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1 r colorectal cancer, one melanoma, and seven multiple myeloma).
2 efficacy also demonstrated in patients with multiple myeloma.
3 at is lost in more than 10% of patients with multiple myeloma.
4 ation-eligible patients with newly diagnosed multiple myeloma.
5 s with intermediate- or high-risk smoldering multiple myeloma.
6 a cells and is approved for the treatment of multiple myeloma.
7 ical exploration found an indolent IgG-kappa multiple myeloma.
8 asone (VTd) in patients with newly diagnosed multiple myeloma.
9 with transplant-ineligible, newly diagnosed multiple myeloma.
10 ll as patient-specific disease signatures in multiple myeloma.
11 cation obtained from patients with high-risk multiple myeloma.
12 omide could delay progression to symptomatic multiple myeloma.
13 pancreatic cancer, lymphocytic leukemia, and multiple myeloma.
14 sone in patients with relapsed or refractory multiple myeloma.
15 in the diagnosis and treatment monitoring of multiple myeloma.
16 rd regimens in patients with newly diagnosed multiple myeloma.
17 nts with relapsed or relapsed and refractory multiple myeloma.
18 as proangiogenic and mitogenic cytokines in multiple myeloma.
19 hly effective and widely used treatments for multiple myeloma.
20 ations for the pathogenesis and treatment of multiple myeloma.
21 n (BCMA), has potential for the treatment of multiple myeloma.
22 dormancy signature genes than patients with multiple myeloma.
23 ant-ineligible patients with newly diagnosed multiple myeloma.
24 ival, and overall survival for patients with multiple myeloma.
25 t genes, leading to bortezomib resistance in multiple myeloma.
26 lineage cancers such as B-ALL, lymphoma and multiple myeloma.
27 apy for patients with relapsed or refractory multiple myeloma.
28 sponse rate in patients with newly diagnosed multiple myeloma.
29 PRL-3 as a valid therapeutic opportunity in multiple myeloma.
30 ppression of bone formation is a hallmark of multiple myeloma.
31 nce therapy in patients with newly diagnosed multiple myeloma.
32 ession and prolong survival in patients with multiple myeloma.
33 one in patients with relapsed and refractory multiple myeloma.
34 mumab in a preclinical model of disseminated multiple myeloma.
35 the unification of treatment approaches for multiple myeloma.
36 izumab in patients with previously untreated multiple myeloma.
37 val in patients with relapsed and refractory multiple myeloma.
38 umab in patients with relapsed or refractory multiple myeloma.
39 file in patients with relapsed or refractory multiple myeloma.
40 ing) CAR T cells in patients with refractory multiple myeloma.
41 phalan with melphalan alone in patients with multiple myeloma.
42 plant-eligible patients with newly diagnosed multiple myeloma.
43 -daratumumab, for immunologic PET imaging of multiple myeloma.
44 ssessed in patients with relapsed/refractory multiple myeloma.
45 treated patients with relapsed or refractory multiple myeloma.
46 nts for patients with relapsed or refractory multiple myeloma.
47 novel therapeutic approach for treatment of multiple myeloma.
48 l neoplasms such as non-Hodgkin lymphoma and multiple myeloma.
49 the current standard of care for smoldering multiple myeloma.
50 phoplasmacytic lymphoma and in 2 patients to multiple myeloma.
51 hereas BMAT was restored after treatment for multiple myeloma.
52 file in patients with relapsed or refractory multiple myeloma.
53 ctivity in patients with heavily pre-treated multiple myeloma.
54 d) is a standard therapy for newly diagnosed multiple myeloma.
55 sone in patients with relapsed or refractory multiple myeloma.
56 tine has shown potential in the treatment of multiple myeloma.
57 ethasone in patients with previously treated multiple myeloma.
58 lvement or other systemic characteristics of multiple myeloma.
59 is a plasma cell dyscrasia and precursor to multiple myeloma.
60 ns of cancer of the pancreas and uterus, and multiple myeloma.
61 patients on dialysis, SMRs were highest for multiple myeloma (30.5), testicular cancer (17.0), and k
64 ease has drawn attention in the treatment of multiple myeloma, a malignant hematologic disorder that
65 ts with a confirmed diagnosis of symptomatic multiple myeloma according to International Myeloma Work
66 if they had confirmed relapsed or refractory multiple myeloma according to International Myeloma Work
67 65% of patients with relapsed and refractory multiple myeloma achieved an overall response with a com
68 nts with hematologic malignancies (lymphoma, multiple myeloma, acute myeloid leukemia, and myelodyspl
69 8 years or older with relapsed or refractory multiple myeloma, an Eastern Cooperative Oncology Group
71 ee survival in patients with newly diagnosed multiple myeloma and a suboptimal response to immunomodu
73 y hematopoietic stem cell transplantation in multiple myeloma and acute myeloid leukemia patients ind
74 usion criteria were the absence of high-risk multiple myeloma and an Eastern Cooperative Oncology Gro
75 e) as a fifth-line therapy for patients with multiple myeloma and as a monotherapy for patients with
76 f proteasome inhibition for the treatment of multiple myeloma and B-cell lymphomas has made the ubiqu
78 initial trial to 9 additional patients with multiple myeloma and ESRD and, more recently, to toleran
79 provide a framework to study the etiology of multiple myeloma and explore strategies for prevention a
81 AT in different preclinical murine models of multiple myeloma and in vitro using myeloma cell-adipocy
84 tients (aged >=18 years) with a diagnosis of multiple myeloma and measurable disease, an Eastern Coop
85 clinical outcomes for patients with de novo multiple myeloma and myeloma cast nephropathy who requir
86 w lesions is crucial in the investigation of multiple myeloma and often dictates the decision to star
87 nificantly delays progression to symptomatic multiple myeloma and the development of end-organ damage
90 s Kd in patients with relapsed or refractory multiple myeloma and was associated with a favourable be
91 le for inclusion if they had newly diagnosed multiple myeloma and were ineligible for high-dose chemo
92 pon additional classification approaches for multiple myelomas and other hematologic malignancies.
94 d-risk and intermediate-risk newly diagnosed multiple myeloma, and is a suitable treatment backbone f
95 PRL-3 that prolongs prosurvival signaling in multiple myeloma, and suggest targeting PRL-3 as a valid
96 Patients aged 18 years or older, who had multiple myeloma, and who had previously been treated wi
97 der with relapsed or relapsed and refractory multiple myeloma (as per International Myeloma Working G
99 , we recruited patients with newly diagnosed multiple myeloma, biopsy-confirmed cast nephropathy, and
101 additional clinical studies of melflufen in multiple myeloma, both in combination with dexamethasone
102 uration antigen (BCMA) have activity against multiple myeloma, but improvements in anti-BCMA CARs are
103 tion has improved outcomes for patients with multiple myeloma, but patients with high-risk multiple m
104 ppaB, which are validated to be related with multiple myeloma by our immunohistochemistry experiment,
106 1), which suppressed HK2 expression in human multiple myeloma cell cultures and human multiple myelom
111 FGF/FGFR system plays a nonredundant role in multiple myeloma cell survival and disease progression,
112 the autocrine FGF/FGFR axis is essential for multiple myeloma cell survival and progression by protec
114 dings were confirmed on bortezomib-resistant multiple myeloma cells as well as on bone marrow-derived
115 tor impaired the growth and dissemination of multiple myeloma cells by inducing mitochondrial oxidati
116 s targeting various cell surface antigens on multiple myeloma cells for the selective delivery of siR
117 d by intercellular mitochondrial transfer to multiple myeloma cells from neighboring nonmalignant bon
118 ls as well as on bone marrow-derived primary multiple myeloma cells from newly diagnosed and relapsed
119 cell survival and progression by protecting multiple myeloma cells from oxidative stress-induced apo
120 -combination achieved synthetic lethality in multiple myeloma cells in culture and prevented HK1(-)HK
122 l multiple myeloma, ST6GAL1 abundance in the multiple myeloma cells negatively correlated with neutro
126 l secretion, highlighting the sensitivity of multiple myeloma cells to the accumulation of protein ag
127 ine xenograft model using CD38-positive OPM2 multiple myeloma cells was used to evaluate CD38-specifi
132 ee survival in patients with newly diagnosed multiple myeloma compared with observation, but did not
136 h aging and obesity, two key risk factors in multiple myeloma disease prevalence, suggesting that BMA
137 aged 18 years and older with newly diagnosed multiple myeloma, Eastern Cooperative Oncology Group per
138 e and timing of mutational processes shaping multiple myeloma evolution in a large cohort of 89 whole
142 and the USA, in which eligible patients with multiple myeloma had received 3 or more previous lines o
143 r older and had symptomatic or non-secretory multiple myeloma, had completed their assigned induction
144 ymptomatic or non-secretory, newly diagnosed multiple myeloma, had completed their assigned induction
145 years or older, had relapsed and refractory multiple myeloma, had received two or more previous line
146 had advanced or metastatic solid tumours or multiple myeloma harbouring RAS-RAF-MEK pathway mutation
147 this drug in patients with solid tumours and multiple myeloma harbouring RAS-RAF-MEK pathway mutation
152 acute lymphoblastic leukemia, lymphomas, and multiple myeloma have led to global implementation of th
155 regimen in the treatment of newly diagnosed multiple myeloma in patients who were not being consider
157 n of Golgi homeostasis induces cell death of multiple myeloma in vitro and in vivo, offering a therap
158 treatment for patients with newly diagnosed multiple myeloma includes combination therapies for pati
159 observation in patients with newly diagnosed multiple myeloma, including cytogenetic risk and transpl
160 e could aid decision making in patients with multiple myeloma ineligible for stem-cell transplantatio
161 s daratumumab for treatment of patients with multiple myeloma involves a lengthy infusion that affect
169 targeting in specific leukemia subtypes and multiple myeloma, linked several polycomb group proteins
170 , as well as those arising in the context of multiple myeloma, may assume a state of dormancy, remain
172 Dramatic overexpression of NSD2 in t(4;14) multiple myeloma (MM) and an activating mutation of NSD2
174 s well as multi-cell computational models of multiple myeloma (MM) and DC were validated using the ob
175 nt consolidation treatment for patients with multiple myeloma (MM) and is thought to prolong the dise
177 ome (MDS) is significantly increased in both multiple myeloma (MM) and monoclonal gammopathy of undet
193 antagonist venetoclax is highly effective in multiple myeloma (MM) patients exhibiting the 11;14 tran
194 ed response rates as well as the survival of multiple myeloma (MM) patients over the past decade and
196 toid dendritic cells (pDCs) in patients with multiple myeloma (MM) promote tumor growth, survival, dr
198 ell transplantation (sASCT) in patients with multiple myeloma (MM) relapsing after a prior autologous
199 c myeloma antigens that can be targeted, and multiple myeloma (MM) remains an incurable disease.
200 l therapeutic advances over the past decade, multiple myeloma (MM) remains largely incurable, indicat
201 y tumors, but the clinical meaning of MRD in multiple myeloma (MM) remains uncertain, particularly wh
203 pathy of undetermined significance (MGUS) to multiple myeloma (MM) such as c-MYC have downstream effe
204 s with robust activity against heterogeneous multiple myeloma (MM) that is resistant to conventional
205 ma cell dyscrasia that consistently precedes multiple myeloma (MM) with a 1% risk of progression per
206 le myeloma (SMM) is a precursor condition of multiple myeloma (MM) with a 10% annual risk of progress
210 immune dysfunction and immunosuppression in multiple myeloma (MM), and various immunotherapeutic app
211 P53 gene are associated with poor outcome in multiple myeloma (MM), but the prognostic value of del17
213 that treatment regimens, including IMiDs in multiple myeloma (MM), lead to aromatase degradation in
214 show that in hematopoietic cells, including multiple myeloma (MM), lymphoma, and leukemia cell lines
217 (MSC), in the maintenance and progression of multiple myeloma (MM), through direct and indirect inter
235 9, with leukaemia; and 3.29, 2.59-4.18, with multiple myeloma), oesophageal (1.96, 1.46-2.64), lung (
241 ficant associations with malignant melanoma, multiple myeloma, oral cancer, and esophageal squamous c
242 on of myeloma cells and BMAds play a role in multiple myeloma pathogenesis and treatment response.
244 asingly established for upfront treatment of multiple myeloma, patients refractory to this drug repre
245 ant-ineligible patients with newly diagnosed multiple myeloma regardless of age, baseline ECOG status
246 In the first randomised study of high-risk multiple myeloma reported to date, the addition of elotu
247 sions from a cohort of 742 patients from the Multiple Myeloma Research Foundation CoMMpass Study.
250 lus dexamethasone in relapsed and refractory multiple myeloma (RRMM), a population with an important
256 y of renal recovery in patients with de novo multiple myeloma, severe acute kidney injury, and myelom
257 intervention with lenalidomide in smoldering multiple myeloma significantly delays progression to sym
259 pen-label, two-arm, phase 2 study done at 58 multiple myeloma specialty centres in eight countries.
263 ng of lymphoproliferative disorders, such as multiple myeloma, that feature increased circulating lev
264 AMG 420 in patients with relapsed/refractory multiple myeloma, the response rate was 70%, including 5
266 1985 ranged from 1.59 (95% CI 1.14-2.21) for multiple myeloma to 4.91 (4.27-5.65) for kidney cancer.
267 ranged from 1.44% (95% CI -0.60 to 3.53) for multiple myeloma to 6.23% (5.32-7.14) for kidney cancer
268 one in patients with relapsed and refractory multiple myeloma to determine the maximum tolerated dose
269 on regimens in patients with newly diagnosed multiple myeloma to result in a substantial survival ben
270 contributed to a substantial advancement in multiple myeloma treatment by improving patient survival
277 volving patients with relapsed or refractory multiple myeloma, we administered bb2121 as a single inf
278 dies in patients with relapsed or refractory multiple myeloma, we observed a high concordance rate wi
279 cohort and 29 patients with solid tumours or multiple myeloma were included in the basket dose-expans
280 ntation-eligible adults with newly diagnosed multiple myeloma were randomly assigned (1:1) to D-VTd o
281 tralia, and Asia with relapsed or refractory multiple myeloma were randomly assigned 2:1 to carfilzom
282 eligible (TIE) patients with newly diagnosed multiple myeloma were randomly assigned to D-Rd (n = 368
283 mmendations were developed for patients with multiple myeloma who are transplantation eligible and th
284 adult patients with relapsed and refractory multiple myeloma who had received at least two previous
285 onvenient treatment option for patients with multiple myeloma who have received one to three previous
287 imen in patients with relapsed or refractory multiple myeloma who previously received lenalidomide.
290 y assigned 737 patients with newly diagnosed multiple myeloma who were ineligible for autologous stem
291 ll survival in patients with newly diagnosed multiple myeloma who were ineligible for stem-cell trans
292 trials done in patients with newly diagnosed multiple myeloma who were ineligible for stem-cell trans
293 aged 18 years or older with newly diagnosed multiple myeloma who were ineligible for, or did not int
294 in patients with solid tumors, lymphomas, or multiple myeloma whose tumors harbored a BRAF(V600) muta
295 aged >=18 years) with relapsed or refractory multiple myeloma with disease progression after three or
297 ent a therapeutic approach for patients with multiple myeloma with poor prognosis and advanced diseas
299 oved efficacious in RPMI8226 and MM.1S human multiple myeloma xenograft mouse models and has been eva