ライフサイエンスコーパス: myeloma cell

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

2 tutively localized on the plasma membrane of myeloma cells.

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

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

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

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

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

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

9 yeloma is associated with CRBN expression in myeloma cells.

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

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

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

13 ein is aberrantly expressed in most multiple myeloma cells.

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

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

16 expression of this protein protects multiple myeloma cells.

17 ple myeloma cells including primary multiple myeloma cells.

18 presses ASK1-dependent apoptosis in multiple myeloma cells.

19 mediated late apoptosis/necrosis of multiple myeloma cells.

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

21 ppaB ligand (RANKL) by heparanase-expressing myeloma cells.

22 nd is aberrantly expressed in human multiple myeloma cells.

23 ll lines as well as freshly isolated patient myeloma cells.

24 ndent on direct contact between Mvarphis and myeloma cells.

25 PRDM1 in lymphoma cells and in PU.1-positive myeloma cells.

26 an resistance in repeatedly exposed multiple myeloma cells.

27 induces substantial cytotoxicity in multiple myeloma cells.

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

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

30 l adhesion-dependent alterations in multiple myeloma cells.

31 redirects T cells to lyse malignant multiple myeloma cells.

32 f these transcription factors kills multiple myeloma cells.

33 he regulation of drug resistance in multiple myeloma cells.

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

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

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

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

38 myeloma cell adhesion, increasing homotypic myeloma cell adhesion while decreasing myeloma heterotro

39 TbetaRIII further regulated myeloma cell adhesion, increasing homotypic myeloma cell

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

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

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

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

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

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

46 irectly transduce prosurvival signals to the myeloma cells and also induce niche production of suppor

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

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

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

50 ppressed proliferation of human leukemia and myeloma cells and downregulated the constitutive express

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

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

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

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

55 bortezomib to induce cytotoxicity of primary myeloma cells and myeloma cell lines.

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

57 t of this disease by targeting both multiple myeloma cells and the bone marrow microenvironment.

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

59 e by retrovirus transduction into P3U1 mouse myeloma cells, and other cell types including murine CD4

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 ism responsible for synergistic induction of myeloma cell apoptosis induced by the combination of tip

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

64 nt mice, and adiponectin was found to induce myeloma cell apoptosis.

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

66 ped a tumor vaccine in which patient-derived myeloma cells are chemically fused with autologous dendr

67 Myeloma cells are dependent on IL6 for their survival an

68 These findings indicate that multiple myeloma cells are dependent on intact MUC1-C function fo

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

70 Dormant myeloma cells are resistant to chemotherapy that targets

71 However, it is not known whether multiple myeloma cells are sensitive to the disruption of MUC1-C

72 Myeloma cells are sensitive to TRAIL through the two dea

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

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

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

76 c molecule, GCS-100, is a potent modifier of myeloma cell biology targeting apoptosis, cell cycle, an

77 e growth and clonogenic capacity of multiple myeloma cells both in vitro and in vivo.

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

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

80 Primary multiple myeloma cells, but not normal B-cells, were also sensiti

81 BN depletion is initially cytotoxic to human myeloma cells, but surviving cells with stable CRBN depl

82 alpha) is exported from the nucleus of human myeloma cells by a CRM1-dependent mechanism at cellular

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

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

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

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

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

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

89 sion of these genes in MSCs, whereas in vivo myeloma cell-conditioned media reduced EphB4 expression

90 Myeloma cells counteracted the metabolic stress by activ

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

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

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

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

95 GAR suppression that contributes to multiple myeloma cell death.

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

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

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

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

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

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

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

103 timulatory receptor CD28 is overexpressed on myeloma cells during disease progression and in the poor

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

105 iver radiation doses sufficient for multiple myeloma cell eradication.

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

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

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

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

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

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

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

113 decan-1 axis regulates angiogenesis, we used myeloma cells expressing either high or low levels of he

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

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

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

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

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

119 rotected both myeloma cell lines and primary myeloma cells from spontaneous and chemotherapy drug-ind

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

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

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

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

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

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

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

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

128 paB pathway in the IL6-independent growth of myeloma cells has not been studied.

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

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

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

132 and CD8 lymphocytes reactive with autologous myeloma cells in 11 of 15 evaluable patients.

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

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

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

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

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

138 igomerization block growth of human multiple myeloma cells in vitro.

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

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

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

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

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

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

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

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

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

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

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

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

151 on studies we demonstrate that expression in myeloma cells is regulated via direct association with t

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

153 Human myeloma cell lines and patient myeloma cells isolated from bone marrow were treated wit

154 inant CDK that phosphorylates Smad2 on T8 in myeloma cells, leading to inhibition of Smad2-Smad4 asso

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

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

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

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

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

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

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

162 toxicity on leukemia, lymphoma, and multiple myeloma cell lines and chronic lymphocytic leukemia (CLL

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

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

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

166 Human myeloma cell lines and patient myeloma cells isolated fr

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

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

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

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

171 Multiple myeloma cell lines and primary multiple myeloma cells st

172 Mvarphis protected both myeloma cell lines and primary myeloma cells from sponta

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

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

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

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

177 nisms of action of GCS-100 are elucidated in myeloma cell lines and primary tumor cells.

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

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

184 ngly suggests that pooled gp96 vaccines from myeloma cell lines can replace gp96 vaccines from autolo

185 sis in primary bone marrow myeloma and human myeloma cell lines due to its inability to activate G(1)

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

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

188 449 antagonized FGFR3 action in the multiple myeloma cell lines OPM2 and KMS11, as evidenced by NF449

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

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

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

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

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

194 Chronic drug exposure produced myeloma cell lines that were tolerant of the direct effe

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

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

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

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

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

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

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

202 paranase to myeloma cells or transfection of myeloma cell lines with the cDNA for heparanase signific

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

204 including rituximab-resistant), and multiple myeloma cell lines, and also patient CLL cells.

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

206 1 against B-lymphoma, leukemia, and multiple myeloma cell lines, and significantly enhanced ADCC agai

207 2b inhibited each of four lymphoma and eight myeloma cell lines, and was more effective than monospec

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

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

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

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

212 hibited various B-cell lymphoma leukemia and myeloma cell lines.

213 ce cytotoxicity of primary myeloma cells and myeloma cell lines.

214 s stabilized in short-lived plasma cells and myeloma cell lines.

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

216 entially abrogates the viability of multiple myeloma cell lines.

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

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

219 ells from MGUS, SMM, and MM specimens; human myeloma cell lines; and normal plasma cell (NPC) samples

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

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

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

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

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

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

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

227 d tumor necrosis factor-alpha and fused with myeloma cells obtained from marrow aspirates.

228 vitro, addition of recombinant heparanase to myeloma cells or transfection of myeloma cell lines with

229 We found that myeloma cells or tumors expressing high levels of hepara

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

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

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

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

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

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

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

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

238 insights into biologic pathways required for myeloma cell proliferation.

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

240 directly transduces a prosurvival signal to myeloma cell, protecting it against chemotherapy and gro

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

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

243 Myeloma cells reduced expression of these genes in MSCs,

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

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

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

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

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

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

250 Multiple myeloma cells secrete more disulfide bond-rich proteins

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

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

253 Primary myeloma cells showed a direct reduction in proliferation

254 ctionally, restoring TbetaRIII expression in myeloma cells significantly inhibited cell growth, proli

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

256 iple myeloma cell lines and primary multiple myeloma cells strongly expressed C/EBPbeta, whereas norm

257 heparan sulfate proteoglycan present on the myeloma cell surface and shed into the tumor microenviro

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

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

260 lts indicate that Mvarphis may contribute to myeloma cell survival and resistance to chemotherapeutic

261 ages (Mvarphis), a type of stromal cells, on myeloma cell survival and response to chemotherapy.

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

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

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

265 In t(4;14)-positive myeloma cells, the normal genome-wide and gene-specific

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

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

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

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

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

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

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

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

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

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

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

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

278 Exposure of multiple myeloma cells to VLX1570 resulted in thermostabilization

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

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

281 Multiple myeloma cells undergo autophagy in response to sorafenib

282 Multiple myeloma cells uniformly overexpress CD38.

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

284 1 in the critical role of DEPTOR in multiple myeloma cell viability.

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

286 n addition, inhibition of MUC1-C in multiple myeloma cells was associated with activation of the intr

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

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

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

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

291 c pathway driven by heparanase expression in myeloma cells whereby elevated levels of VEGF and shed s

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

293 13 expression was localized to BM-associated myeloma cells, while elevated MMP-13 serum levels were a

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

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

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

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

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

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

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

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