ライフサイエンスコーパス: MGUS

1 MGUS is a premalignant disorder frequently encountered i

2 MGUS is considered an obligate precursor to several lymp

3 MGUS patients frequently mount a humoral and cellular im

4 MGUS patients had an 8.01-fold (5.40-11.43) increased ri

5 MGUS was identified in 694 (3.2 percent) of these person

6 MGUS was present in 100.0% (87.2%-100.0%), 98.3% (90.8%-

7 g multiple myeloma (SMM) or MGUS (11 SMM, 17 MGUS) who had normal karyotype, 11 cases of hyperdiploid

8 n-based data from Sweden, we identified 4458 MGUS patients, 17505 population-based controls, and firs

9 ne mineral density (vBMD) measurements in 50 MGUS patients (20 females, 30 males; mean +/- SEM age, 7

10 omography imaging of the distal radius in 50 MGUS patients and 100 age-, gender-, and body mass index

11 drome (OFD1) had response in 6 of 29 (20.6%) MGUS patients but 0 of 11 newly diagnosed MM patients.

12 ne-hundred eleven relatives of 232 MM and 97 MGUS probands were studied.

13 The SIR for glaucoma was 1.60 after MGUS, 1.76 after WM and 2.18 after AL amyloidosis.

14 ct was significantly increased to 1.80 after MGUS, 1.70 after MM, 1.85 after WM and 2.31 after AL amy

15 or Hodgkin lymphoma was not increased among MGUS relatives.

16 ives of MM (RR, 2.0; 95% CI, 1.4 to 2.8) and MGUS probands (RR, 3.3; 95% CI, 2.1 to 4.8).

17 quent to both MM (SIR = 2.22; 1.74-2.80) and MGUS (SIR = 3.30; 2.76-3.90).

18 Associations between pesticide exposures and MGUS prevalence were assessed by logistic regression mod

19 imately 25 cluster, miR-181a and b in MM and MGUS samples with respect to healthy PCs.

20 black) with a discharge diagnosis of MM and MGUS, respectively.

21 l evaluation, CBC and CRP every 3 months and MGUS as usually recommended.

22 r the increased risk of multiple myeloma and MGUS in blacks is related to socioeconomic status, genet

23 y had prostate cancer, multiple myeloma, and MGUS.

24 re expressed by the majority of myelomas and MGUS tumors and are a potential immune target.

25 As MGUS prevalence is around 3% at 60 years and close to 10

26 tic schema, they are frequently diagnosed as MGUS.

27 for MGUS; the aim of the study was to assess MGUS risk in relation to obesity and race.

28 In the present study, an asymptomatic MGUS stage consistently preceded MM.

29 ways preceded by a premalignant asymptomatic MGUS stage.

30 isk by type of first-degree relative, age at MGUS (above/below 65 years), or sex.

31 vation that a low M-protein concentration at MGUS diagnosis was associated with poorer MM survival ma

32 , low M-protein concentration (<0.5 g/dL) at MGUS diagnosis was associated with poorer MM survival (H

33 f 214 patients with MM, 27% were found to be MGUS-L.

34 Because MGUS is already a genetically complex lesion, applicatio

35 n active multiple myeloma clone and a benign MGUS clone, and thus provides a unique model to assess t

36 no differences in clinical outcomes between MGUS patients and KT controls.

37 ultiple myeloma in patients with light-chain MGUS was 0.3% (0.1-0.8) per 100 person-years.

38 Prevalence of light-chain MGUS was 0.8% (95% CI 0.7-0.9), contributing to an overa

39 Light-chain MGUS was defined as an abnormal free light-chain ratio w

40 30 (23%) of 129 patients with light-chain MGUS were diagnosed with renal disease.

41 renal disorders in patients with light-chain MGUS.

42 light chain and met criteria for light-chain MGUS.

43 corresponding precursor entity, light-chain MGUS.

44 In contrast, MGUS, but not MM, patients generate high-titer anti-MICA

45 Relative to controls, MGUS patients had decreased aBMD at the femoral neck (P

46 Compared with controls, MGUS patients had both significantly higher cortical por

47 e disorders for light-chain and conventional MGUS and assessed incidence of renal disorders in patien

48 g the light-chain equivalent of conventional MGUS and posing a risk of progression to light-chain mul

49 pression that was diagnostic of conventional MGUS.

50 n=22) and patients with stringently defined MGUS/smoldering MM (n=24) and symptomatic MM (n=351) (P<

51 To determine MGUS clone susceptibly to therapy, future studies might

52 Thirty-nine (8.1%) subjects developed MGUS after KT.

53 0-fold (2.3-170) elevated risk of developing MGUS, MM, and LPL/WM, respectively.

54 By electrophoresis, MGUS was detected in 55 (6%) relatives, and immunofixati

55 sed cohort, previously assembled to estimate MGUS prevalence, of 21,463 residents of Olmsted County,

56 n epidemiology and risk factors for familial MGUS and myeloma, the risk of lymphoproliferative disord

57 , represented the only predictive factor for MGUS development.

58 strongest molecular defined risk factors for MGUS, MM, and WM.

59 urrent prognostic and therapeutic models for MGUS and MM.

60 Because treatment is not recommended for MGUS, appropriate therapy is commonly withheld.

61 ranslated into a 2.4-fold increased risk for MGUS in Ranch Hand veterans than comparison veterans aft

62 Risks for MGUS were generally of similar magnitude.

63 9 years) of similar socioeconomic status for MGUS; the aim of the study was to assess MGUS risk in re

64 In conclusion, routine testing for MGUS before transplantation is not prognostic nor a cont

65 study conducted in 2013 to 2014, testing for MGUS in serum specimens collected and stored in 2002 by

66 d CCN1 was associated with a longer time for MGUS/AMM to progress to overt MM.

67 Eighty-four MGUS cases developed a lymphoid disorder, representing a

68 expression is increased on plasma cells from MGUS patients compared with normal donors, whereas MM pa

69 sion and profiled CD138(+) plasma cells from MGUS, SMM, and MM specimens; human myeloma cell lines; a

70 M, 44 with MGUS (24+20), and 16 with MM from MGUS created 2 major cluster branches, one containing 82

71 reened for reactivity with paraproteins from MGUS, MM, and WM patients.

72 way are associated with the progression from MGUS to MM and raise the possibility that anti-MICA mono

73 e mechanisms underlying the progression from MGUS to MM are incompletely understood but include the s

74 The average annual risk of progression from MGUS to multiple myeloma is 0.5% to 1.0%.

75 ylation of the genome at the transition from MGUS to presentation myeloma.

76 uding IgM cases, 0/14), and immunoglobulin G MGUS (0/9) patients as well as healthy donors (0/40; P <

77 of 39 (3.9%) blacks and 21 (2.1%) whites had MGUS.

78 an 50 years (n = 555), 38 were found to have MGUS, yielding a prevalence of 6.8% (95% CI, 5.0%-9.3%).

79 follow-up of individuals diagnosed as having MGUS depending on risk stratification.

80 .7%) had previously been diagnosed as having MGUS.

81 However, studies comparing how MGUS and multiple myeloma plasma cell clones respond to

82 We aimed to identify how MGUS and multiple myeloma plasma cell clones responded t

83 Relatives of patients with IgG/IgA MGUS had a 4.0-fold (1.7-9.2), 2.9-fold (1.7-4.9), and 2

84 gammopathy multiple myeloma with IgG or IgA MGUS clones were subsequently identified from the three

85 k MGUS patients (>/= 1.5 g/dL and/or non-IgG MGUS) were more likely to be optimally followed (81% vs

86 in 97 of 104 (93%) WM and 13 of 24 (54%) IgM MGUS patients and was either absent or rarely expressed

87 P as a widely present mutation in WM and IgM MGUS patients using highly sensitive and specific AS-PCR

88 iation between peripheral neuropathy and IgM MGUS with characteristic clinical, electrophysiology and

89 8q11-18q23] progressively increased from IgM MGUS and smoldering WM vs symptomatic WM (18% vs 20% and

90 notypic profiles for clonal B cells from IgM MGUS, smoldering, and symptomatic WM patients.

91 Real-time AS-PCR identified IgM MGUS patients progressing to WM and showed a high rate o

92 clonal B cells that, albeit benign (ie, IgM MGUS and smoldering WM), already harbor the phenotypic a

93 The finding of this mutation in many IgM MGUS patients suggests that MYD88 L265P may be an early

94 Risk was confined to IgG/IgA, while no IgM MGUS patients developed AML/MDS; patients with monoclona

95 Relatives of IgM MGUS patients had 5.0-fold (1.1-23) increased CLL risk a

96 gammopathy of undetermined significance (IgM MGUS).

97 cells from newly diagnosed patients with IgM MGUS (n = 22), smoldering (n = 16), and symptomatic WM (

98 1q and 4q when patients with WM and with IgM MGUS were both considered affected; nonparametric linkag

99 for AML/MDS following IgG/IgA (but not IgM) MGUS, and the highest risk associated with M-protein con

100 diagnostic tool for patients with WM or IgM-MGUS.

101 gammopathy of undetermined significance (IgM-MGUS), 84 with splenic marginal zone lymphoma (SMZL), an

102 Compared to IgM-MGUS patients with wild-type MYD88, those carrying MYD88

103 During follow-up, 9 patients with IgM-MGUS progressed to WM or to marginal zone lymphoma.

104 100%) patients with WM, 36/77 (47%) with IgM-MGUS, 5/84 (6%) with SMZL, and 3/52 (4%) with B-CLPD.

105 The frequency of Amp1q21 was 0% in MGUS, 45% in SMM, 43% in newly diagnosed MM, and 72% in

106 marks the clonogenic CD138(-) compartment in MGUS.

107 Death in MGUS patients was not associated with progression of the

108 P < .01) were all significantly decreased in MGUS patients, suggestive of impaired bone formation.

109 P < .05) also were significantly elevated in MGUS patients.

110 GE proteins is stronger and more frequent in MGUS compared with myeloma with a predominantly CD45RA(-

111 supports a role for susceptibility genes in MGUS.

112 antigenic targets of spontaneous immunity in MGUS differ from MM.

113 the occurrence of fractures, is increased in MGUS.

114 oma also may be associated with bone loss in MGUS.

115 t evidence of altered bone microstructure in MGUS and suggest that cytokines elevated in osteolytic m

116 plasmocytes from MM patients but neither in MGUS patients nor in healthy individuals, suggesting tha

117 ied in MM subjects and cell lines but not in MGUS subjects or healthy PCs.

118 e confirmed T-cell responses against OFD1 in MGUS and observed down-regulation of GLI1/PTCH1 and p-be

119 ed fracture risk, which has been reported in MGUS patients.

120 ntified, with specific antibody responses in MGUS.

121 explain the increased fracture risk seen in MGUS patients.

122 approaches to enhance immune surveillance in MGUS and to break down immune tolerance in MM.

123 in signal transduction and tumorigenesis in MGUS and MM.

124 Each SNP independently influenced MGUS risk with statistically significant associations (P

125 mong residents of Olmsted County, Minnesota, MGUS was found in 3.2 percent of persons 50 years of age

126 28% of the MM patients, termed MGUS-like MM (MGUS-L MM).

127 rvals (CIs) for the relationship between MM, MGUS, and specific prior medical conditions.

128 ated conditions might act as triggers for MM/MGUS development.

129 Among first-degree relatives of a nationwide MGUS cohort, we found elevated risks of MGUS, MM, LPL/WM

130 MM, but not MGUS, patients harbor circulating sMICA, which triggers

131 Genetic analyses of MGUS cells have provided evidence that it is a genetical

132 and glaucoma and tested the associations of MGUS, MM, WM and AL amyloidosis with subsequent eye dise

133 The cause of MGUS is largely unknown.

134 are few reports about the clinical course of MGUS or risk profile in long-term immunosuppressed patie

135 nt questions that arise during the course of MGUS.

136 olyclonal phase preceding the development of MGUS.

137 At diagnosis of MGUS, the average age was 52 +/- 9.2 years, and 23% of t

138 credited to hematologists, the discovery of MGUS is most often incidental and made by nonhematologis

139 To better define the skeletal effects of MGUS, we performed aBMD and high-resolution peripheral q

140 Age-adjusted prevalence estimates of MGUS were compared with MGUS prevalence in 9469 men from

141 tion, its role in fostering the evolution of MGUS or SMM into MM is yet to be proven.

142 The 2-fold excess of MGUS among blacks compared with whites of similar socioe

143 Although the genetic features of MGUS or SMM cells at baseline may predict disease risk,

144 ty to SOX2 inhibits the clonogenic growth of MGUS cells in vitro.

145 risk factors could improve identification of MGUS patients at high risk for progression.

146 Interactions of MGUS cells with immune cells, bone cells, and others in

147 than MM patients without prior knowledge of MGUS (median survival, 2.1 years), although MM patients

148 Prior knowledge of MGUS among MM patients.

149 Patients with MM with prior knowledge of MGUS had better MM survival, suggesting that earlier tre

150 atients with (vs without) prior knowledge of MGUS had more comorbidities (P < .001).

151 Patients with MM with prior knowledge of MGUS had significantly (HR, 0.86; 95% CI, 0.77-0.96; P <

152 Among MM patients with prior knowledge of MGUS, low M-protein concentration (<0.5 g/dL) at MGUS di

153 nts with vs those without prior knowledge of MGUS.

154 s for improving individualized management of MGUS and SMM patients, as well as the potential for deve

155 Recent advances in mouse modeling of MGUS suggest that the clinical dormancy of the clone may

156 Occurrence of MGUS was not influenced by age and sex.

157 Prevalence and clinical outcomes of MGUS in kidney transplant (KT) recipients have been prev

158 NA damage, contribute to the pathogenesis of MGUS and MM.

159 In summary, the prevalence of MGUS among pesticide applicators was twice that in a pop

160 ay contribute to the increased prevalence of MGUS among relatives of probands with MGUS, MM, and othe

161 determined longitudinally the prevalence of MGUS and characterized patterns of monoclonal immunoglob

162 ry techniques to ascertain the prevalence of MGUS in a large population in a well-defined geographic

163 how that there is an increased prevalence of MGUS in blood relatives of persons with lymphoproliferat

164 The prevalence of MGUS in relatives increased with age (1.9%, 6.9%, 11.6%,

165 The prevalence of MGUS in relatives was compared with population-based rat

166 om Minnesota, the age-adjusted prevalence of MGUS was 1.9-fold (95% CI, 1.3- to 2.7-fold) higher amon

167 The prevalence of MGUS was 5.3 percent among persons 70 years of age or ol

168 he biology and probability of progression of MGUS and SMM.

169 ed risk of MGUS in first-degree relatives of MGUS or MM patients implies shared environment and/or ge

170 red with relatives of controls, relatives of MGUS patients had increased risk of MGUS (relative risk

171 malignancies among first-degree relatives of MGUS patients.

172 tives of MGUS patients had increased risk of MGUS (relative risk [RR] = 2.8; 1.4-5.6), multiple myelo

173 Analyses of populations at increased risk of MGUS also suggest the possible existence of a polyclonal

174 s (n = 58387) with the aim to assess risk of MGUS and lymphoproliferative malignancies among first-de

175 The increased risk of MGUS in first-degree relatives of MGUS or MM patients im

176 etection methods, there was a higher risk of MGUS in relatives (age-adjusted risk ratio [RR], 2.6; 95

177 Risk of MGUS measured by prevalence, odds ratios (ORs), and 95%

178 (95% CI, 1.1- to 5.3-fold) increased risk of MGUS prevalence was observed among users of the chlorina

179 erans have a significantly increased risk of MGUS, supporting an association between Agent Orange exp

180 ependently associated with an excess risk of MGUS.

181 wide MGUS cohort, we found elevated risks of MGUS, MM, LPL/WM, and CLL, supporting a role for germlin

182 DNA expression library to screen the sera of MGUS patients to identify tumor-associated antigens.

183 Studies of MGUS revealed that some samples shared biologic features

184 marrow of MM patients compared with those of MGUS patients and control subjects.

185 dy suggests that routine annual follow-up of MGUS may not be required in low-risk MGUS.

186 gnosing and conducting clinical follow-up of MGUS on MM survival is unclear.

187 f 116 patients, 69% had optimal follow-up of MGUS.

188 To examine the impact of these 7 SNPs on MGUS, we analyzed two case-control series totaling 492 c

189 Emerging evidence from molecular studies on MGUS and SMM, involving cytogenetics, gene-expression pr

190 hieved with anti-multiple myeloma therapy on MGUS (which we defined as M2) and multiple myeloma (M1)

191 ividuals from all backgrounds; however, only MGUS, MM, and WM patients who were HSP90-SUMO1 carriers

192 degree relatives of multiple myeloma (MM) or MGUS patients.

193 ts with smoldering multiple myeloma (SMM) or MGUS (11 SMM, 17 MGUS) who had normal karyotype, 11 case

194 (95% CI 0.7-0.9), contributing to an overall MGUS prevalence of 4.2% (3.9-4.5).

195 The crude prevalence of overall MGUS was 7.1% (34 of 479) in Ranch Hand veterans and 3.1

196 tion of earlier stages, which we term as pre-MGUS Analyses of populations at increased risk of MGUS a

197 phoproliferative disorders and pretransplant MGUS.

198 as NPCs transition to MM, create a high-risk MGUS gene signature, and subgroup International Staging

199 High-risk MGUS patients (>/= 1.5 g/dL and/or non-IgG MGUS) were mo

200 M, which comprised the basis for a high-risk MGUS signature.

201 timal frequency of monitoring in higher-risk MGUS patients.

202 w-up of MGUS may not be required in low-risk MGUS.

203 Secondary MGUS was more common in patients after stem cell transpl

204 ts with MM, 128 (6.6%) developed a secondary MGUS, at a median of 12 months from the diagnosis of MM.

205 erior in MM patients who developed secondary MGUS compared with the rest of the cohort (73 vs 38 mont

206 The median duration of secondary MGUS was 5.9 months.

207 time of onset and the duration of secondary MGUS, as well as failure to resolve spontaneously, had a

208 y, characteristics, and outcome of secondary MGUS.

209 nal gammopathy of undetermined significance (MGUS) (n = 6), and normal donors (n = 6).

210 nal gammopathy of undetermined significance (MGUS) and healthy individuals is presented.

211 nal gammopathy of undetermined significance (MGUS) and multiple myeloma (MM) comprise heterogeneous d

212 nal gammopathy of undetermined significance (MGUS) and multiple myeloma for expression of cancer-test

213 nal gammopathy of undetermined significance (MGUS) and smoldering multiple myeloma (SMM), suggesting

214 nal gammopathy of undetermined significance (MGUS) and smoldering myeloma.

215 nal gammopathy of undetermined significance (MGUS) are at increased fracture risk, and we have previo

216 nal gammopathy of undetermined significance (MGUS) can progress to multiple myeloma (MM).

217 nal gammopathy of undetermined significance (MGUS) has been observed in case reports and in smaller s

218 nal gammopathy of undetermined significance (MGUS) have increased cortical bone porosity and reduced

219 nal gammopathy of undetermined significance (MGUS) is a common disorder of aging and a precursor lesi

220 nal gammopathy of undetermined significance (MGUS) is a premalignant plasma-cell proliferative disord

221 nal gammopathy of undetermined significance (MGUS) is an asymptomatic plasma cell proliferative disor

222 nal gammopathy of undetermined significance (MGUS) is an asymptomatic premalignant plasma cell disord

223 nal gammopathy of undetermined significance (MGUS) is associated with a long-term risk of progression

224 nal gammopathy of undetermined significance (MGUS) is defined by expression of heavy-chain immunoglob

225 nal gammopathy of undetermined significance (MGUS) is increased in first-degree relatives of multiple

226 nal gammopathy of undetermined significance (MGUS) is present in approximately 2% of individuals age

227 nal gammopathy of undetermined significance (MGUS) is the most commonly found monoclonal gammopathy a

228 nal gammopathy of undetermined significance (MGUS) is unknown.

229 nal gammopathy of undetermined significance (MGUS) is, in many ways, a unique hematologic entity.

230 nal gammopathy of undetermined significance (MGUS) or asymptomatic multiple myeloma (AMM).

231 nal gammopathy of undetermined significance (MGUS) or smoldering myeloma (SMM).

232 nal gammopathy of undetermined significance (MGUS) patients diagnosed between 1986 and 2005.

233 nal gammopathy of undetermined significance (MGUS) patients.

234 nal gammopathy of undetermined significance (MGUS) referred to our hospital for acute painless drop o

235 nal gammopathy of undetermined significance (MGUS) remain undetermined.

236 nal gammopathy of undetermined significance (MGUS) represents a precursor lesion to myeloma (MM).

237 nal gammopathy of undetermined significance (MGUS) than with multiple myeloma.

238 nal gammopathy of undetermined significance (MGUS) to lymphoplasmacellular and myeloid malignancies i

239 nal gammopathy of undetermined significance (MGUS) to multiple myeloma (MM) is driven by defects in d

240 nal gammopathy of undetermined significance (MGUS) to multiple myeloma (MM) is thought to be associat

241 nal gammopathy of undetermined significance (MGUS) to multiple myeloma are unclear but may include th

242 nal gammopathy of undetermined significance (MGUS), a precursor to multiple myeloma (MM), is one of t

243 nal gammopathy of undetermined significance (MGUS), a premalignant plasma-cell disorder, among person

244 nal gammopathy of undetermined significance (MGUS), and five cases of prostate cancer in two generati

245 nal gammopathy of undetermined significance (MGUS), asymptomatic myeloma (AMM), and multiple myeloma

246 nal gammopathy of undetermined significance (MGUS), followed up to 30 years (median, 10 years), we es

247 nal gammopathy of undetermined significance (MGUS), have been described.

248 nal gammopathy of undetermined significance (MGUS), multiple myeloma (MM), Waldenstrom macroglobuline

249 l gammopathies of undetermined significance (MGUS), multiple myelomas (MM), and Waldenstrom's macrogl

250 nal gammopathy of undetermined significance (MGUS), which is usually only treated by a form of anti-m

251 nal gammopathy of undetermined significance (MGUS).

252 nal gammopathy of undetermined significance (MGUS).

253 nal gammopathy of undetermined significance (MGUS).

254 nal gammopathy of undetermined significance (MGUS).

255 nal gammopathy of undetermined significance (MGUS).

256 nal gammopathy of undetermined significance (MGUS).

257 nal gammopathy of undetermined significance (MGUS); however, to our knowledge, no studies have uncove

258 nal gammopathy of undetermined significance (MGUS; n = 14), smoldering multiple myeloma (SMM; n = 31)

259 nal gammopathy of undetermined significance (MGUS; n=17), smoldering multiple myeloma (SMM; n=40), an

260 noclonal gammopathy of unknown significance (MGUS) and smoldering multiple myeloma (SMM) are asymptom

261 noclonal gammopathy of unknown significance (MGUS), PBC, and healthy donors.

262 nal gammopathy of undetermined significance [MGUS]).

263 nal gammopathy of undetermined significance [MGUS], presentation myeloma, and plasma cell leukemia).

264 Using similar MGUS detection methods, there was a higher risk of MGUS

265 Despite their larger radial bone size, MGUS patients have significantly increased cortical bone

266 rmal karyotype, 11 cases of hyperdiploid SMM/MGUS were detected.

267 Although some MGUS clones exhibited a complete response, many did not

268 ceptible to therapy are present in only some MGUS plasma cell clones.

269 ed from a population-based prevalence study (MGUS) and the Mayo Clinic (MM).

270 er containing 28% of the MM patients, termed MGUS-like MM (MGUS-L MM).

271 nst multiple myeloma plasma cell clones than MGUS plasma cell clones.

272 produce about four folds more exosomes than MGUS and healthy individuals.

273 We noted that MGUS diagnosis often coincided with diagnoses of senile

274 ture risk, and we have previously shown that MGUS patients have altered trabecular bone microarchitec

275 The MGUS group had a significantly higher prevalence of mono

276 The MGUS-L signature was also seen in plasma cells from 15 o

277 geneity is also established early during the MGUS phase.

278 Cs) accumulate in the bone marrow during the MGUS-to-MM progression.

279 DLI response; 2 of 12 (17%) patients in the MGUS pretreatment control population also had detectable

280 cluster branches, one containing 82% of the MGUS patients and the other containing 28% of the MM pat

281 n AMM patients predicted low risk similar to MGUS.

282 polygenic model of disease susceptibility to MGUS.

283 l failure, anemia, and bone lesions, whereas MGUS and smoldering myeloma are diagnosed based on labor

284 d epigenetic alterations that affect whether MGUS plasma cell clones are responsive to anti-multiple

285 en at Mayo Clinic between 1973 and 2004 with MGUS who subsequently progressed to MM.

286 clustering of 351 patients with MM, 44 with MGUS (24+20), and 16 with MM from MGUS created 2 major c

287 discuss the potential harms associated with MGUS diagnosis, a topic that is rarely, if ever, broache

288 valence estimates of MGUS were compared with MGUS prevalence in 9469 men from Minnesota.

289 of individuals with MGUS is consistent with MGUS being a marker of inherited genetic susceptibility

290 yeloma (MM) in relatives of individuals with MGUS is consistent with MGUS being a marker of inherited

291 lure, and mortality between KT patients with MGUS and a matched cohort of KT recipients without MGUS.

292 ncies among blood-relatives of patients with MGUS and MM, and discusses future directions for researc

293 dividualized risk profiles for patients with MGUS and SMM represents an ongoing challenge that has to

294 he current standard of care of patients with MGUS and SMM, the use of risk models, including flow cyt

295 the frequency and outcomes of patients with MGUS identified pretransplant.

296 ing personalized management of patients with MGUS or smoldering myeloma, as well as the potential for

297 tance of clinical follow-up in patients with MGUS, regardless of risk stratification.

298 r predict progression to MM in patients with MGUS.

299 nce of MGUS among relatives of probands with MGUS, MM, and other blood malignancies.

300 nd a matched cohort of KT recipients without MGUS.