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1 lymph node lesions, 27 liver lesions, and 50 bone lesions).
2 (hypercalcaemia, renal failure, anaemia, and bone lesions).
3 ic MM is a well-demarcated, focal osteolytic bone lesion.
4 d bone colonization and decreased osteolytic bone lesions.
5 lving extramedullary hematopoiesis, skin and bone lesions.
6 y Medical Center Groningen were reviewed for bone lesions.
7 ons exhibit defective osteoclastogenesis and bone lesions.
8 reviewed to identify patients with malignant bone lesions.
9 of tumor cells to the bone marrow and lytic bone lesions.
10 could be used to detect osteoclasts in lytic bone lesions.
11 of bone tumors with no development of lytic bone lesions.
12 teoblastic character of most prostate cancer bone lesions.
13 d were associated with the presence of focal bone lesions.
14 contrast, only 4% of beta3-/- mice developed bone lesions.
15 eloma (MM) is commonly associated with lytic bone lesions.
16 mpared with other forms of therapy for lytic bone lesions.
17 or RANKL, prevented the development of lytic bone lesions.
18 ation, and radiologic evidence of osteolytic bone lesions.
19 logies in 15 specimens, including 10 primary bone lesions.
20 nd inhibition of radiographic progression of bone lesions.
21 e not significantly different from those for bone lesions.
22 nohistochemistry was performed on metastatic bone lesions.
23 tures from other processes such as malignant bone lesions.
24 rum M spikes, bone marrow insufficiency, and bone lesions.
25 vator (CIITA) contributes to myeloma-induced bone lesions.
26 tiorgan secondary metastases that arise from bone lesions.
27 as dramatically upregulated in AR-V7-induced bone lesions.
28 y Medical Center Groningen were reviewed for bone lesions.
29 r the initial assessment of MM-related lytic bone lesions.
30 aracterized by the development of osteolytic bone lesions.
31 ifests with bone marrow tumors causing lytic bone lesions.
32 associated with osteoporosis and metastatic bone lesions.
33 d NOS (not otherwise specified), nonspecific bone lesions.
34 sound diathermy may be associated with focal bone lesions.
35 tricle, leading to disseminated visceral and bone lesions.
36 een osteoclasts and osteoblasts and leads to bone lesions.
37 properties on cancer cells disseminated from bone lesions.
38 cycle by 27% for lymph nodes and by 33% for bone lesions.
39 erozygous mice; none of these mice developed bone lesions.
40 ial advantages over PET/CT for evaluation of bone lesions.
41 T for anatomic delineation and allocation of bone lesions.
42 ntification was reduced by a factor of 4 for bone lesions (10.24% for Dixon PET and 2.68% for ZeDD PE
43 re found for PET/MR than for PET/CT both for bone lesions (12.4% +/- 15.5%) and for regions of normal
44 ate liver lesions, 2 patients with sclerotic bone lesions, 2 patients with breast abnormalities, 1 pa
46 er sensitivity than MRI or (18)F-FDG PET for bone lesions (95.8% vs. 90.7% and 89.3%, respectively).
47 ditions, AR-V7 strongly induced osteoblastic bone lesions, a response not observed with AR-FL overexp
48 of hematopoiesis and formation of osteolytic bone lesions also known as myeloma bone disease (MBD).
50 nt, mimicking progressive disease with "new" bone lesions, although there was an overall treatment re
51 Experience of scintigraphic detection of bone lesion and active bone marrow involvement of multip
52 ith breast cancer who had at least one lytic bone lesion and who were receiving hormonal therapy were
53 (11)C-acetate-avid and (18)F-FDG-avid focal bone lesions and (11)C-acetate general marrow activity-s
61 analyzed by ex vivo 3-dimensional imaging of bone lesions and by proteomic analysis and were further
62 by PCs correlates with the presence of lytic bone lesions and distinguishes MM from reactive plasmacy
63 ZOL showed fast uptake and high retention in bone lesions and fast clearance from the bloodstream in
64 2.8 mo) in the 19 patients who showed no new bone lesions and final TLA lower than the median of 750
65 it reached a plateau at three specimens for bone lesions and four specimens for soft-tissue lesions.
66 Obtaining a minimum of three specimens in bone lesions and four specimens in soft-tissue lesions o
67 ibuting factor to the increase in osteolytic bone lesions and hypercalcemia found in ATL patients.
70 ination of tumor cells leading to osteolytic bone lesions and liver metastases, common sites of clini
71 etal coccidioidomycosis manifests with lytic bone lesions and may produce peripherally enhancing flui
73 o significantly different between metastatic bone lesions and normal-appearing bone tissue (P <= .02)
76 lary disease, as well as the number of focal bone lesions and SUV(max), has been reported in several
77 IL-1 signaling can cause aseptic osteolytic bone lesions and that the absence of IL-10 signaling cau
78 hatase to confirm the presence of osteolytic bone lesions and the presence of osteoclasts, respective
79 e useful in yielding the precise location of bone lesions and thus helping avoid misdiagnosis of bone
80 integrated (18)F-FDG PET/MR specifically for bone lesions and to analyze differences in standardized
81 entiating between benign and malignant focal bone lesions and to propose a Bone Tumor Imaging Reporti
82 cer type, chemotherapy status, and number of bone lesions and were compared by using Fisher exact tes
85 mponents: diffuse marrow infiltration, focal bone lesions, and soft-tissue (extramedullary) disease.
87 (18)F-DCFBC PET detection of lymph nodes, bone lesions, and visceral lesions was superior to CIM.
88 aemia, renal failure, anaemia, or osteolytic bone lesions-and a detailed diagnostic investigation is
89 gnosis should be considered when superficial bone lesions appear time-related to therapy and in areas
90 The present study demonstrates that NOMID bone lesions are derived from the same osteoblast progen
92 e metastases as well as decreased osteolytic bone lesion area and reduced numbers of osteoclasts at t
93 astasis, treatment with GANT58-NPs decreased bone lesion area by 49% (p<.01) and lesion number by 38%
94 lveolar processes for presence of osteolytic bone lesions around causative teeth roots and we found t
95 ficant decrease in the incidence and size of bone lesions as compared with the results in control or
96 rP may reduce the development of destructive bone lesions as well as the growth of tumor cells in bon
98 compared management recommendations based on bone lesion assessment by (18)F-FDG PET plus contrast-en
99 GE2 inhibition may be therapeutic targets in bone lesions associated with defects of these two pathwa
101 acid; 0.77, 0.65-0.92; p=0.0038) and without bone lesions at baseline (29 [10%] of 302 vs 48 [17%] of
103 and PET-CT with respect to the detection of bone lesions at diagnosis and the prognostic value of th
105 n There is no difference in the detection of bone lesions at diagnosis when comparing PET-CT and MRI.
106 ved were ganglia, unspecific lymph node, and bone lesions, at a rate of 43%, 31%, and 24% for (18)F-P
107 ercalcemia, renal failure, anemia, and lytic bone lesions attributable to clonal expansion of plasma
109 d nonpigmented schwannomas and fibro-osseous bone lesions beginning at approximately 6 months of age.
110 coisolated with N-type cells from metastatic bone lesions, but to date their ability to induce cooper
111 Our current approach to quantify metastatic bone lesions, called the Bone Scan Index, is based on an
112 icance, additional criteria were included: a bone lesion, Castleman disease, organomegaly (or lymphad
113 by PCs correlated with the presence of lytic bone lesions (chi-square, 33.39: P <0.000; odds ratio, 1
114 ed prevalence of knee OA-related subchondral bone lesions compared with those reporting no use of the
115 sensitive for bone metastases, detecting 341 bone lesions, compared with 246 by conventional imaging.
117 most of the patients have revealed the mixed bone lesions, comprising both osteolytic and osteoblasti
120 ally and clinically robust for evaluation of bone lesions despite differences in attenuation correcti
122 lobulin free light chain ratio, and multiple bone lesions detected only by modern imaging) should be
123 knockout significantly decreased MDA-MB-231 bone lesion development in both the cardiac and tibial i
124 The mechanism by which bFGF rescued the bone lesion development was by promotion of tumor cell p
128 tivariate predictors: SPECT detection of new bone lesions during treatment (P < 0.0001) and final SPE
129 h use of imaging to assess whether sclerotic bone lesions, effusions, and organomegaly are present.
130 ND FINDINGS: Fifty-eight adult patients with bone lesions, either as a solitary site or as a componen
131 in acts as an important determinant in mixed bone lesions, especially in controlling osteoblastic eff
132 ant differences in activity were seen in the bone lesion evaluated on the baseline and initial postal
134 one scan plus CT detected an equal number of bone lesions for 14 patients (64%), PSMA PET/CT detected
135 14 patients (64%), PSMA PET/CT detected more bone lesions for six patients (27%), and bone scan plus
137 skeletal complications associated with lytic bone lesions for up to 1 year in women with stage IV bre
138 ion of prostate cancer metastases, including bone lesions for which there is no current reliable agen
139 a(+/-) and Prkar1a(+/-)Prkar2b(+/-) animals, bone lesions formed that looked like those of the Prkar1
147 of clinical manifestations including anemia, bone lesions, hypercalcemia, renal dysfunction, and comp
149 corresponding CT morphology features of 146 bone lesions identified in these 25 patients were follow
150 n species of Penicillium was isolated from a bone lesion in a young dog with osteomyelitis of the rig
151 a-PSMA-11 PET/CT imaging revealed additional bone lesions in 6% of patients, but without significantl
152 FPyL PET, whereas (18)F-DCFPyL PET localized bone lesions in 8 of 38 (21%) patients with negative res
157 hough IL-1beta is known as the key driver of bone lesions in CRMO, the signaling events leading to pa
158 t is unknown whether assessment of potential bone lesions in metastatic breast cancer (MBC) by (18)F-
160 ondin1 (RSpo1) were sufficient to repair the bone lesions in multiple myeloma and rheumatoid arthriti
165 tal complications associated with osteolytic bone lesions in patients with breast cancer and multiple
170 luation Criteria in Solid Tumors (RECIST) or bone lesions in the absence of measurable disease, witho
174 c yield is higher in lytic than in sclerotic bone lesions, in larger lesions, and for longer specimen
176 lesions that closely mirror the osteoblastic bone lesions induced by metastatic prostate tumors in hu
177 Strong TGF-beta signaling in osteolytic bone lesions is suppressed directly by genetic and pharm
178 opoiesis, widespread extramedullary disease, bone lesions, kidney abnormalities, preserved programmed
179 for uncontrolled growth causing destructive bone lesions, kidney injury, anemia, and hypercalcemia.
182 most organs was higher than zero, except for bone lesions (mean DDR, -2.8%; 95% CI, -17.8 to 12.2).
184 cells that manifests as one or more of lytic bone lesions, monoclonal protein in the blood or urine,
186 e important in the hypercalcemia, osteolytic bone lesions, neutrophilia, elevation of C-reactive prot
187 myeloma (MM) is characterized by osteolytic bone lesions (OBL) that arise as a consequence of osteob
188 3 years) with a confirmed malignant solitary bone lesion of maximum dimension of 8 cm or smaller that
189 We now report somatic SMAD3 mutations in bone lesions of four unrelated patients with endosteal p
195 ize of bone lesions or the appearance of new bone lesions on CT after treatment with (177)Lu-octreota
197 ration-resistant prostate cancer, numbers of bone lesions on CT, FDG PET, and FDHT PET scans and the
198 ho had atypically distributed, purely cystic bone lesions on CT; measuring the Hounsfield (HU) of the
201 clinical presentations ranging from a single bone lesion or trivial skin rash to an explosive dissemi
202 with NETs, the apparent increase in size of bone lesions or the appearance of new bone lesions on CT
203 major criteria (Castleman disease, sclerotic bone lesions, or elevated VEGF) and at least one minor c
207 bgroup of patients with metabolically active bone lesions (P = 0.02), but no difference was highlight
210 logy, growth pattern, and development of new bone lesions, possible bone metastases were classified a
211 ow, but the generalized osteopenia and focal bone lesions present in many adult patients are refracto
213 are pustular rash, marked osteopenia, lytic bone lesions, respiratory insufficiency, and thrombosis.
214 patients, (18)F-FDG PET versus BS to assess bone lesions resulted in clinically relevant management
217 n on normal tissue, soft-tissue lesions, and bone lesions; standardized uptake values were quantitati
218 tect highly significant progression of lytic bone lesions, subchondral sclerosis, and osteophyte size
220 pathologies, effusion, tendon, cartilage and bone lesions, tendon and ligament pathology at the site
221 ty in an orthotopic model of diffuse myeloma bone lesions than in conventional subcutaneous xenograft
222 ysmal bone cyst (ABC) is a locally recurrent bone lesion that has been regarded as a reactive process
223 as the rhizomelic dwarfism and nonossifying bone lesions that are characteristic of the disorder.
224 nted patients develop osteoporosis and other bone lesions that are related, at least in part, to thei
225 Prostate cancer (CaP) develops metastatic bone lesions that consist of a mixture of osteosclerosis
226 ession of MVNP (MVNP mice) developed PD-like bone lesions that required MVNP-dependent induction of h
227 plasma cells, frequently develop osteolytic bone lesions that severely impact quality of life and cl
228 f protein kinase A (PKA) activity, developed bone lesions that were derived from cAMP-responsive oste
229 m) and malignant lesions (pulmonary nodules, bone lesions); the regression line was y = 0.85x + 0.15,
231 lay a major role in the development of lytic bone lesions, the major clinical feature distinguishing
233 ma, extravascular volume overload, sclerotic bone lesions, thrombocytosis, elevated VEGF, and abnorma
238 zed the responses of adult LCH patients with bone lesions to three primary chemotherapy treatments to
241 ce (P < 0.01) in the ratio of lymph node and bone lesion uptake to kidney uptake between responders a
242 ating osteoclast activity within deep-seated bone lesions using appropriate fluorescent probes, despi
243 we established a novel mouse model of mixed bone lesions using intratibial injection of TM40D-MB cel
244 how PSTPIP2 deficiency causes osteopenia and bone lesions, using the mouse PSTPIP2 mutations, cmo, wh
251 presence or absence of metabolically active bone lesions was also recorded for each patient, and pat
252 The critical role of PD-1H in myeloma lytic bone lesions was confirmed using a Pd-1h(-/-) myeloma bo
253 rence in correct classification of malignant bone lesions was found among sets A (85/90), B (84/90),
254 To address how Notch affects prostate cancer bone lesions, we manipulated Notch expression in mouse t
255 oxic chemotherapy and had at least one lytic bone lesion were given either placebo or pamidronate (90
256 three patient groups Four or more sclerotic bone lesions were detected in all 25 (100%) of those wit
270 aphy (CT) in the identification of malignant bone lesions when the PET and CT findings are discordant
272 ased the capacity of the cells to repair the bone lesion, whereas BIO treatment had no significant ef
273 ng hypercalcemia, renal failure, anemia, and bone lesions, whereas MGUS and smoldering myeloma are di
274 n bone disease and is characterized by focal bone lesions which contain large numbers of abnormal ost
275 been described in both benign and malignant bone lesions, which can lead to false-positive findings
276 ancer (BCa) bone metastases cause osteolytic bone lesions, which result from the interactions of meta
277 r and area of radiographically evident lytic bone lesions, which, at the highest dose, were undetecta
278 omen with metastatic breast cancer and lytic bone lesions who received chemotherapy were randomly ass
279 s or older with measurable disease/evaluable bone lesions, whose disease progressed after 1-2 lines o
282 d shape, size, and distribution of sclerotic bone lesions with subsequent calculation of differences