ライフサイエンスコーパス: myeloma

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

2 tient outcomes for the treatment of Multiple Myeloma.

3 pecific T cells in a mouse model of multiple myeloma.

4 breast cancer, prostate cancer, or multiple myeloma.

5 treatment for patients with newly diagnosed myeloma.

6 vestigated for patients with newly diagnosed myeloma.

7 but also acute myeloid leukemia and multiple myeloma.

8 ove access to oral therapy for patients with myeloma.

9 omponents of treatment regimens for multiple myeloma.

10 the clinical evaluation of PAK4 modulator in myeloma.

11 atients with relapsed or refractory multiple myeloma.

12 with B-cell malignancies, including multiple myeloma.

13 s of compounds for the treatment of relapsed myeloma.

14 enograft mouse model of established multiple myeloma.

15 atients with relapsed or refractory multiple myeloma.

16 ermining Bcl-2 family dependence in multiple myeloma.

17 ythematosis and relapsed/refractory multiple myeloma.

18 lofibrosis and Waldenstrom macroglobulinemia/myeloma.

19 only 1 (2.5%) patient progressed to multiple myeloma.

20 diagnosed with biclonal gammopathy multiple myeloma.

21 relapsed or refractory lymphoma and multiple myeloma.

22 methasone in relapsed or refractory multiple myeloma.

23 ed to quantify IL-10 levels in patients with myeloma.

24 efficacy in relapsed or refractory multiple myeloma.

25 drome and is overexpressed in human multiple myeloma.

26 ul tool to evaluate the prognosis of de novo myeloma.

27 t efficacy in the setting of newly diagnosed myeloma.

28 dissemination and overt relapse in multiple myeloma.

29 ibody approved for the treatment of multiple myeloma.

30 ystem for therapeutic management of multiple myeloma.

31 ASCT in patients with refractory or relapsed myeloma.

32 could be an effective treatment strategy in myeloma.

33 impact on the pathogenesis of human multiple myeloma.

34 pendence is highly heterogeneous in multiple myeloma.

35 on as a target for immunotherapy in multiple myeloma.

36 s chronic lymphocytic leukemia, and multiple myeloma.

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

38 omide causing a deadly ADR when used against myeloma, a likely result of the disease itself; multipli

39 ave developed a system, Ex vivo Mathematical Myeloma Advisor (EMMA), consisting of patient-specific m

40 uited patients with newly diagnosed multiple myeloma aged 18 years and older from participating South

41 rum sclerostin level is elevated in multiple myeloma, an osteolytic malignancy, where it might serve

42 me inhibitors benefit patients with multiple myeloma and B cell-dependent autoimmune disorders but ex

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

44 e activation that is upregulated in multiple myeloma and is a critical component of the immunosuppres

45 The inhibitors are far more cytotoxic for myeloma and lymphoma cell lines than for hepatocarcinoma

46 stablished targets overexpressed in multiple myeloma and non-Hodgkin lymphoma, respectively.

47 ((18)F-FDG) PET/CT in patients with multiple myeloma and other plasma cell disorders, including smoul

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

49 ain cause of acute kidney injury in multiple myeloma and persistent reduction in kidney function stro

50 y as an effective treatment against multiple myeloma and provide novel insights into the consequences

51 set of data supports PAK4 as an oncogene in myeloma and provide the rationale for the clinical evalu

52 ll disorders, including smouldering multiple myeloma and solitary plasmacytoma.

53 One patient exhibited M2 progression to myeloma and subsequently died.

54 r older, had relapsed or refractory multiple myeloma, and had received between one and three previous

55 as seen when using daratumumab in refractory myeloma, and trials for both elotuzumab and daratumumab

56 noglobulin light-chain amyloidosis, multiple myeloma, and Waldenstrom macroglobulinemia.

57 n patients with biclonal gammopathy multiple myeloma, anti-multiple myeloma therapies exert a greater

58 evidence that lung cancer, anal cancer, and myeloma are diagnosed at modestly younger ages, and also

59 identify, with biclonal gammopathy multiple myeloma as an investigative model, the genetic and epige

60 nduction treatment in patients with multiple myeloma at first relapse after a first ASCT.

61 ssed in osteocytes from bones from naive and myeloma-bearing mice.

62 iagnosed and relapsed or refractory multiple myeloma because it assesses bone damage with relatively

63 from a therapeutic perspective for multiple myeloma because we have shown that targeting Rab GTPase

64 In conclusion, our results implicate IL-8 in myeloma bone disease and point to the potential utility

65 d patients with biclonal gammopathy multiple myeloma by central laboratory analysis of 6399 newly dia

66 (BM) infiltration in patients with multiple myeloma by using a virtual noncalcium (VNCa) technique.

67 tment regimens is therefore a cornerstone in myeloma care.

68 ial involving 98 patients with biopsy-proven myeloma cast nephropathy requiring hemodialysis treated

69 Among patients with myeloma cast nephropathy treated with a bortezomib-based

70 nce rate among patients newly diagnosed with myeloma cast nephropathy treated with hemodialysis using

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 presses ASK1-dependent apoptosis in multiple myeloma cells.

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

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

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

104 induces substantial cytotoxicity in multiple myeloma cells.

105 sed by the coexistence of an active multiple myeloma clone and a benign MGUS clone, and thus provides

106 against fibronectin inhibited the ability of myeloma-derived exosomes to stimulate endothelial cell i

107 e that adiponectin protects against multiple myeloma development, particularly among overweight and o

108 nd have been shown to contribute to multiple myeloma development; yet, little is known of the role of

109 g event was associated with a younger age at myeloma diagnosis (difference = 4; P = .01), and CD4 cou

110 2), and kidney cancers (difference = 2) and myeloma (difference = 4).

111 chedules with combinations of these new anti-myeloma drug classes.

112 6399 newly diagnosed patients with multiple myeloma enrolled in three UK clinical trials (Myeloma IX

113 usly treated relapsed or refractory multiple myeloma from five cancer centres in the USA.

114 Although transcriptome profiles in multiple myeloma has been described, landscape of expressed fusio

115 The standard treatment of relapsed multiple myeloma has been either lenalidomide-dexamethasone (RD)

116 e management of RI in patients with multiple myeloma, high fluid intake is indicated along with antim

117 e most recurrently mutated genes in multiple myeloma; however its role in disease pathogenesis has no

118 uish between smouldering and active multiple myeloma, if whole-body X-ray (WBXR) is negative and whol

119 of renal significance in 30 (60%), multiple myeloma in 17 (34%), and chronic lymphocytic leukemia in

120 entified Part D beneficiaries diagnosed with myeloma in 2007 to 2011.

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

122 leukemia, mantle cell lymphoma, and multiple myeloma in vitro.

123 y and the evolutionary processes in multiple myeloma.In multiple myeloma, malignant cells expand with

124 Survivors of multiple myeloma (incidence rate ratio [IRR], 1.70; P < .01), car

125 ment with anti-sclerostin antibody prevented myeloma-induced bone loss, reduced osteolytic bone lesio

126 Multiple myeloma is a plasma cell malignancy characterized by rec

127 Biclonal gammopathy multiple myeloma is characterised by the coexistence of an active

128 ells require Mcl-1 for survival, a subset of myeloma is codependent on Bcl-2 and/or Bcl-xL We investi

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

130 Multiple myeloma is consistently preceded by monoclonal gammopath

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

132 ever, an imbalanced distribution of multiple myeloma is frequently observed in medical imaging.

133 Multiple myeloma is highly dependent on the bone marrow microenvi

134 -737 to study the factors regulating whether myeloma is Mcl-1 dependent, and thus resistant to ABT-73

135 yeloma enrolled in three UK clinical trials (Myeloma IX, Myeloma XI, and TEAMM) between July 7, 2004,

136 kin lymphoma; non-Hodgkin lymphoma; multiple myeloma; leukemia; and all other cancers combined.

137 variety of human cancer cell lines, multiple myeloma lines consistently exhibiting high sensitivity.

138 n MGUS (which we defined as M2) and multiple myeloma (M1) clones-overall, within patients, and betwee

139 In multiple myeloma malignant plasma cells expand within the bone ma

140 ry processes in multiple myeloma.In multiple myeloma, malignant cells expand within bone marrow.

141 o resolution of medullary and extramedullary myeloma manifestations in a murine xenograft model in vi

142 In an analysis of >800 primary multiple myelomas, MAX alterations occurred at a frequency of app

143 n implicated as efficacy targets in multiple myeloma (MM) and 5q deletion associated myelodysplastic

144 30% of de novo and 70% of relapsed multiple myeloma (MM) and is correlated with disease progression

145 insight into the clonal dynamics of multiple myeloma (MM) and its possible influence on patient outco

146 PRIT approach for the treatment of multiple myeloma (MM) and other B-cell malignancies, for which we

147 g (IMiDs) with clinical efficacy in multiple myeloma (MM) and other late B-cell neoplasms.

148 in the bone marrow of patients with multiple myeloma (MM) and to determine a threshold ADC that may h

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

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

151 s highly and uniformly expressed on multiple myeloma (MM) cells, and at relatively low levels on norm

152 nhibitor that induces cell death in multiple myeloma (MM) cells, particularly in those harboring t(11

153 Notably, multiple myeloma (MM) expresses high levels of ADK, and 6-ETI was

154 Multiple myeloma (MM) has benefited from significant advancements

155 Multiple myeloma (MM) is a hematological cancer for which immune-

156 Multiple myeloma (MM) is a nearly always incurable malignancy of

157 Multiple myeloma (MM) is a plasma B-cell hematologic cancer that

158 Multiple myeloma (MM) is a plasma cell cancer that develops in th

159 t can circumvent chemoresistance in Multiple Myeloma (MM) is a priority.

160 Multiple myeloma (MM) is characterized by the expansion of malign

161 Multiple myeloma (MM) is characterized by wide variability in the

162 Multiple myeloma (MM) is the second most common hematological mal

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

164 ion profiles (GEP) from a cohort of multiple myeloma (MM) patients and normal individuals using globa

165 Primed CD56bright cells from multiple myeloma (MM) patients displayed superior responses to au

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

167 ibition is an effective therapy for multiple myeloma (MM) patients; however, the emergence of drug re

168 AL PCs, in comparison with primary multiple myeloma (MM) PCs, the prototypical PI-responsive cells.

169 between the number of patients with multiple myeloma (MM) treated annually at a treatment facility (v

170 to microfluidic devices by treating multiple myeloma (MM) tumor cells with two MM drugs (bortezomib (

171 l lineage marker FcRH5 expressed in multiple myeloma (MM) tumor cells.

172 NAs are aberrantly overexpressed in multiple myeloma (MM) tumor plasma cells compared to their normal

173 Survival following a diagnosis of multiple myeloma (MM) varies between patients and some of these d

174 llenges for effective management of multiple myeloma (MM), a plasma cell cancer.

175 In multiple myeloma (MM), a plasma cell malignancy, most tumors disp

176 se forms of malignancies, including multiple myeloma (MM), and thus represent potential therapeutic t

177 a promising therapeutic target for multiple myeloma (MM), but expression is variable, and early repo

178 iRNA) in several cancers, including multiple myeloma (MM), by controlling the expression of target pr

179 for the treatment of patients with multiple myeloma (MM), including alkylators, steroids, immunomodu

180 In both AL and multiple myeloma (MM), soluble immunoglobulin light chains (LC) a

181 atients with relapsed or refractory multiple myeloma (MM).

182 are important imaging techniques in multiple myeloma (MM).

183 th relapsed lenalidomide-refractory multiple myeloma (MM).

184 epth of response in newly diagnosed multiple myeloma (MM).

185 emonstration of a role for CARM1 in multiple myeloma (MM).

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

187 matological malignancies, including multiple myeloma (MM).

188 malignant plasma cell (PC) disease multiple myeloma (MM).

189 ith several cancer types, including multiple myeloma (MM).

190 dual disease (MRD) in patients with multiple myeloma (MM).

191 ting exosomal microRNAs (miRNAs) in multiple myeloma (MM).

192 et for pharmacological treatment of multiple myeloma (MM).

193 ly impact outcomes in patients with multiple myeloma (MM).

194 odgkin lymphoma (HL, N = 1,465) and multiple myeloma (MM, N = 3,790).

195 aratumumab was performed using CD38(+) human myeloma MM1.S-luciferase (MM1.S) cells.

196 Furthermore, using an intramedullary myeloma model, ACAR T cells caused regression of an esta

197 s) of patients with newly diagnosed multiple myeloma (NDMM).

198 ukemia, acute lymphocytic leukemia, multiple myeloma, non-Hodgkin lymphoma, Hodgkin lymphoma, myelopr

199 se of incomplete targeting of other critical myeloma oncogenic kinases.

200 fic antibodies for the treatment of multiple myeloma: one targets FcRH5 expressed on B cells, whereas

201 essed by plasma cells from 630 patients with myeloma or 54 myeloma cell lines.

202 study, 34 consecutive patients with multiple myeloma or monoclonal gammopathy of unknown significance

203 identify FAM46C mutation as a contributor to myeloma pathogenesis and disease progression via perturb

204 d may serve as a key determinant of multiple myeloma pathophysiology.

205 t and venetoclax, in a cohort of 19 multiple myeloma patient samples, yielded consistent results with

206 b, using both myeloma cell lines and primary myeloma patient specimens.

207 contrast, FAM46C mutations found in multiple myeloma patients abrogate this cytotoxicity, indicating

208 Samples from multiple myeloma patients also revealed a decreased copy number o

209 have benefits in breast cancer and multiple myeloma patients and have been used with adoptive immuno

210 tion of CgA-derived polypeptides in multiple myeloma patients and the subsequent implications for dis

211 d poor prognosis in newly diagnosed multiple myeloma patients and was associated with an increase in

212 or CD138(+) bone marrow cells from multiple myeloma patients compromised their ability to induce bon

213 Moreover, multiple myeloma patients treated with pomalidomide demonstrated

214 y untreated and in relapsed/refractory (R/R) myeloma patients who had received previous treatment wit

215 diagnosed and homogeneously treated multiple myeloma patients with long follow-up.

216 estingly, MAX alterations define a subset of myeloma patients with lower MYC expression and a better

217 to predict therapeutic response in multiple myeloma patients within a clinically actionable time fra

218 mosensitivity of primary cells from multiple myeloma patients, allowing us to predict clinical respon

219 From a cohort of 52 multiple myeloma patients, EMMA correctly classified 96% as respo

220 e potent in specimens obtained from relapsed myeloma patients, suggesting that relapse may occur at a

221 ppression is associated with poor outcome in myeloma patients, where proteasome inhibitors are a main

222 ies, but single-agent activity is limited in myeloma patients.

223 and induced comparable toxicities in elderly myeloma patients.

224 nstrate that HIF-2alpha upregulates multiple myeloma PC CXCL12 expression, decreasing migration towar

225 CCR1 activation potently induces multiple myeloma PC migration toward CCL3 while abrogating the mu

226 on toward CCL3 while abrogating the multiple myeloma PC migratory response to CXCL12.

227 ition, increased CCR1 expression by multiple myeloma PCs conferred poor prognosis in newly diagnosed

228 regulation in driving the egress of multiple myeloma PCs from the bone marrow.

229 ted with an increase in circulating multiple myeloma PCs in these patients.

230 n of the chemokine receptor CCR1 in multiple myeloma PCs.

231 ted with increased recirculation of multiple myeloma PCs.

232 , thereby enabling dissemination of multiple myeloma PCs.

233 diagnosis and at relapse, therefore requires myeloma physicians to carefully balance efficacy and tox

234 ver, studies comparing how MGUS and multiple myeloma plasma cell clones respond to these therapies ar

235 We aimed to identify how MGUS and multiple myeloma plasma cell clones responded to anti-multiple my

236 a greater depth of response against multiple myeloma plasma cell clones than MGUS plasma cell clones.

237 is dependent on the ability of the multiple myeloma plasma cells (PC) to reenter the circulation and

238 the underlying features that render multiple myeloma plasma cells susceptible to therapy are present

239 DK4/6 inhibitors has been modest in multiple myeloma, potentially because of incomplete targeting of

240 roliferative activity of VLX1570 in multiple myeloma, primarily associated with inhibition of USP14 a

241 neity, providing novel insight into multiple myeloma progression and evolution.

242 The results support a model for multiple myeloma progression with clonal sweeps in the early phas

243 able for relapsed and/or refractory multiple myeloma (R/R MM) after a long period in which dexamethas

244 remain the cornerstone of the management of myeloma-related RI (grade A).

245 Multiple myeloma remains treatable but incurable.

246 nts with relapsed and/or refractory multiple myeloma (RRMM) have poor prognosis.

247 , patients with relapsed/refractory multiple myeloma (RRMM) received elotuzumab with bortezomib and d

248 n patients with relapsed/refractory multiple myeloma (RRMM).

249 Among adults with multiple myeloma, RVD therapy plus transplantation was associated

250 nfused in NSG mice previously engrafted with myeloma, SE cells mediated tumor rejection without induc

251 of histone methyltransferase (HMT) multiple myeloma SET domain (MMSET) in mouse B cells and the CH12

252 Overexpression of the multiple myeloma set domain (MMSET) Wolf-Hirschhorn syndrome cand

253 als targeting BCMA in patients with multiple myeloma should consider possible effects on pDCs.

254 tly in clinical trials for relapsed multiple myeloma, significantly inhibited in vivo tumor growth.

255 nscriptomics analysis was performed on mouse myeloma SP2/0, Chinese hamster ovary (CHO), and human em

256 6 remain unprocessed in the nucleus and show myeloma-specific expression, STAiRs 15 and 18 are splice

257 ation therapy involving strategies to expand myeloma-specific T cells and T-cell activation via PD-1/

258 -1 precisely identified marrow-infiltrating, myeloma-specific T cells in a mouse model of multiple my

259 essfully address the clinical ambiguities of myeloma spectrum diseases.

260 Targeting postulated CD19(+) myeloma stem cells with anti-CD19 CAR-Ts is a novel appr

261 Group for Hematology Oncology and the Nordic Myeloma Study Group (the HOVON87/NMSG18 trial).

262 s displayed superior responses to autologous myeloma targets, and furthermore, CD56bright NK cells fr

263 RPRETATION: In patients with newly diagnosed myeloma, the addition of bortezomib to lenalidomide and

264 breast cancer, prostate cancer, or multiple myeloma, the use of zoledronic acid every 12 weeks compa

265 l gammopathy multiple myeloma, anti-multiple myeloma therapies exert a greater depth of response agai

266 Integration of CAR-Ts with other myeloma therapies is an important area of future researc

267 ally only treated by a form of anti-multiple myeloma therapy if it is causing substantial disease thr

268 lasma cell clones responded to anti-multiple myeloma therapy in patients newly diagnosed with biclona

269 ence in response achieved with anti-multiple myeloma therapy on MGUS (which we defined as M2) and mul

270 of separate clones to the same anti-multiple myeloma therapy, in the same patient, at the same time.

271 cell clones are responsive to anti-multiple myeloma therapy.

272 relapsed or relapsed and refractory multiple myeloma to receive bortezomib (1.3 mg per square meter o

273 randomly assigned 700 patients with multiple myeloma to receive induction therapy with three cycles o

274 mmon nonhematological adverse events of anti-myeloma treatment regimens containing proteasome inhibit

275 , carfilzomib is the first and only multiple myeloma treatment that extends overall survival in the r

276 mental therapeutic to dually attack multiple myeloma tumor cell survival and tumor angiogenesis.

277 ficity and sensitivity for detecting CD38(+) myeloma tumors of variable sizes (8.5-128 mm(3)) with st

278 men for patients with relapsed or refractory myeloma undergoing an autologous stem-cell transplant (A

279 ve extramedullary manifestations of multiple myeloma undergoing CXCR4-directed endoradiotherapy.

280 Following hospital admission, multiple myeloma was diagnosed and confirmed by bone marrow biops

281 Using the Vk*MYC mouse model of multiple myeloma, we further demonstrate that exogenously adminis

282 new mechanisms of tumorigenesis in multiple myeloma, we performed RNA sequencing in a cohort of 255

283 progression, death, or death as a result of myeloma were all higher with placebo or observation vers

284 s prognostic value in patients with multiple myeloma who are treated with IMiDs.

285 Conclusion Medicare beneficiaries with myeloma who do not receive LISs face a substantial finan

286 cer, metastatic prostate cancer, or multiple myeloma who had at least 1 site of bone involvement were

287 patients with primary refractory or relapsed myeloma who had received treatment with bortezomib, an i

288 patients with previously untreated multiple myeloma who were not planned for immediate autologous st

289 SA, patients (age >/=18 years) with multiple myeloma who were previously treated with at least three

290 diagnosed or relapsed or refractory multiple myeloma who were treated in clinical trials with IMiD-co

291 de and thalidomide) among beneficiaries with myeloma, who can receive either orally administered or p

292 n patients with relapsed/refractory multiple myeloma with >/=2 prior lines of therapy who were refrac

293 4 patients with biclonal gammopathy multiple myeloma with IgG or IgA MGUS clones were subsequently id

294 ng BM infiltration in patients with multiple myeloma with precision comparable to that of MR imaging.

295 been validated in the treatment of multiple myeloma, with several FDA-approved therapeutics.

296 The International Myeloma Working Group consensus aimed to provide recomme

297 mission in accordance with the International Myeloma Working Group criteria.

298 ly classified 79% according to International Myeloma Working Group stratification of level of respons

299 sequencing tumor data for 333 patients from Myeloma XI, a UK phase 3 trial and 434 patients from the

300 led in three UK clinical trials (Myeloma IX, Myeloma XI, and TEAMM) between July 7, 2004, and June 2,