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1 tal cancer, one melanoma, and seven multiple myeloma).
2 tandard therapy for newly diagnosed multiple myeloma.
3 atients with relapsed or refractory multiple myeloma.
4 shown potential in the treatment of multiple myeloma.
5 tentially explaining their high frequency in myeloma.
6 erapeutic approach for treatment of multiple myeloma.
7 in patients with previously treated multiple myeloma.
8 cytic lymphoma and in 2 patients to multiple myeloma.
9 r other systemic characteristics of multiple myeloma.
10 eting as a promising therapeutic strategy in myeloma.
11 n patients with heavily pre-treated multiple myeloma.
12 ation-eligible and -ineligible patients with myeloma.
13 sma cell dyscrasia and precursor to multiple myeloma.
14 cer of the pancreas and uterus, and multiple myeloma.
15 of undetermined significance and smoldering myeloma.
16 also demonstrated in patients with multiple myeloma.
17 t in more than 10% of patients with multiple myeloma.
18 gible patients with newly diagnosed multiple myeloma.
19 termediate- or high-risk smoldering multiple myeloma.
20 nd is approved for the treatment of multiple myeloma.
21 oration found an indolent IgG-kappa multiple myeloma.
22 d) in patients with newly diagnosed multiple myeloma.
23 nsplant-ineligible, newly diagnosed multiple myeloma.
24 ient-specific disease signatures in multiple myeloma.
25 changes detected at the time of diagnosis of myeloma.
26 ke was visualized at PET in sites of osseous myeloma.
27 tained from patients with high-risk multiple myeloma.
28 ld delay progression to symptomatic multiple myeloma.
29 c cancer, lymphocytic leukemia, and multiple myeloma.
30 atients with relapsed or refractory multiple myeloma.
31 agnosis and treatment monitoring of multiple myeloma.
32 e spliceosome as a specific vulnerability in myeloma.
33 ns in patients with newly diagnosed multiple myeloma.
34 relapsed or relapsed and refractory multiple myeloma.
35 tive and widely used treatments for multiple myeloma.
36 r the pathogenesis and treatment of multiple myeloma.
37 giogenic and mitogenic cytokines in multiple myeloma.
38 has potential for the treatment of multiple myeloma.
39 signature genes than patients with multiple myeloma.
40 gible patients with newly diagnosed multiple myeloma.
41 or auto-HCT in patients with newly diagnosed myeloma.
42 overall survival for patients with multiple myeloma.
43 leading to bortezomib resistance in multiple myeloma.
44 cancers such as B-ALL, lymphoma and multiple myeloma.
45 of bone formation is a hallmark of multiple myeloma.
46 a preclinical model of disseminated multiple myeloma.
47 atients with relapsed or refractory multiple myeloma.
48 mab, for immunologic PET imaging of multiple myeloma.
49 n patients with relapsed/refractory multiple myeloma.
50 atients with relapsed or refractory multiple myeloma.
51 atients with relapsed or refractory multiple myeloma.
52 ms such as non-Hodgkin lymphoma and multiple myeloma.
53 ent standard of care for smoldering multiple myeloma.
54 AT was restored after treatment for multiple myeloma.
55 atients with relapsed or refractory multiple myeloma.
56 ients with refractory cancers, lymphomas, or myelomas.
57 8% lower risk), kidney (11%-17% lower risk), myeloma (14%-19% lower risk), liver (18%-27% lower risk)
60 drawn attention in the treatment of multiple myeloma, a malignant hematologic disorder that can produ
61 whole-body MRI for directing patient care in myeloma, a multidisciplinary, international, and expert
62 ad confirmed relapsed or refractory multiple myeloma according to International Myeloma Working Group
63 confirmed diagnosis of symptomatic multiple myeloma according to International Myeloma Working Group
64 tients with relapsed and refractory multiple myeloma achieved an overall response with a combination
65 Single-agent belantamab mafodotin shows anti-myeloma activity with a manageable safety profile in pat
66 hematologic malignancies (lymphoma, multiple myeloma, acute myeloid leukemia, and myelodysplastic syn
67 patients are able to recognize and eliminate myeloma, although this is subverted in the majority of p
68 r older with relapsed or refractory multiple myeloma, an Eastern Cooperative Oncology Group performan
70 oietic stem cell transplantation in multiple myeloma and acute myeloid leukemia patients indicate tha
72 teria were the absence of high-risk multiple myeloma and an Eastern Cooperative Oncology Group perfor
73 ifth-line therapy for patients with multiple myeloma and as a monotherapy for patients with relapsed
74 ome inhibition for the treatment of multiple myeloma and B-cell lymphomas has made the ubiquitin path
76 framework to study the etiology of multiple myeloma and explore strategies for prevention and early
78 ferent preclinical murine models of multiple myeloma and in vitro using myeloma cell-adipocyte cocult
79 The evolution and progression of multiple myeloma and its precursors over time is poorly understoo
81 ged >=18 years) with a diagnosis of multiple myeloma and measurable disease, an Eastern Cooperative O
84 atients with relapsed or refractory multiple myeloma and was associated with a favourable benefit-ris
85 clusion if they had newly diagnosed multiple myeloma and were ineligible for high-dose chemotherapy w
87 d intermediate-risk newly diagnosed multiple myeloma, and is a suitable treatment backbone for the de
88 nts aged 18 years or older, who had multiple myeloma, and who had previously been treated with one to
89 e are currently a limited number of specific myeloma antigens that can be targeted, and multiple myel
90 relapsed or relapsed and refractory multiple myeloma (as per International Myeloma Working Group 2014
91 Although treatment of bone metastases and myeloma bone disease is rarely curative, disease control
93 rlein and colleagues demonstrate in multiple myeloma, bone marrow stromal cells transfer mitochondria
94 al clinical studies of melflufen in multiple myeloma, both in combination with dexamethasone as well
95 ntigen (BCMA) have activity against multiple myeloma, but improvements in anti-BCMA CARs are needed.
96 38 antibody, is approved in the treatment of myeloma, but its efficacy and safety in light-chain (AL)
97 improved outcomes for patients with multiple myeloma, but patients with high-risk multiple myeloma ha
100 omib-based regimens in patients with initial myeloma cast nephropathy (CN) and acute kidney injury (A
103 urvival and subsequent expansion of a single myeloma cell following treatment with high-dose melphala
104 eloma revealed significant loss of BMAT with myeloma cell infiltration of the marrow, whereas BMAT wa
108 system plays a nonredundant role in multiple myeloma cell survival and disease progression, and indic
109 rine FGF/FGFR axis is essential for multiple myeloma cell survival and progression by protecting mult
112 iprocal interactions and cross-regulation of myeloma cells and BMAds play a role in multiple myeloma
114 e confirmed on bortezomib-resistant multiple myeloma cells as well as on bone marrow-derived primary
115 , heat shock may also be especially toxic to myeloma cells by causing protein unfolding, increasing f
116 red the growth and dissemination of multiple myeloma cells by inducing mitochondrial oxidative stress
117 ng various cell surface antigens on multiple myeloma cells for the selective delivery of siRNA target
118 l as on bone marrow-derived primary multiple myeloma cells from newly diagnosed and relapsed/refracto
119 vival and progression by protecting multiple myeloma cells from oxidative stress-induced apoptosis.
120 bidirectional interactions between BMAds and myeloma cells have significant implications for the path
123 ke 13 nonmyeloma cell lines, even though the myeloma cells induced heat-shock proteins and increased
128 vealed that the alpha(4) integrin subunit on myeloma cells stimulated vascular cell adhesion molecule
131 arrow stromal cells transfer mitochondria to myeloma cells to increase cellular respiration, resultin
133 on, highlighting the sensitivity of multiple myeloma cells to the accumulation of protein aggregates.
134 raft model using CD38-positive OPM2 multiple myeloma cells was used to evaluate CD38-specificity of (
143 high-risk disease, renal disease, suboptimal myeloma control (active or progressive disease), and 1 o
144 with specific expertise in whole-body MRI in myeloma convened to discuss the technical performance st
147 Evaluation of CNV Radar in a public multiple myeloma dataset demonstrated that CNV Radar was able to
149 nd obesity, two key risk factors in multiple myeloma disease prevalence, suggesting that BMAds may in
150 apy as a result of the moderate graft-versus-myeloma effect of allogeneic stem cell transplantation.
151 ing of mutational processes shaping multiple myeloma evolution in a large cohort of 89 whole genomes
155 SA, in which eligible patients with multiple myeloma had received 3 or more previous lines of therapy
156 gical malignancies (leukaemia, lymphoma, and myeloma) had a more severe COVID-19 trajectory compared
157 older, had relapsed and refractory multiple myeloma, had received two or more previous lines of ther
162 Recent advances in the treatment of multiple myeloma have increased the need for accurate diagnosis o
163 phoblastic leukemia, lymphomas, and multiple myeloma have led to global implementation of these novel
168 in the treatment of newly diagnosed multiple myeloma in patients who were not being considered for im
170 i homeostasis induces cell death of multiple myeloma in vitro and in vivo, offering a therapeutic str
171 t for patients with newly diagnosed multiple myeloma includes combination therapies for patients who
172 umab for treatment of patients with multiple myeloma involves a lengthy infusion that affects quality
178 prevention recommendations and compared with Myeloma IX, more patients received thromboprophylaxis (8
182 er a shift from 37 to 43 degrees C, all four myeloma lines studied underwent extensive apoptosis in 4
183 as those arising in the context of multiple myeloma, may assume a state of dormancy, remaining quies
186 Longer survival in patients with multiple myeloma (MM) after treatment with novel agents (NA) such
187 c overexpression of NSD2 in t(4;14) multiple myeloma (MM) and an activating mutation of NSD2 discover
189 is significantly increased in both multiple myeloma (MM) and monoclonal gammopathy of undetermined s
201 t venetoclax is highly effective in multiple myeloma (MM) patients exhibiting the 11;14 translocation
203 ritic cells (pDCs) in patients with multiple myeloma (MM) promote tumor growth, survival, drug resist
204 plantation (sASCT) in patients with multiple myeloma (MM) relapsing after a prior autologous stem-cel
206 utic advances over the past decade, multiple myeloma (MM) remains largely incurable, indicating a nee
207 but the clinical meaning of MRD in multiple myeloma (MM) remains uncertain, particularly when assess
208 undetermined significance (MGUS) to multiple myeloma (MM) such as c-MYC have downstream effects on in
209 bust activity against heterogeneous multiple myeloma (MM) that is resistant to conventional CAR-T cel
210 a (SMM) is a precursor condition of multiple myeloma (MM) with a 10% annual risk of progression.
213 ysfunction and immunosuppression in multiple myeloma (MM), and various immunotherapeutic approaches h
214 atment regimens, including IMiDs in multiple myeloma (MM), lead to aromatase degradation in human meg
216 Based on outcomes of daratumumab in multiple myeloma (MM), the phase 3 ANDROMEDA study (NCT03201965)
224 ated bone lining cell subtypes from a murine myeloma model, we find that bone morphogenetic protein (
225 ed bone formation is a direct consequence of myeloma-MSC contact that promotes the differentiation of
228 gnosed in 4 of 33 patients (12%) (smoldering myeloma, n = 2; chronic lymphoid leukemia, n = 1; and re
232 ht chain cast nephropathy (LCCN) in multiple myeloma often leads to severe and poorly reversible acut
233 ticipants were excluded if they had multiple myeloma or any other B cell lymphoproliferative disorder
237 sociations with malignant melanoma, multiple myeloma, oral cancer, and esophageal squamous cell carci
239 kinase (MAPK) signaling are found in half of myeloma patients and contribute to proteasome inhibitor
241 n the BD group and 4 in the C-BD group) from myeloma progression and 3 (0 in the BD group and 3 in th
242 gible patients with newly diagnosed multiple myeloma regardless of age, baseline ECOG status, or dept
243 first randomised study of high-risk multiple myeloma reported to date, the addition of elotuzumab to
246 inical Excellence in the United Kingdom, the Myeloma Response Assessment and Diagnosis System (or MY-
247 marrow biopsies from patients with multiple myeloma revealed significant loss of BMAT with myeloma c
248 ant inhibition of proliferation of the human myeloma RPMI8226 cell line was observed after 3 d of inc
249 atients with relapsed or refractory multiple myeloma (RRMM) have limited treatment options and poor s
250 ethasone in relapsed and refractory multiple myeloma (RRMM), a population with an important unmet med
254 ion with lenalidomide in smoldering multiple myeloma significantly delays progression to symptomatic
256 ll disorders, collected by the International Myeloma Society to understand the initial challenges fac
260 Moreover, they argue these mutations promote myeloma survival by reducing cellular stress, thereby di
262 n patients with relapsed/refractory multiple myeloma, the response rate was 70%, including 50% MRD-ne
265 tients with relapsed and refractory multiple myeloma to determine the maximum tolerated dose of melfl
266 ns in patients with newly diagnosed multiple myeloma to result in a substantial survival benefit.
267 ition of prophylactic levofloxacin to active myeloma treatment during the first 12 weeks of therapy s
272 udy was to describe the genomic landscape of myeloma using deep whole-genome sequencing (WGS) and dev
275 atients with relapsed or refractory multiple myeloma, we observed a high concordance rate with FISH f
276 d 29 patients with solid tumours or multiple myeloma were included in the basket dose-expansion cohor
277 ligible adults with newly diagnosed multiple myeloma were randomly assigned (1:1) to D-VTd or VTd.
278 nd Asia with relapsed or refractory multiple myeloma were randomly assigned 2:1 to carfilzomib, dexam
279 (TIE) patients with newly diagnosed multiple myeloma were randomly assigned to D-Rd (n = 368) or Rd (
280 to evaluate direct spliceosome inhibition in myeloma, which synergizes with carfilzomib and shows pot
281 tients with relapsed and refractory multiple myeloma who had received at least two previous lines of
282 treatment option for patients with multiple myeloma who have received one to three previous lines of
283 al in patients with newly diagnosed multiple myeloma who were ineligible for stem-cell transplantatio
284 years or older with newly diagnosed multiple myeloma who were ineligible for, or did not intend to ha
285 ts with solid tumors, lymphomas, or multiple myeloma whose tumors harbored a BRAF(V600) mutation.
287 years) with relapsed or refractory multiple myeloma with disease progression after three or more lin
288 rapeutic approach for patients with multiple myeloma with poor prognosis and advanced disease stage.
289 XI trial protocol incorporated International Myeloma Working Group (IMWG) thrombosis prevention recom
291 ctory multiple myeloma (as per International Myeloma Working Group 2014 criteria), who had received o
292 Following guidance from the International Myeloma Working Group and the National Institute for Cli
293 multiple myeloma according to International Myeloma Working Group criteria who had achieved at least
294 multiple myeloma according to International Myeloma Working Group criteria; received at least three
296 cacious in RPMI8226 and MM.1S human multiple myeloma xenograft mouse models and has been evaluated as
297 outcome data from Myeloma IX (n = 1936) and Myeloma XI (n = 4358) phase 3 randomized controlled tria