ライフサイエンスコーパス: MIBG

1 MIBG imaging was significantly more sensitive than FDG-P

2 MIBG scan is significantly more sensitive for individual

3 MIBG scans showed no BM disease in 15 of 38 patients wit

4 MIBG scores >/= 3 following induction therapy identifies

5 to patient/body region was 80%/65% for 123I-MIBG and 88%/70% for [18F]FDA-PET.

6 s pretreatment (80%/65%) sensitivity of 123I-MIBG scintigraphy.

7 False-negative results on 123I-MIBG scintigraphy and/or [18F]FDA-PET were not predicted

8 of regions that were false negative on 123I-MIBG scintigraphy or [18F]FDA-PET were detected by [18F]

9 131I-MIBG with myeloablative chemotherapy is feasible and eff

10 r, currently used methods of estimating 131I-MIBG uptake in vivo may be too inaccurate to properly mo

11 ration of 131I-metaiodobenzylguanidine (131I-MIBG) continues to be a promising treatment for neurobla

12 ter iodine-131-metaiodobenzylguanidine (131I-MIBG) treatment of patients with resistant neuroblastoma

13 e initial dose level using 12 mCi/kg of 131I-MIBG and reduced chemotherapy, one in six patients had d

14 in vivo localization and measurement of 131I-MIBG uptake in tumors.

15 n = 148) were treated with 18 mCi/kg of 131I-MIBG.

16 imilar before and after chemotherapy or 131I-MIBG treatment, except for a trend toward lower post- (6

17 mal GFR (> or = 100 mL/min/1.73 m2) was 131I-MIBG 12 mCi/kg, carboplatin 1,500 mg/m2, etoposide 1,200

18 te and low nonhematologic toxicity with 131I-MIBG suggest incorporation of this agent into initial mu

19 adionuclide studies consisting of PET-CT and MIBG scintigraphy.

20 up and further characterized with PET-CT and MIBG scintigraphy.

21 d pressure monitoring, echocardiography, and MIBG imaging.

22 esions identified on concomitant FDG-PET and MIBG scans and gave scans a semiquantitative score.

23 ase responses makes extensive BM testing and MIBG scintigraphy prerequisites for accurate determinati

24 cant difference in light units expressed as (MIBG - MIBI)/maximal MIBG value between laser channels a

25 rdiac sympathetic denervation as assessed by MIBG imaging is a useful prognostic marker in transthyre

26 or patients with neuroblastoma detectable by MIBG or marrow analysis.

27 ocardial sympathetic denervation detected by MIBG imaging in transthyretin familial amyloid polyneuro

28 The scintigraphic response was evaluated by MIBG and bone scans using a semi-quantitative scoring sy

29 Patients with disease evaluable only by MIBG and/or BM histology had a 21.7% CR rate to hu14.8-I

30 t always correlate with complete response by MIBG uptake.

31 as to correlate early response to therapy by MIBG scan, using a semiquantitative scoring method, with

32 han (11)C-HED and 12 times slower than (11)C-MIBG.

33 Nonradioactive carrier MIBG molecules inhibit uptake of (131)I-MIBG, theoretica

34 tial exposure to standard-dose chemotherapy, MIBG scintigraphy merely confirms the findings of other

35 ncordance of positive lesions on concomitant MIBG and FDG-PET scans was 39.6% when examining the 139

36 The estimated MIBG distribution volumes (V(d)) for transduced Jurkat,

37 ucose-positron emission tomography scans for MIBG-nonavid disease, replace technetium-99m diphosphona

38 Eligible patients had MIBG-positive lesions and tumor-free, cryopreserved hema

39 Mean light units for the regions with high MIBG relative to MIBI were significantly higher than the

40 ients injected with (68)Ga-DOTATOC or (123)I MIBG emitted an average EDR-1m roughly half that of pati

41 (123) I-FP-CIT SPECT and (123) I-MIBG myocardial scintigraphy have similar sensitivity fo

42 cts of diabetes and heart disease on (123) I-MIBG myocardial scintigraphy results might have been ove

43 s underwent (123) I-FP-CIT SPECT and (123) I-MIBG myocardial scintigraphy within a few weeks of clini

44 B were respectively 93% and 100% for (123) I-MIBG myocardial scintigraphy, and 90% and 76% for (123)

45 omitant parkinsonism) who had normal (123) I-MIBG myocardial uptake.

46 pposed to potentially interfere with (123) I-MIBG uptake.

47 y (P < 0.05) for (201)Tl (2.04-fold), (123)I-MIBG (3.25-fold), and (3)H-l-methionine (3.11-fold).

48 g (99m)Tc-tetrofosmin (26 +/- 6 MBq), (123)I-MIBG (54 +/- 14 MBq), and a CZT camera.

49 exposure, (18)F-FDG (one occasion) or (123)I-MIBG (other occasion) was administered.

50 ish the optimal time interval between (123)I-MIBG administration and subsequent SPECT/CT acquisition

51 SPECT/CT scans acquired at 4 h after (123)I-MIBG administration and the SPECT/CT scans acquired at 2

52 SPECT/CT was performed at 24 h after (123)I-MIBG administration, the magnitude of BAT activity measu

53 SPECT/CT scans acquired at 24 h after (123)I-MIBG administration.

54 A total of 113 paired (123)I-MIBG and (18)F-FDG PET scans in 60 patients with neurobl

55 (123)I-MIBG and (18)F-FDG showed equal numbers of lesions in 1

56 (123)I-MIBG and (18)F-FDG were equal in 2 of 15 scans, and 4 of

57 (123)I-MIBG and (18)F-FDG were equivalent or complementary in 1

58 ts with tumors that weakly accumulate (123)I-MIBG and at major decision points during therapy (i.e.,

59 )F-FDG and semiquantitative uptake of (123)I-MIBG at 24 h after administration (r = 0.64, P = 0.04).

60 )F-FDG and semiquantitative uptake of (123)I-MIBG at 4 h after administration.

61 (123)I-MIBG cardiac washout was lower during carvedilol than me

62 In contrast, (18)F-LMI1195 and (123)I-MIBG demonstrated stable storage at the nerve terminal w

63 euroblastoma (15 scans, 10 patients), (123)I-MIBG depicted more extensive primary neuroblastoma or lo

64 euroblastoma (85 scans, 40 patients), (123)I-MIBG depicted more neuroblastoma sites in 44 of 85 scans

65 sulted as an independent predictor of (123)I-MIBG early and late heart:mediastinum ratio and single-p

66 EAT thickness correlated with (123)I-MIBG early and late heart:mediastinum ratio and single-p

67 s on cardiac sympathetic denervation ((123)I-MIBG early and late heart:mediastinum ratio and single-p

68 I-MIBG small-animal PET compared with (123)I-MIBG gamma-camera/SPECT.

69 Although (123)I-MIBG has been in clinical use for the imaging of pheochr

70 raphic and clinical variables and the (123)I-MIBG heart-to-mediastinum ratio (H/M).

71 the independent predictive ability of (123)I-MIBG imaging for mortality outcomes.

72 (123)I-MIBG imaging has several limitations that can be overcom

73 (123)I-MIBG imaging is a mainstay in the evaluation of neurobla

74 2%-88% and specificity of 82%-84% for (123)I-MIBG imaging used in the diagnostic assessment of primar

75 on of (18)F-LMI1195 was compared with (123)I-MIBG in MENX mut/mut rats (n = 6) and correlated with hi

76 -LMI1195, (11)C-hydroxyephedrine, and (123)I-MIBG in rabbit hearts.

77 To clarify the normal kinetics of (123)I-MIBG in vivo over time, we designed an experimental prot

78 nderwent planar acquisition 4 h after (123)I-MIBG injection (191 +/- 41 [mean +/- SD] MBq).

79 G SPECT/CT, when performed 24 h after (123)I-MIBG injection, as a method to visualize and quantify sy

80 /CT was performed at 4 and 24 h after (123)I-MIBG injection.

81 (123)I-MIBG is overall superior in the evaluation of stage 4 ne

82 stage 1 and 2 neuroblastoma, although (123)I-MIBG may be needed to exclude higher-stage disease.

83 s sympathetic activity as measured by (123)I-MIBG myocardial washout.

84 se Criteria or (for MP) by changes in (123)I-MIBG or PET scans.

85 nificant additive predictive value on (123)I-MIBG planar and single-photon emission computed tomograp

86 disease present; 49, disease absent), (123)I-MIBG planar scintigraphy had a sensitivity and specifici

87 (123)I-MIBG scan is essential for valid estimation of the durat

88 (123)I-MIBG scan was the most reliable study for revealing unsu

89 Among asymptomatic patients, (123)I-MIBG scan was the sole positive study indicating relapse

90 Patients whose monitoring included (123)I-MIBG scan were significantly less likely than patients m

91 Without monitoring that includes (123)I-MIBG scan, caution should be used when comparing RFS bet

92 efractory VT underwent 15-min and 4-h (123)I-MIBG scans before and 6 mo after the ablation procedure.

93 A retrospective analysis of (123)I-MIBG scans obtained from patients who had been prospecti

94 (123)I-MIBG scans were evaluated at 2 time points, diagnosis (n

95 Among the 18 tumors with concomitant (123)I-MIBG scans, 4 tumors with viable cells were (123)I-MIBG-

96 (123)I-MIBG scans, or [(18)F]fluorodeoxyglucose-positron emissi

97 If (18)F-DA PET is not available, (123)I-MIBG scintigraphy (for nonmetastatic or adrenal PHEO) an

98 emonstrated a higher sensitivity than (123)I-MIBG scintigraphy (n = 18; P = 0.0455) or (18)F-FDG PET

99 atients and might be complementary to (123)I-MIBG scintigraphy and (18)F-FDG PET.

100 ve confirmation of the performance of (123)I-MIBG scintigraphy for the evaluation of patients with kn

101 EO, because it is more sensitive than (123)I-MIBG scintigraphy or SRS.

102 was 90.2% for (18)F-DA PET, 76.0% for (123)I-MIBG scintigraphy, and 22.0% for SRS.

103 was 75.4% for (18)F-DA PET, 63.4% for (123)I-MIBG scintigraphy, and 64.0% for SRS.

104 ar medicine modalities: (18)F-DA PET, (123)I-MIBG scintigraphy, or SRS.

105 (123)I-MIBG SPECT has been shown to be complementary to planar

106 Moreover, (123)I-MIBG SPECT has been used in numerous studies to document

107 This review examines recent trends in (123)I-MIBG SPECT imaging and evidence that provides the basis

108 s superior quantitative capabilities, (123)I-MIBG SPECT is, for the foreseeable future, the only wide

109 erity of innervation abnormalities in (123)I-MIBG SPECT, programs and protocols specifically for (123

110 We aimed to determine whether (123)I-MIBG SPECT/CT and (18)F-FDG PET/CT identify the same ana

111 de SPECT/CT studies and 186 MBq in 10 (123)I-MIBG SPECT/CT studies.

112 Moreover, when (123)I-MIBG SPECT/CT was performed at 24 h after (123)I-MIBG ad

113 (123)I-MIBG SPECT/CT, as a marker of sympathetic activity, and

114 ically influenced but also identifies (123)I-MIBG SPECT/CT, when performed 24 h after (123)I-MIBG inj

115 Most cardiac (123)I-MIBG studies have relied on measurements from anterior p

116 diac innervation has been observed in (123)I-MIBG studies of multiple-system atrophy (MSA) and progre

117 3D dynamic analysis of (123)I-MIBG suggests that myocardial peak uptake is reached mor

118 (123)I-MIBG targets cell membrane and vesicular catecholamine t

119 mine chase did not change the cardiac (123)I-MIBG uptake (delayed heart-to-mediastinum ratio, 1.99 +/

120 take of (18)F-LMI1195 correlated with (123)I-MIBG uptake (r = 0.91), histological tumor volume (r = 0

121 glands by evaluating semiquantitative (123)I-MIBG uptake and to examine genotype-specific differences

122 All subjects who showed (123)I-MIBG uptake in BAT also showed (18)F-FDG uptake in BAT.

123 Liver-normalized semiquantitative (123)I-MIBG uptake may be helpful to distinguish between pheoch

124 (123)I-MIBG uptake significantly correlated with maximum tumor

125 ermination of the late HMR of cardiac (123)I-MIBG uptake using dual-isotope ((123)I and (99m)Tc) acqu

126 observed in 8 of 10 subjects, whereas (123)I-MIBG uptake was observed in 7 of 10 subjects in both the

127 tistically significant differences in (123)I-MIBG uptake were found across PPGLs of different genotyp

128 (123)I-MIBG uptake, however, did not correlate with either NET

129 do not translate into differences in (123)I-MIBG uptake.

130 The myocardial MSI of (123)I-MIBG was reached within 5.57 +/- 4.23 min (range, 2-12 m

131 contemporaneous images obtained using (123)I-MIBG were also reviewed for the presence of BAT.

132 ch as (123)I-metaiodobenzylguanidine ((123)I-MIBG) and (11)C-(-)-meta-hydroxyephedrine ((11)C-HED) ar

133 with (123)I-metaiodobenzylguanidine ((123)I-MIBG) and somatostatin receptor scintigraphy (SRS) with

134 cs of (123)I-metaiodobenzylguanidine ((123)I-MIBG) are scarce and have always been obtained using pla

135 with (123)I-metaiodobenzylguanidine ((123)I-MIBG) has demonstrated extensive losses of cardiac sympa

136 ce of (123)I-metaiodobenzylguanidine ((123)I-MIBG) imaging in heart failure subjects (median follow-u

137 (123)I-metaiodobenzylguanidine ((123)I-MIBG) imaging is a tool for evaluating one of the fundam

138 (123)I-meta-iodobenzylguanidine ((123)I-MIBG) imaging is currently a mainstay in the evaluation

139 y by (123)I-meta-iodobenzylguanidine ((123)I-MIBG) imaging when either beta-blocker is used.

140 ed by (123)I-metaiodobenzylguanidine ((123)I-MIBG) imaging.

141 r iodine-123-metaiodobenzylguanidine ((123)I-MIBG) scan, urine catecholamines, and bone marrow (BM) h

142 ty of (123)I-metaiodobenzylguanidine ((123)I-MIBG) scintigraphy and (18)F-FDG PET in neuroblastoma.

143 se of (123)I-metaiodobenzylguanidine ((123)I-MIBG) scintigraphy and (18)F-FDG PET, using tumor histol

144 (123)I-metaiodobenzylguanidine ((123)I-MIBG) scintigraphy plays an important role in the diagno

145 ative (123)I-metaiodobenzylguanidine ((123)I-MIBG) scoring method (the Curie score, or CS) was previo

146 R) of (123)I-metaiodobenzylguanidine ((123)I-MIBG) uptake obtained using a multipinhole cadmium-zinc-

147 e and (123)I-metaiodobenzylguanidine ((123)I-MIBG) was examined by PET and planar scintigraphy, respe

148 nalog (123)I-metaiodobenzylguanidine ((123)I-MIBG).

149 ed by (123)I-metaiodobenzylguanidine ((123)I-MIBG).

150 3.39 for (201)TlCl, 9.77 +/- 6.06 for (123)I-MIBG, 37.30 +/- 14.42 for (99m)Tc-MIBI, 5.47 +/- 4.44 fo

151 BAT uptake of (18)F- or (3)H-FDG, (123)I-MIBG, and (3)H-l-methionine was significantly increased

152 eased uptake with (18)F- or (3)H-FDG, (123)I-MIBG, and (3)H-l-methionine, and the immunohistostaining

153 taneously with the bolus injection of (123)I-MIBG, and data were collected every 5 min for the first

154 All patients exhibited (123)I-MIBG-avid, International Neuroblastoma Staging System st

155 cans, 4 tumors with viable cells were (123)I-MIBG-negative but were successfully detected by (18)F-FD

156 nderwent one (18)F-FDG PET/CT and two (123)I-MIBG-SPECT/CT scans within a 2-wk interval.

157 h after (18)F-FDG administration, and (123)I-MIBG-SPECT/CT was performed at 4 and 24 h after (123)I-M

158 PECT 24 h after the administration of (123)I-MIBG.

159 tudied with (18)F-FDG, (18)F-F-DA, or (123)I-MIBG.

160 c innervations in a manner similar to (123)I-MIBG.

161 at can be noninvasively assessed with (123)I-MIBG.

162 at later imaging times; at 73 h after (124)I-MIBG injection, the C6/hNET-IRES-GFP xenograft-to-muscle

163 ts demonstrated several advantages of (124)I-MIBG small-animal PET compared with (123)I-MIBG gamma-ca

164 The planned treatment was (131)I-MIBG (444 or 666 MBq/kg) intravenously on day 1 plus ars

165 The treatment dose of NCA (131)I-MIBG (specific activity, 165 MBq/mug) was adjusted as ne

166 All patients received (131)I-MIBG 12 mCi/kg on day -21, followed by carboplatin (1,50

167 en compared with historical data with (131)I-MIBG alone.

168 published dosimetric organ values for (131)I-MIBG and (90)Y-DOTATOC along with critical organ-dose li

169 Combining (131)I-MIBG and (90)Y-DOTATOC for radiotherapy of neuroendocrin

170 Fourteen patients received (131)I-MIBG and arsenic trioxide, both at maximal dosages; 2 pa

171 sibility of a novel regimen combining (131)I-MIBG and myeloablative chemotherapy with autologous stem

172 Combinations of PJ34 and (131)I-MIBG and of PJ34 and (131)I-MIBG/topotecan were also ass

173 Dose-intensified treatment with (131)I-MIBG at a fixed dose of 11.1 GBq (300 mCi) per cycle is

174 The addition of arsenic trioxide to (131)I-MIBG did not significantly improve response rates when c

175 Cumulative (131)I-MIBG given to achieve the target RMI ranged from 22 to 5

176 the evaluation of neuroblastoma, and (131)I-MIBG has been used for the treatment of relapsed high-ri

177 (131)I-MIBG has essentially been only palliative in paraganglio

178 Treatment with (131)I-MIBG in combination with myeloablative chemotherapy and

179 termine the maximum-tolerated dose of (131)I-MIBG in two consecutive infusions at a 2-week interval,

180 ion of topotecan and PJ34 or PJ34 and (131)I-MIBG induced supraadditive toxicity in both cell lines.

181 The (131)I-MIBG infusion and myeloablative chemotherapy were both w

182 The primary toxicity of (131)I-MIBG is myelosuppression, which might necessitate autolo

183 oblastoma were treated with 18 mCi/kg (131)I-MIBG on a phase I/II protocol.

184 -agent therapy with respect to either (131)I-MIBG or (90)Y-DOTATOC.

185 treatment with 11.1 GBq (300 mCi) of (131)I-MIBG per cycle.

186 atients received a 666 MBq/kg dose of (131)I-MIBG plus a 0.15 mg/kg dose of arsenic trioxide.

187 atients received a 444 MBq/kg dose of (131)I-MIBG plus a 0.15 mg/kg dose of arsenic trioxide; and 3 p

188 (131)I-MIBG plus arsenic trioxide was well tolerated, with an a

189 Administration of HSV1716/NAT and (131)I-MIBG resulted in decreased tumor growth and enhanced sur

190 which was superior to the rates with (131)I-MIBG scan (64%; P = .1), bone scan (36%; P < .001), and

191 ed with one (4.5%) of 22 patients for (131)I-MIBG scan (P = .04) and 0% to 6% of patients for each of

192 ess likely than patients monitored by (131)I-MIBG scan to have an extensive osteomedullary relapse an

193 It is superior to (131)I-MIBG scintigraphy and conventional imaging (CT/MR imagin

194 A combination of CT/MR imaging and (131)I-MIBG scintigraphy detected only 53 of 78 (67.9%) lesions

195 (131)I-MIBG scintigraphy showed only 30 of the 78 lesions and w

196 tive improvements in semiquantitative (131)I-MIBG scores were observed in 6 patients.

197 (123)I/(131)I-MIBG theranostics have been applied in the clinical eval

198 se, and longer time from diagnosis to (131)I-MIBG therapy (P <or=.04).

199 erse event profile similar to that of (131)I-MIBG therapy alone.

200 (131)I-MIBG therapy was administered on days 0 and 14.

201 atotoxicity associated with high-dose (131)I-MIBG therapy, with severe thrombocytopenia an early and

202 Mean absorbed dose of (131)I-MIBG to blood was 0.134 cGy/MBq, well below myeloablativ

203 am treatment enhanced the toxicity of (131)I-MIBG to spheroids and xenografts expressing the noradren

204 pression and the need for AHSCT after (131)I-MIBG treatment.

205 dose per megabecquerel divided by the (131)I-MIBG tumor dose per megabecquerel.

206 0 y old with resistant neuroblastoma, (131)I-MIBG uptake, and cryopreserved hematopoietic stem cells.

207 (131)I-MIBG was administered on day -21, CEM was administered o

208 The NCA (131)I-MIBG was escalated from 444 to 777 MBq/kg (12-21 mCi/kg)

209 (131)I-MIBG was escalated in groups of three to six patients, s

210 A diagnostic dose of NCA (131)I-MIBG was followed by 3 dosimetry scans to assess radiati

211 NCA (131)I-MIBG with autologous peripheral blood stem cell transpla

212 We previously reported that combining (131)I-MIBG with the topoisomerase I inhibitor topotecan induce

213 agent (131)I-metaiodobenzylguanidine ((131)I-MIBG) and tested the combination in a phase II clinical

214 Iodine-131-metaiodobenzylguanidine ((131)I-MIBG) has been shown to be active against refractory neu

215 using (131)I-metaiodobenzylguanidine ((131)I-MIBG) has produced remissions in some neuroblastoma pati

216 Iodine-131-metaiodobenzylguanidine ((131)I-MIBG) provides targeted radiotherapy with more than 30%

217 body (131)I-metaiodobenzylgunanidine ((131)I-MIBG) scintigraphy and conventional imaging (CT/MR imagi

218 Iodine-131-metaiodobenzylguanidine ((131)I-MIBG) selectively targets radiation to catecholamine-pro

219 temic (131)I-metaiodobenzylguanidine ((131)I-MIBG) therapy of neuroendocrine tumors comprises differe

220 n and (131)I-metaiodobenzylguanidine ((131)I-MIBG), a radiopharmaceutical used for the therapy of neu

221 geted radiotherapy using radiolabeled (131)I-MIBG, a strategy that has already shown promise for comb

222 The antitumor efficacy of topotecan, (131)I-MIBG, and (131)I-MIBG/topotecan combination treatment wa

223 rier MIBG molecules inhibit uptake of (131)I-MIBG, theoretically resulting in less tumor radiation an

224 owed dramatic dose intensification of (131)I-MIBG, with minimal toxicity and promising activity.

225 erated dose of no-carrier-added (NCA) (131)I-MIBG, with secondary aims of assessing tumor and organ d

226 ced the capacity for active uptake of (131)I-MIBG.

227 of the maximum tolerated activity of (131)I-MIBG.

228 nd 11 with other tumors) treated with (131)I-MIBG.

229 d radionuclide therapy in the form of (131)I-MIBG.

230 The PJ34 and (131)I-MIBG/topotecan combination treatment induced G(2) arrest

231 ficacy of topotecan, (131)I-MIBG, and (131)I-MIBG/topotecan combination treatment was increased by PA

232 vitro and in vivo, to further enhance (131)I-MIBG/topotecan efficacy.

233 ll scheduled combinations of PJ34 and (131)I-MIBG/topotecan induced supraadditive toxicity and increa

234 multaneous administration of PJ34 and (131)I-MIBG/topotecan significantly delayed the growth of SK-N-

235 and UVW/NAT xenografts, compared with (131)I-MIBG/topotecan therapy.

236 PJ34 and (131)I-MIBG and of PJ34 and (131)I-MIBG/topotecan were also assessed using similar scheduli

237 y, iodine-131-metaiodobenzylguanidine (131)I-MIBG; through November 1999) or iodine-123-metaiodobenzy

238 ography (PET) after i.v. infusion of [(123)I]MIBG or [(124)I]MIBG, respectively.

239 Response was evaluated by [(123)I]MIBG scans, computed tomography/magnetic resonance imagi

240 tro and also selectively accumulated [(123)I]MIBG.

241 ter i.v. infusion of [(123)I]MIBG or [(124)I]MIBG, respectively.

242 Cumulative [(131)I]MIBG administered ranged from 492 to 3,191 mCi.

243 ge 10 to 64 years, were treated with [(131)I]MIBG doses ranging from 492 to 1,160 mCi (median, 12 mCi

244 cryopreserved before treatment with [(131)I]MIBG greater than 12 mCi/kg or with a total dose greater

245 Sixty-nine [(131)I]MIBG infusions were given, which included infusions to 3

246 sponse rates achieved with high-dose [(131)I]MIBG suggest its utility in the management of selected p

247 Differences in MIBG accumulation between cell lines were primarily due

248 (MIBI) and meta-[(123)I]iodobenzylguanidine (MIBG) were performed on 42 patients admitted with SAH to

249 ET) substrates [123I]-m-iodobenzylguanidine (MIBG) and [11C]-m-hydroxyephedrine (HED) are used as mar

250 131I-meta-iodobenzylguanidine (MIBG) was used to assess integrity of the norepinephrine

251 on emission tomography scans if the tumor is MIBG nonavid.

252 ified from the color table on the map as low MIBG relative to MIBI were significantly lower than rema

253 ght units expressed as (MIBG - MIBI)/maximal MIBG value between laser channels and unmarked myocardia

254 was compared with late heart-to-mediastinum MIBG uptake ratio (H/M; either in relation to the estima

255 Metaiodobenzylguanidine (MIBG), specifically taken up in cells of sympathetic ori

256 e-123 or iodine-131 metaiodobenzylguanidine (MIBG) scan, bone scan, computed tomography (and/or magne

257 iodine-131 (131I) -metaiodobenzylguanidine (MIBG), 111In-pentetreotide, and Tc-99m-methylene diphosp

258 enzyl)guanidine), a metaiodobenzylguanidine (MIBG) analog, for the detection of pheochromocytoma in a

259 oradrenaline analog metaiodobenzylguanidine (MIBG).

260 odine-123 ((123)I) -metaiodobenzylguanidine (MIBG) scans or [(18)F]fluorodeoxyglucose-positron emissi

261 administered (131)I-metaiodobenzylguanidine (MIBG) activity to tumor and whole-body dosimetry, tumor

262 (123)I-metaiodobenzylguanidine (MIBG) and (111)In-pentetrotide SPECT have been used for

263 (131)I-Metaiodobenzylguanidine (MIBG) and (90)Y-DOTA-D-Phe1-Tyr3-octreotide (DOTATOC) ha

264 with 37 MBq (125)I-metaiodobenzylguanidine (MIBG) followed in 3 h with 1,110 MBq (99m)Tc-sestamibi;

265 (131)I-metaiodobenzylguanidine (MIBG) is specifically taken up in neuroblastoma, with a

266 ride (TlCl), (123)I-metaiodobenzylguanidine (MIBG), (99m)Tc-sestamibi (MIBI), (18)F- or (3)H-FDG, (3)

267 s (18)F-FDG, (123)I-metaiodobenzylguanidine (MIBG), and (99m)Tc-tetrofosmin have demonstrated uptake

268 ble only by [(123)I]metaiodobenzylguanidine (MIBG) scintigraphy and/or bone marrow (BM) histology (st

269 essed by 123-iodine metaiodobenzylguanidine (MIBG) imaging occurs early in disease progression.

270 ts targeting NET is metaiodobenzylguanidine (MIBG), a guanethidine analog of norepinephrine.

271 - or (124)I-labeled metaiodobenzylguanidine (MIBG) to high levels compared with the wild-type parent

272 not make mandatory, metaiodobenzylguanidine (MIBG) scans.

273 for neuroblastoma: metaiodobenzylguanidine (MIBG) scan for uptake by the norepinephrine transporter

274 radiolabeled probe, metaiodobenzylguanidine (MIBG).

275 or MRI), bone scan, metaiodobenzylguanidine (MIBG) scan, bone marrow tests, and urine catecholamine m

276 such as bone scans, metaiodobenzylguanidine (MIBG) scans, and (111)In-diethylenetriaminepentaacetic a

277 In hibernating myocardium, MIBG deposition was decreased in each layer, with the gr

278 In comparison with patients with normal MIBG uptake, those with evidence of functional denervati

279 er global (n=9) or regional (n=3) absence of MIBG uptake.

280 ntrast, there were no spatial alterations of MIBG deposition in sham-instrumented animals.

281 zylguanidine ((18)F-MFBG) is a PET analog of MIBG that may allow for single-day, high-resolution quan

282 t-free survival and survival from the day of MIBG infusion for all patients at 3 years was 0.31 +/- 0

283 We present the first report on the effect of MIBG scans on the classification of response to dose-int

284 nd slow clearance (half-time, 63 +/- 6 h) of MIBG from transduced xenografts compared with that from

285 an doses were 0.92, 0.82, and 1.2 mGy/MBq of MIBG for the liver, lung, and kidney, respectively.

286 This review focuses on the use of MIBG (which is a false transmitter) and octreotide (whic

287 therapy from diagnosis at MSKCC, the use of MIBG scintigraphy increased the incomplete response numb

288 with versus without osteomedullary uptake on MIBG scintigraphs at diagnosis was seen (35% +/- 11% v 8

289 as observed in patients with a postinduction MIBG score of >/= 3 compared to those with scores of les

290 The use of two reporter probes (MIBG and 2'-deoxy-2'-fluoro-beta-d-arabinofuranosyl-5-io

291 Reduced MIBG relative to regional flow was seen in surrounding t

292 The median relative MIBG scores after two, four, and six cycles were 0.5, 0.

293 nd relative (score divided by initial score) MIBG scores were then correlated with overall pretranspl

294 Semiquantitative MIBG score early in therapy provides valuable prognostic

295 Responses by semiquantitative MIBG score occurred in eight patients, soft tissue respo

296 s became completely negative more often than MIBG scans after treatment.

297 The MIBG image was subtracted from the methoxyisobutylisonit

298 e referral to MSKCC for intensified therapy, MIBG findings changed the response classification of one

299 Similar to MIBG, FDG skeletal uptake was diffusely increased with e

300 d by exposure to hyperglycemia combined with MIBG to improve therapeutic response.