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1 (hypercalcaemia, renal failure, anaemia, and bone lesions).
2 ic MM is a well-demarcated, focal osteolytic bone lesion.
3 ons exhibit defective osteoclastogenesis and bone lesions.
4 reviewed to identify patients with malignant bone lesions.
5  of tumor cells to the bone marrow and lytic bone lesions.
6 could be used to detect osteoclasts in lytic bone lesions.
7  of bone tumors with no development of lytic bone lesions.
8 teoblastic character of most prostate cancer bone lesions.
9 d were associated with the presence of focal bone lesions.
10 contrast, only 4% of beta3-/- mice developed bone lesions.
11 eloma (MM) is commonly associated with lytic bone lesions.
12 mpared with other forms of therapy for lytic bone lesions.
13 or RANKL, prevented the development of lytic bone lesions.
14 ation, and radiologic evidence of osteolytic bone lesions.
15 logies in 15 specimens, including 10 primary bone lesions.
16 nd inhibition of radiographic progression of bone lesions.
17 e not significantly different from those for bone lesions.
18 nohistochemistry was performed on metastatic bone lesions.
19 tures from other processes such as malignant bone lesions.
20 erozygous mice; none of these mice developed bone lesions.
21 ial advantages over PET/CT for evaluation of bone lesions.
22 T for anatomic delineation and allocation of bone lesions.
23 d bone colonization and decreased osteolytic bone lesions.
24 lving extramedullary hematopoiesis, skin and bone lesions.
25 ntification was reduced by a factor of 4 for bone lesions (10.24% for Dixon PET and 2.68% for ZeDD PE
26 re found for PET/MR than for PET/CT both for bone lesions (12.4% +/- 15.5%) and for regions of normal
27 ate liver lesions, 2 patients with sclerotic bone lesions, 2 patients with breast abnormalities, 1 pa
28 of hematopoiesis and formation of osteolytic bone lesions also known as myeloma bone disease (MBD).
29                Lesions were scored on CT and bone lesions also on SRS before and after treatment.
30 nt, mimicking progressive disease with "new" bone lesions, although there was an overall treatment re
31     Experience of scintigraphic detection of bone lesion and active bone marrow involvement of multip
32 ith breast cancer who had at least one lytic bone lesion and who were receiving hormonal therapy were
33  (11)C-acetate-avid and (18)F-FDG-avid focal bone lesions and (11)C-acetate general marrow activity-s
34  choline-avid metastases were identified: 44 bone lesions and 23 lymph node lesions.
35                      Yield was 87% for lytic bone lesions and 57% for sclerotic bone lesions (P = .00
36                                 In total, 30 bone lesions and 60 soft-tissue lesions were evaluated.
37                 Diagnostic yield was 77% for bone lesions and 76% for soft-tissue lesions (P = .88).
38 by PCs correlates with the presence of lytic bone lesions and distinguishes MM from reactive plasmacy
39  it reached a plateau at three specimens for bone lesions and four specimens for soft-tissue lesions.
40    Obtaining a minimum of three specimens in bone lesions and four specimens in soft-tissue lesions o
41 ibuting factor to the increase in osteolytic bone lesions and hypercalcemia found in ATL patients.
42  acute ATL patients is the presence of lytic bone lesions and hypercalcemia.
43 ow plasma cells characterized by destructive bone lesions and is fatal in most patients.
44 ination of tumor cells leading to osteolytic bone lesions and liver metastases, common sites of clini
45                         Patients with 1 to 3 bone lesions and negative bone marrows are often treated
46 th paclitaxel would inhibit experimental FTC bone lesions and preserve bone structure.
47                                          For bone lesions and regions of normal bone, a highly signif
48  IL-1 signaling can cause aseptic osteolytic bone lesions and that the absence of IL-10 signaling cau
49 hatase to confirm the presence of osteolytic bone lesions and the presence of osteoclasts, respective
50 e useful in yielding the precise location of bone lesions and thus helping avoid misdiagnosis of bone
51 integrated (18)F-FDG PET/MR specifically for bone lesions and to analyze differences in standardized
52 cer type, chemotherapy status, and number of bone lesions and were compared by using Fisher exact tes
53 yeloma-induced bone loss, reduced osteolytic bone lesions, and increased fracture resistance.
54 lonal gammopathy, BM infiltration with lytic bone lesions, and protein deposition in the kidney.
55 mponents: diffuse marrow infiltration, focal bone lesions, and soft-tissue (extramedullary) disease.
56 docrinopathy, skin changes, edema, sclerotic bone lesions, and thrombocytosis.
57    (18)F-DCFBC PET detection of lymph nodes, bone lesions, and visceral lesions was superior to CIM.
58    The present study demonstrates that NOMID bone lesions are derived from the same osteoblast progen
59 tasis burden but becomes less effective when bone lesions are well established.
60 lveolar processes for presence of osteolytic bone lesions around causative teeth roots and we found t
61 ficant decrease in the incidence and size of bone lesions as compared with the results in control or
62 rP may reduce the development of destructive bone lesions as well as the growth of tumor cells in bon
63 s (PC3-AR9) results in decreased invasion in bone lesion assays and in vivo mouse models.
64 GE2 inhibition may be therapeutic targets in bone lesions associated with defects of these two pathwa
65 acid; 0.77, 0.65-0.92; p=0.0038) and without bone lesions at baseline (29 [10%] of 302 vs 48 [17%] of
66          Conclusion: The number of sclerotic bone lesions at body CT is of potential value in the dia
67  and PET-CT with respect to the detection of bone lesions at diagnosis and the prognostic value of th
68   The primary end point was the detection of bone lesions at diagnosis by MRI versus PET-CT.
69 n There is no difference in the detection of bone lesions at diagnosis when comparing PET-CT and MRI.
70 ercalcemia, renal failure, anemia, and lytic bone lesions attributable to clonal expansion of plasma
71                                In 1 patient, bone lesions became visible on CT after treatment, mimic
72 d nonpigmented schwannomas and fibro-osseous bone lesions beginning at approximately 6 months of age.
73 coisolated with N-type cells from metastatic bone lesions, but to date their ability to induce cooper
74  Our current approach to quantify metastatic bone lesions, called the Bone Scan Index, is based on an
75 icance, additional criteria were included: a bone lesion, Castleman disease, organomegaly (or lymphad
76 by PCs correlated with the presence of lytic bone lesions (chi-square, 33.39: P <0.000; odds ratio, 1
77 ed prevalence of knee OA-related subchondral bone lesions compared with those reporting no use of the
78 sensitive for bone metastases, detecting 341 bone lesions, compared with 246 by conventional imaging.
79                      The risk for osteolytic bone lesion complications in metastatic breast cancer wa
80 most of the patients have revealed the mixed bone lesions, comprising both osteolytic and osteoblasti
81                          The number of focal bone lesions correlates inversely with outcome.
82 ally and clinically robust for evaluation of bone lesions despite differences in attenuation correcti
83                      Multiple sites of focal bone lesions detected on MR studies allow a more appropr
84 lobulin free light chain ratio, and multiple bone lesions detected only by modern imaging) should be
85  knockout significantly decreased MDA-MB-231 bone lesion development in both the cardiac and tibial i
86      The mechanism by which bFGF rescued the bone lesion development was by promotion of tumor cell p
87                                   Metastatic bone lesion development was compared by analysis of both
88 ons that facilitate tumor growth and control bone lesion development.
89 br2 KO mice rescued the inhibited metastatic bone lesion development.
90 ND FINDINGS: Fifty-eight adult patients with bone lesions, either as a solitary site or as a componen
91 in acts as an important determinant in mixed bone lesions, especially in controlling osteoblastic eff
92 ant differences in activity were seen in the bone lesion evaluated on the baseline and initial postal
93           Purpose: To determine if sclerotic bone lesions evident at body computed tomography (CT) ar
94 skeletal complications associated with lytic bone lesions for up to 1 year in women with stage IV bre
95 ion of prostate cancer metastases, including bone lesions for which there is no current reliable agen
96 a(+/-) and Prkar1a(+/-)Prkar2b(+/-) animals, bone lesions formed that looked like those of the Prkar1
97  of skeletal-related events in patients with bone lesions from multiple myeloma.
98 ET-derived SUV imaging metrics in individual bone lesions from patients in a multicenter study.
99 new bone formation is frequently seen in the bone lesions from prostate cancer.
100 sed by 70% in anti-CCL2-treated animals with bone lesions from VCaP cells.
101                       Finally, patients with bone lesions had relatively higher levels of M-CSF and o
102 of clinical manifestations including anemia, bone lesions, hypercalcemia, renal dysfunction, and comp
103  corresponding CT morphology features of 146 bone lesions identified in these 25 patients were follow
104 n species of Penicillium was isolated from a bone lesion in a young dog with osteomyelitis of the rig
105 ective and minimally toxic treatment for LCH bone lesions in adults.
106 old woman presented with bone pain and lytic bone lesions in April 2010.
107 etic role in the establishment of osteolytic bone lesions in breast cancer.
108                   The majority of metastatic bone lesions in cervical cancer seem to be of osteolytic
109 y, and its serum level correlates with focal bone lesions in MM.
110 ondin1 (RSpo1) were sufficient to repair the bone lesions in multiple myeloma and rheumatoid arthriti
111  Th1 phenotype may profoundly diminish lytic bone lesions in multiple myeloma.
112 s (MILs) in OC activation and development of bone lesions in myeloma patients.
113 icantly reduced the occurrence of osteolytic bone lesions in myeloma-bearing mice.
114 tal complications associated with osteolytic bone lesions in patients with breast cancer and multiple
115 lls is associated with the presence of lytic bone lesions in patients with multiple myeloma.
116 ive therapeutic approach to treat osteolytic bone lesions in patients with myeloma.
117 mor-induced bone gain, a response resembling bone lesions in prostate cancer patients.
118 luation Criteria in Solid Tumors (RECIST) or bone lesions in the absence of measurable disease, witho
119 cancer cell lines in vitro and in metastatic bone lesions in vivo.
120 K-1, or MCP-1 were each sufficient to reduce bone lesions in vivo.
121 c yield is higher in lytic than in sclerotic bone lesions, in larger lesions, and for longer specimen
122                                      Whereas bone lesions increased in size, soft-tissue lesions decr
123 lesions that closely mirror the osteoblastic bone lesions induced by metastatic prostate tumors in hu
124      Strong TGF-beta signaling in osteolytic bone lesions is suppressed directly by genetic and pharm
125                               A total of 411 bone lesions larger than 1.5 cm(3) were automatically se
126 T imaging allowed high-contrast detection of bone lesions, lymph node, and liver metastases.
127                                      Sixteen bone lesions (midtibia, n = 14; distal fibula, n = 1; an
128 cells that manifests as one or more of lytic bone lesions, monoclonal protein in the blood or urine,
129  less than 5% for soft tissue and in or near bone lesions (n = 91).
130 e important in the hypercalcemia, osteolytic bone lesions, neutrophilia, elevation of C-reactive prot
131  myeloma (MM) is characterized by osteolytic bone lesions (OBL) that arise as a consequence of osteob
132 3 years) with a confirmed malignant solitary bone lesion of maximum dimension of 8 cm or smaller that
133 nt had no significant effect on cartilage or bone lesions of OA.
134 able disease (91%), and/or appearance of new bone lesions on bone scan (83%).
135 herapy, regardless of presence of osteolytic bone lesions on conventional radiography.
136 ize of bone lesions or the appearance of new bone lesions on CT after treatment with (177)Lu-octreota
137                           We have noted that bone lesions on CT respond differently from soft-tissue
138 ration-resistant prostate cancer, numbers of bone lesions on CT, FDG PET, and FDHT PET scans and the
139                   The intensity or number of bone lesions on SRS decreased after treatment in 19 of 2
140                                              Bone lesions on the spine of a male skeleton excavated a
141 clinical presentations ranging from a single bone lesion or trivial skin rash to an explosive dissemi
142  with NETs, the apparent increase in size of bone lesions or the appearance of new bone lesions on CT
143 major criteria (Castleman disease, sclerotic bone lesions, or elevated VEGF) and at least one minor c
144 ependent of the number of syndrome features, bone lesions, or plasma cells at diagnosis.
145 han FDG-PET overall and for the detection of bone lesions (P < .001).
146 for lytic bone lesions and 57% for sclerotic bone lesions (P = .002).
147 bgroup of patients with metabolically active bone lesions (P = 0.02), but no difference was highlight
148                               Improvement in bone lesions, pain, diabetes insipidus, and other manife
149 ling pathway has a significant impact on the bone lesion phenotype.
150 logy, growth pattern, and development of new bone lesions, possible bone metastases were classified a
151 ow, but the generalized osteopenia and focal bone lesions present in many adult patients are refracto
152                   A high correlation between bone lesion quantity as determined visually and automati
153  are pustular rash, marked osteopenia, lytic bone lesions, respiratory insufficiency, and thrombosis.
154                                          For bone lesions, significant underestimations of -16% and -
155 n on normal tissue, soft-tissue lesions, and bone lesions; standardized uptake values were quantitati
156 tect highly significant progression of lytic bone lesions, subchondral sclerosis, and osteophyte size
157 g to multiple neoplasias, is associated with bone lesions such as osteochondromyxomas (OMX).
158 pathologies, effusion, tendon, cartilage and bone lesions, tendon and ligament pathology at the site
159 ty in an orthotopic model of diffuse myeloma bone lesions than in conventional subcutaneous xenograft
160 ysmal bone cyst (ABC) is a locally recurrent bone lesion that has been regarded as a reactive process
161  as the rhizomelic dwarfism and nonossifying bone lesions that are characteristic of the disorder.
162 nted patients develop osteoporosis and other bone lesions that are related, at least in part, to thei
163    Prostate cancer (CaP) develops metastatic bone lesions that consist of a mixture of osteosclerosis
164 ession of MVNP (MVNP mice) developed PD-like bone lesions that required MVNP-dependent induction of h
165 f protein kinase A (PKA) activity, developed bone lesions that were derived from cAMP-responsive oste
166 m) and malignant lesions (pulmonary nodules, bone lesions); the regression line was y = 0.85x + 0.15,
167                                           In bone lesions, the average underestimation was -7.4% +/-
168 lay a major role in the development of lytic bone lesions, the major clinical feature distinguishing
169 ma, extravascular volume overload, sclerotic bone lesions, thrombocytosis, elevated VEGF, and abnorma
170 l for clinically quantifying the response of bone lesions to therapy.
171 zed the responses of adult LCH patients with bone lesions to three primary chemotherapy treatments to
172                               In this model, bone lesions typical of the human disease develop in mic
173                                          For bone lesions, underestimation of PET standardized uptake
174  we established a novel mouse model of mixed bone lesions using intratibial injection of TM40D-MB cel
175 how PSTPIP2 deficiency causes osteopenia and bone lesions, using the mouse PSTPIP2 mutations, cmo, wh
176 m one to the other class identified apparent bone lesion volume change (Delta BLV).
177                         The median number of bone lesions was 1 (range: 1-6).
178                   The detection rate for all bone lesions was 35% (247 of 698) for MPRs and 74% (520
179                   The accuracy in diagnosing bone lesions was 89.7% for planar bone scanning versus 9
180  presence or absence of metabolically active bone lesions was also recorded for each patient, and pat
181 rence in correct classification of malignant bone lesions was found among sets A (85/90), B (84/90),
182 oxic chemotherapy and had at least one lytic bone lesion were given either placebo or pamidronate (90
183  three patient groups Four or more sclerotic bone lesions were detected in all 25 (100%) of those wit
184                                        Lytic bone lesions were detected using x-rays in all the hyper
185                                 In total, 98 bone lesions were identified in 33 of 119 patients, and
186                                         Most bone lesions were in the skull, spine, or jaw.
187                                      Because bone lesions were not visible on CT before treatment in
188                                              Bone lesions were present in 40 of the 51 MM patients an
189                                     Solitary bone lesions were reported on 21 radiographic surveys an
190         Results: Most commonly the sclerotic bone lesions were round, measured 0.3 cm (range, 0.2-3.2
191                       Subcutaneous and lytic bone lesions were strongly associated with B. quintana,
192 aphy (CT) in the identification of malignant bone lesions when the PET and CT findings are discordant
193                     Specifically, osteolytic bone lesions, where bone is destroyed, lead to debilitat
194 ased the capacity of the cells to repair the bone lesion, whereas BIO treatment had no significant ef
195 ng hypercalcemia, renal failure, anemia, and bone lesions, whereas MGUS and smoldering myeloma are di
196 n bone disease and is characterized by focal bone lesions which contain large numbers of abnormal ost
197 ancer (BCa) bone metastases cause osteolytic bone lesions, which result from the interactions of meta
198 r and area of radiographically evident lytic bone lesions, which, at the highest dose, were undetecta
199 omen with metastatic breast cancer and lytic bone lesions who received chemotherapy were randomly ass
200 r flare (eg, >5 sites of visceral disease or bone lesions with impending fracture).
201        The P394L mutant mice developed focal bone lesions with increasing age and by 12 months, 14/18
202 d shape, size, and distribution of sclerotic bone lesions with subsequent calculation of differences
203        We therefore compared the response of bone lesions with that of soft-tissue lesions to treatme
204  myeloma (MM) is characterized by osteolytic bone lesions with uncoupled bone remodeling.

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