma cell crosstalk, versikine induced components of

85 suppressed HK2 expression in human multiple myeloma cell cultures and human multiple myeloma mouse x

86 ect Usp24 KD resulted in marked induction of myeloma cell death that was associated with a reduction

87 massive apoptosis (PRIMA-1(Met)) in inducing myeloma cell death, using 27 human myeloma cell lines (H

88 with ABT-737 (a Bcl-2 inhibitor) in inducing myeloma cell death.

89 ms by which FGF antagonists promote multiple myeloma cell death.

90 GAR suppression that contributes to multiple myeloma cell death.

91 bition of c-MYC activity efficiently induces myeloma cell death.

92 ce injected with 5TGM1-eGFP, 5T2MM, or MM1.S myeloma cells demonstrated significant bone loss, which

93 e tested in cell transfection using multiple myeloma cells, demonstrating efficient knockdown in the

94 In primary myeloma cells derived from bone marrow aspirates, CD46-A

95 ovo GSL synthesis and is further enhanced by myeloma cell-derived GSLs.

96 nd how it exerts cell-extrinsic control over myeloma cell dormancy and reactivation.

97 he endosteal niche is pivotal in controlling myeloma cell dormancy highlights the potential for targe

98 CD166 silencing in multiple myeloma cells enabled longer survival, a smaller tumor b

99 iver radiation doses sufficient for multiple myeloma cell eradication.

100 ABC294640 effectively induced apoptosis of myeloma cells, even in the presence of BM stromal cells.

101 tosis, illuminating a new possible driver of myeloma cell evolution in a drug-resistant clone.

102 One proposed reason for myeloma cells' exceptional sensitivity to proteasome inh

103 Our data demonstrate that myeloma cells exhibit reliance on constitutively cell su

104 locations of NF-kappaB and STAT3 in multiple myeloma cells exposed to different conditions, including

105 As a model we study myeloma cells exposed to the proteasome inhibitor bortez

106 Our analyses show that dormant myeloma cells express a distinct transcriptome signature

107 We found that myeloma cells express high levels of the matrix metallop

108 hermore, osteocytes in contact with multiple myeloma cells expressed high levels of Sost/sclerostin,

109 any other malignant tumors, freshly isolated myeloma cells expressed several carcinoembryonic antigen

110 he rates of methylation and demethylation in myeloma cells expressing high vs. low levels of the meth

111 ngly, donor-derived IL-17A acted directly on myeloma cells expressing the IL-17 receptor to induce a

112 urvival and subsequent expansion of a single myeloma cell following treatment with high-dose melphala

113 ng various cell surface antigens on multiple myeloma cells for the selective delivery of siRNA target

114 These stromal cells protect multiple myeloma cells from apoptosis induced by chemotherapeutic

115 Overexpression of PARP14 completely rescued myeloma cells from apoptosis induced by JNK2 knockdown,

116 uently, the IRF4 protein required to protect myeloma cells from apoptosis is markedly reduced in pG1

117 ormal donor MSC depleted mature and immature myeloma cells from clinical aphereses while expanding th

118 rcellular mitochondrial transfer to multiple myeloma cells from neighboring nonmalignant bone marrow

119 l as on bone marrow-derived primary multiple myeloma cells from newly diagnosed and relapsed/refracto

120 vival and progression by protecting multiple myeloma cells from oxidative stress-induced apoptosis.

121 (+) myeloma cell proliferation and protected myeloma cells from spontaneous and stress-induced apopto

122 ence the transcriptome of individual dormant myeloma cells from the bones of tumor-bearing mice.

123 C2-2b-2b efficiently depleted lymphoma and myeloma cells from whole human blood but also exhibited

124 Together these results implicate FAM46C in myeloma cell growth and survival and identify FAM46C mut

125 interaction in a hypoxic environment affects myeloma cell growth and their response to drug treatment

126 etion of endogenous FAM46C enhanced multiple myeloma cell growth, decreased Ig light chain and HSPA5/

127 Annexin A2 (ANXA2) promotes myeloma cell growth, reduces apoptosis in myeloma cell l

128 ticularly Notch3 and 4, stimulating multiple myeloma cell growth.

129 o, whereas IFN-gamma had no direct effect on myeloma cell growth.

130 bidirectional interactions between BMAds and myeloma cells have significant implications for the path

131 CD166(+) multiple myeloma cells homed more efficiently than CD166(-) cells

132 fine CD166 as a pivotal director in multiple myeloma cell homing to the bone marrow and multiple myel

133 a target because of its strong expression on myeloma cells in 100% of patients.

134 ion achieved synthetic lethality in multiple myeloma cells in culture and prevented HK1(-)HK2(+) mult

135 es and prevented outgrowth of human multiple myeloma cells in immunodeficient mice.

136 Importantly, J6M0-mcMMAF rapidly eliminates myeloma cells in subcutaneous and disseminated mouse mod

137 minated well-established 5T33P and MOPC-315P myeloma cells in the bone marrow of tumor-bearing mice.

138 hat BMAds may influence and be influenced by myeloma cells in the marrow.

139 In this study, we i) cultured myeloma cells in the presence/absence of OCs under normo

140 Multiple myeloma cells in this way take a double hit: immunoprote

141 )-specific CTLs can effectively lyse primary myeloma cells in vitro.

142 ysis of previously untreated and R/R primary myeloma cells in vitro.

143 owed high selectivity toward mitochondria in myeloma cells in vivo and allowed their visualization in

144 f human MM physically interact with multiple myeloma cells in vivo, undergo caspase-3-dependent apopt

145 reases survival of stroma-dependent multiple myeloma cells including primary multiple myeloma cells.

146 ced a synergistic effect in killing multiple myeloma cells, including those that were resistant to bo

147 ke 13 nonmyeloma cell lines, even though the myeloma cells induced heat-shock proteins and increased

148 eloma revealed significant loss of BMAT with myeloma cell infiltration of the marrow, whereas BMAT wa

149 Myeloma cells inhibit osteoblastogenesis from mesenchyma

150 n revealed that CD166 expression in multiple myeloma cells inhibited osteoblastogenesis of bone marro

151 graft models, silencing MMP-13 expression in myeloma cells inhibited the development of osteolytic le

152 suggesting that targeting osteocyte-multiple myeloma cell interactions through specific Notch recepto

153 ture, and subcutaneous injection of MSCs and myeloma cells into mice.

154 Intravenous injection of 10(6) 5T33 mouse myeloma cells into the Syngeneic mouse strain C57BL/KaLw

155 despite development of therapies that target myeloma cell-intrinsic pathways.

156 Higher ANXA2 expression in myeloma cells is associated with significantly inferior

157 leagues demonstrate that PSGL-1 expressed on myeloma cells is involved with regulating tumor cell ext

158 Its silencing in multiple myeloma cells is sufficient to induce cytotoxicity, sugg

159 ion, we generated a derivative of the KMS-11 myeloma cell line (FGFR(Y373C)) with acquired resistance

160 t ThB-BP analogue was assessed in a multiple myeloma cell line and found to be equipotent to the best

161 (STAT3) facilitates survival in the multiple myeloma cell line INA-6 and therefore represents an onco

162 of MM patients, and in three of seven human myeloma cell lines (HMCLs) analyzed.

163 inducing myeloma cell death, using 27 human myeloma cell lines (HMCLs) and 23 primary samples.

164 wn, although it has been reported that human myeloma cell lines (HMCLs) are highly sensitive to Gln d

165 proves the efficacy of sorafenib in multiple myeloma cell lines and CD138(+)-enriched primary cells i

166 Using exosomes isolated from myeloma cell lines and from myeloma patients, we identif

167 hat sorafenib induces cell death in multiple myeloma cell lines and in CD138(+)-enriched primary mult

168 cell antigen overexpressed on the surface of myeloma cell lines and on neoplastic plasma cells of pat

169 We found that exposure of myeloma cell lines and patient tumor samples to GSIs mar

170 apoptosis and cell-cycle arrest in multiple myeloma cell lines and prevented outgrowth of human mult

171 iscovered to be highly expressed in multiple myeloma cell lines and primary bone marrow cells from pa

172 gene expression profiling studies involving myeloma cell lines and primary cells as well as normal l

173 bitor carfilzomib in lymphoma, leukemia, and myeloma cell lines and primary lymphoma and leukemia cel

174 ic when combined with bortezomib, using both myeloma cell lines and primary myeloma patient specimens

175 addiction is responsible for rapid death of myeloma cell lines and primary myeloma tumor cells treat

176 As a substantial number of multiple myeloma cell lines and primary samples were found to exp

177 Treatment of multiple myeloma cell lines and primary samples with ON123300 in

178 ltiple myeloma treatments, in three multiple myeloma cell lines and seven patient-derived primary mul

179 ISH analyses, we have identified in multiple myeloma cell lines and tumors a novel and recurrent type

180 with four siRNAs per gene in three multiple myeloma cell lines and two non-myeloma cell lines, catal

181 resinol was the only compound active against myeloma cell lines and was also active against colon can

182 The majority of human multiple myeloma cell lines are HK1(-)HK2(+).

183 dependent DNA double-strand breaks (DSBs) in myeloma cell lines as well as primary MM cells.

184 of MYC-MAX heterodimerization, 10058-F4, on myeloma cell lines as well as primary myeloma cells, and

185 In the present study, myeloma cell lines expressing either high or low levels

186 We established myeloma cell lines expressing wild-type (WT), constituti

187 inhibition and cytotoxicity against multiple myeloma cell lines in vitro and remarkable tumor growth

188 CD166 deficiency in multiple myeloma cell lines or CD138(+) bone marrow cells from mu

189 Whole-genome sequencing of myeloma cell lines revealed additional TSIs, demonstrati

190 singly, analysis of Mcl-1-dependent multiple myeloma cell lines revealed codependence on Bcl-2/Bcl-x(

191 Analysis of myeloma cell lines revealed that loss of IKZF1 and IKZF3

192 Treatment of human myeloma cell lines such as MM1.S, OPM2, and U266 with th

193 involved, we developed bortezomib-resistant myeloma cell lines that, unlike previously reported mode

194 Selective targeting of multiple myeloma cell lines through CBP/EP300 bromodomain inhibit

195 apeutic susceptibility across human multiple myeloma cell lines to a gamut of standard-of-care therap

196 ll line and several NSCLC and human multiple myeloma cell lines to identify conserved interacting pro

197 plasma cell differentiation and in multiple myeloma cell lines upon induction of pharmacological ER

198 In vitro cytotoxicity against multiple myeloma cell lines was directly correlated with DEPTOR p

199 D46-ADC) potently inhibited proliferation in myeloma cell lines with little effect on normal cells.

200 d reduced clonogenic growth in BMSC-adherent myeloma cell lines, aldehyde dehydrogenase-positive MM c

201 es myeloma cell growth, reduces apoptosis in myeloma cell lines, and increases osteoclast formation.

202 hree multiple myeloma cell lines and two non-myeloma cell lines, cataloging a total of 57 potent mult

203 ctiveness in inducing cell death in multiple myeloma cell lines, in the presence of OPG secreted by s

204 nd T cells, plus human leukemia and multiple myeloma cell lines, recruitment of c-Rel to the first in

205 tin, exhibited apparent cytotoxic effects on myeloma cell lines, without any difference in suppressio

206 idated in several Ewing sarcoma and multiple myeloma cell lines.

207 GF-beta produced by cultured human and mouse myeloma cell lines.

208 entially abrogates the viability of multiple myeloma cell lines.

209 ed a submicromolar IC50 in 10 of 10 multiple myeloma cell lines.

210 FNDC3A was lost in some multiple myeloma cell lines.

211 a cells from 630 patients with myeloma or 54 myeloma cell lines.

212 and triggers necrotic cell death in multiple myeloma cell lines.

213 C by short hairpin RNA induced cell death in myeloma cell lines; however, cell lines are generated fr

214 relapse is thought to originate from dormant myeloma cells, localized in specialized niches, which re

215 steocyte apoptosis was initiated by multiple myeloma cell-mediated activation of Notch signaling and

216 uate and to monitor the effect of therapy on myeloma-cell metabolism.

217 c-Jun under normoxic condition; (2) blocked myeloma cell migration and invasion by reducing the expr

218 oreover, exposure to GSK3 inhibitors renders myeloma cells more efficient to activate NK cell degranu

219 e myeloma, ST6GAL1 abundance in the multiple myeloma cells negatively correlated with neutrophil abun

220 In primary myeloma cells, nutlin-3a increased DR5 expression and le

221 The reliance of multiple myeloma cells on oxidative phosphorylation was caused by

222 TP53 wild-type myeloma cells overexpressed DR5 in correlation with sens

223 transgenic mice, we here describe that some myeloma cells persisted in a dormant state and, eventual

224 egy targeting mature and immature clonogenic myeloma cell populations in the autograft.

225 s and seven patient-derived primary multiple myeloma cell populations.

226 ictive) but is also an intrinsic property of myeloma cells (prognostic).

227 K2 specific inhibitor) effectively inhibited myeloma cell proliferation and induced caspase 3-mediate

228 Autocrine SHH enhanced CD138(+) myeloma cell proliferation and protected myeloma cells f

229 rofile as an oral agent and that it inhibits myeloma cell proliferation, resulting in survival advant

230 insights into biologic pathways required for myeloma cell proliferation.

231 Conversely, CD166 expression in multiple myeloma cells promoted osteoclastogenesis by activating

232 The immunoglobulin type produced by myeloma cells provides an excellent marker to follow cha

233 rect contact between osteocytes and multiple myeloma cells reciprocally activated Notch signaling and

234 Myeloma cells reduced BMAT in different preclinical muri

235 ned the mechanisms by which p38 signaling in myeloma cells regulates osteoblastogenesis, osteoclastog

236 These results suggest that multiple myeloma cells remodel their trafficking machinery to cop

237 While myeloma cells require a basal level of autophagy for sur

238 though normal plasma cells and most multiple myeloma cells require Mcl-1 for survival, a subset of my

239 rpin RNA-mediated knockdown (KD) of Usp9x in myeloma cells resulted in transient induction of apoptos

240 endent cohorts of 332 and 701 CD138-purified myeloma cell samples from previously untreated patients

241 d this issue in a model in which MHC II(NEG) myeloma cells secrete a monoclonal Ig containing a V reg

242 Multiple myeloma cells secrete more disulfide bond-rich proteins

243 naling and was further amplified by multiple myeloma cell-secreted TNF.

244 In addition, multiple myeloma cells sensitive to ON123300 were found to have a

245 ar Programming approach to infer OC-mediated myeloma cell-specific signaling pathways under normoxic

246 vealed that the alpha(4) integrin subunit on myeloma cells stimulated vascular cell adhesion molecule

247 Next, we performed myeloma cell surface screenings of phage-displayed patie

248 system plays a nonredundant role in multiple myeloma cell survival and disease progression, and indic

249 Usp24 was found to sustain myeloma cell survival and Mcl-1 regulation in the absenc

250 rine FGF/FGFR axis is essential for multiple myeloma cell survival and progression by protecting mult

251 Abrogation of PRL-3 reduced myeloma cell survival, clonogenicity, and tumorigenesis,

252 ne marrow microenvironment are essential for myeloma cell survival, mirroring the same dependence of

253 ssion was shown to be essential for multiple myeloma cell survival.

254 Reconstitution of FAM46C in multiple myeloma cells that had lost it induced apoptosis and ER

255 Drug-resistant dormant myeloma cells that reside in specific niches within the

256 Interestingly, in multiple myeloma cells the IL-8 release is not increased by borte

257 Daratumumab targets CD38-expressing myeloma cells through a variety of immune-mediated mecha

258 SLAMF7), selectively kills SLAMF7-expressing myeloma cells through direct activation and engagement o

259 indings reveal a novel regulatory pathway in myeloma cells through which JNK2 signals cell survival v

260 indings reveal a novel regulatory pathway in myeloma cells through which JNK2 signals cell survival v

261 liver live oncolytic virus to human multiple myeloma cells, thus augmenting GVM by transfer of active

262 tion of tunneling nanotubes that connect the myeloma cell to the stromal cell and is dependent on sur

263 Shifting myeloma cells to 43, 41, or 39 degrees C (which was not

264 played a role in the acquired resistance of myeloma cells to bortezomib, which could be overcome by

265 ntially target the bone microenvironment and myeloma cells to enhance the drug availability at the my

266 unfolded protein stress response in multiple myeloma cells to generate a mass response that was tempo

267 Here, we performed a screen of human myeloma cells to identify pro-osteoclastogenic agents th

268 d enhances the sensitivity of human multiple myeloma cells to IMiDs.

269 arrow stromal cells transfer mitochondria to myeloma cells to increase cellular respiration, resultin

270 ecreased proteasome activity, and sensitized myeloma cells to PIs.

271 on, highlighting the sensitivity of multiple myeloma cells to the accumulation of protein aggregates.

272 We found that p53 affects the sensitivity of myeloma cells to the DR5 agonistic human antibody lexatu

273 of the trypsin-like site sensitize multiple myeloma cells to these agents.

274 degranulation and to enhance the ability of myeloma cells to trigger NK cell-mediated cytotoxicity.

275 Exposure of multiple myeloma cells to VLX1570 resulted in thermostabilization

276 For example, in multiple myeloma cells treated with the proteasome inhibitor bort

277 egrin/FAK signaling pathway was activated in myeloma cells under hypoxic condition.

278 Multiple myeloma cells undergo autophagy in response to sorafenib

279 Multiple myeloma cells uniformly overexpress CD38.

280 Here, we report that multiple myeloma cells use mitochondrial-based metabolism as well

281 d a genome-scale lethality study in multiple myeloma cells using siRNAs.

282 Upregulation of PRL-3 increased myeloma cell viability and rephosphorylated STAT3 in a b

283 1 in the critical role of DEPTOR in multiple myeloma cell viability.

284 the clinic, high TJP1 expression in patient myeloma cells was associated with a significantly higher

285 raft model using CD38-positive OPM2 multiple myeloma cells was used to evaluate CD38-specificity of (

286 es between multiple myeloma and non-multiple myeloma cells were found to occur within the 20S proteas

287 Nontoxic to myeloma cells when used as a single agent, 4a sensitized

288 sp24 were expressed and activated in primary myeloma cells whereas Usp24 protein overexpression was n

289 totoxicity was seen against primary multiple myeloma cells, whereas normal hematopoietic colony forma

290 ival and chemoprotective factor for multiple myeloma cells, which is pathophysiologically linked to b

291 13 expression was localized to BM-associated myeloma cells, while elevated MMP-13 serum levels were a

292 level of CD46 was markedly higher in patient myeloma cells with 1q gain than in those with normal 1q

293 udies demonstrate that treatment of multiple myeloma cells with a MUC1-C inhibitor is associated with

294 Interaction of myeloma cells with osteoclasts (OC) can enhance tumor ce

295 H5N1 virus were developed by fusion of mouse myeloma cells with spleen cells isolated from an H5N1-vi

296 cell-specific pathways showed that targeting myeloma cells with the combination of PI3K and integrin

297 Thus, engagement of myeloma cells with the osteoblastic niche induces expres

298 ABC294640 inhibited primary human CD1381 myeloma cells with the same efficacy as with MM cell lin

299 Treatment of multiple myeloma cells with VLX1570 induced the accumulation of p

300 also prevented DEPTOR-mTOR binding in human myeloma cells, with subsequent activation of mTORC1 and