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1 te mutation appeared to arise de novo in the metastatic lesion.
2  and the presence or absence of a measurable metastatic lesion.
3 pectrum of resistance mutations present in a metastatic lesion.
4 minantly associated with cancer cells in the metastatic lesions.
5  confirmed folate uptake in both primary and metastatic lesions.
6 r primary tumor inflammation and early stage metastatic lesions.
7 s significantly elevated in both primary and metastatic lesions.
8 tases (superscan) to recognizable individual metastatic lesions.
9 e localization of panitumumab at primary and metastatic lesions.
10 ed core biopsies that corresponded to MRI of metastatic lesions.
11 lls and continuously associates with growing metastatic lesions.
12  the primary tumor and/or in detecting small metastatic lesions.
13 8)F-FDG or (18)F-FLT uptake when focusing on metastatic lesions.
14 ue to hypersecretion of biogenic amines from metastatic lesions.
15 ic melanoma cell lines and human tissue from metastatic lesions.
16 n of clear cell RCC as the primary tumor for metastatic lesions.
17 nd slowed tumor progression and formation of metastatic lesions.
18 tic melanoma cell lines and in patients with metastatic lesions.
19 ession, only at the invasive front of larger metastatic lesions.
20  areas of the body in patients with multiple metastatic lesions.
21  tracer uptake in residual primary tumor and metastatic lesions.
22 n is decreased in primary tumors and lost in metastatic lesions.
23 ) in poorly differentiated primary tumors or metastatic lesions.
24               Twenty-nine of 30 patients had metastatic lesions.
25 nd in particular, extensive staining of bone metastatic lesions.
26  may promote progression of breast tumors to metastatic lesions.
27 t sites where they extravasate and establish metastatic lesions.
28 ique could elucidate the tissue of origin of metastatic lesions.
29 ctive Smad signaling in human and mouse bone-metastatic lesions.
30 cell growth, angiogenesis and development of metastatic lesions.
31 s, including differences between primary and metastatic lesions.
32 ficantly higher in primary melanomas than in metastatic lesions.
33 tly inhibited the number of spontaneous lung metastatic lesions.
34 CC and may not adequately characterize small metastatic lesions.
35 tic tumors, but is dramatically increased in metastatic lesions.
36 anying normal epithelium and preinvasive and metastatic lesions.
37 y occurs only in neoplasia, most strongly in metastatic lesions.
38 east a macroscopic complete resection of the metastatic lesions.
39 s, but not from biologically late primary or metastatic lesions.
40 for 90% of 175 carcinomas, including 9 of 12 metastatic lesions.
41 as maintained both in the primary tumors and metastatic lesions.
42 and increased significantly to nearly 60% in metastatic lesions.
43  in 44% of primary breast cancers and 90% of metastatic lesions.
44 in ductal carcinoma in situ to nearly 50% in metastatic lesions.
45         None of the nine ras/p21+/+ mice had metastatic lesions.
46 wth of primary tumors and the development of metastatic lesions.
47 and independently according to the number of metastatic lesions.
48 on in primary prostate cancer and associated metastatic lesions.
49  in 44% of primary breast cancers and 90% of metastatic lesions.
50 s common in some cancers and particularly in metastatic lesions.
51 or angiogenesis and leukocyte recruitment to metastatic lesions.
52 geting potential was assessed in primary and metastatic lesions.
53 n of focal therapy-activated T cells between metastatic lesions.
54 ile maintaining the capacity to develop into metastatic lesions.
55 rs were from regional lymph node and distant metastatic lesions.
56 n also favor the rapid growth of preexisting metastatic lesions.
57 P NETs, taking into account both primary and metastatic lesions.
58 s describing the growth of primary tumors or metastatic lesions.
59 oRNA is significantly decreased in the brain metastatic lesions.
60 e growth of the primary tumor or the size of metastatic lesions.
61 stasis leading to the formation of focal pre-metastatic lesions.
62 biopsies of 73 primary breast cancers and 19 metastatic lesions.
63  and in situ characterization of primary and metastatic lesions.
64  cancers, SOD2 is significantly increased in metastatic lesions.
65 n sites where they extravasate and establish metastatic lesions.
66 ssing osteosarcoma, and particularly for its metastatic lesions.
67 itates localization of the primary tumor and metastatic lesions.
68 rowth of primary tumors and the formation of metastatic lesions.
69 ors confer the capability of tumor growth at metastatic lesions.
70 erapeutic effects on both primary tumors and metastatic lesions.
71 odstream before the appearance of detectable metastatic lesions.
72  in the management of patients with multiple metastatic lesions.
73 effect of drugs on suppressing initiation of metastatic lesions.
74  relief at the site of primary tumor or from metastatic lesions.
75 rodeoxyglucose at detecting non-glucose-avid metastatic lesions.
76  tumors, the measured mean peritumoral MD of metastatic lesions, 0.733 x 10(-3) mm(2)/sec +/- 0.061 (
77  therapy was not influenced by the number of metastatic lesions (1 vs 2-4, interaction HR = 0.98).
78                            The proportion of metastatic lesions (12 of 13) with reduced expression of
79   According to biopsy analysis, only 9 of 20 metastatic lesions (45%) were pigmented with high melani
80 n in patient tumor samples was restricted to metastatic lesions (5/22; 23%) and no expression was det
81                   Because of the location of metastatic lesions, a surgical approach is limited and m
82 downregulated in primary prostate tumors and metastatic lesions across multiple data sets and is by i
83 ble to deliver their therapeutic payloads to metastatic lesions after systemic administration.
84                                              Metastatic lesions also showed (18)F- FPPRGD2 2-fluoropr
85 cancer models, EZC3 facilitated detection of metastatic lesions although total prostate luciferase ex
86 ed the expression of miR-7 and KLF4 in brain-metastatic lesions and found that these genes were signi
87 t TRAMP mice but was dramatically reduced in metastatic lesions and in androgen-independent disease.
88 04 and (99m)Tc-MIP-1405 identified most bone metastatic lesions and rapidly detected soft-tissue PCa
89 nsight into the etiology of both primary and metastatic lesions and rationalizations for tumor recurr
90 ET in the detection of paraganglioma and its metastatic lesions and to evaluate whether tracer uptake
91 ver, was reduced in primary prostate cancer, metastatic lesions, and androgen-independent disease.
92 ls into BALB/c mice results in tumor growth, metastatic lesions, and death.
93  modulate the ability of tumor cells to form metastatic lesions, and host genetic polymorphism could
94 ility-surface area product were observed for metastatic lesions, and significantly higher arterial fr
95 c colon cancer in liver, liver away from the metastatic lesions, and skin from three patients with me
96 s of dissemination are poorly understood and metastatic lesions are genetically divergent from the ma
97                      Alternatively, multiple metastatic lesions are seeded from different clones pres
98                                     Multiple metastatic lesions are usually treated with whole-brain
99 ultures of breast cancer cells isolated from metastatic lesions as compared with cells that produced
100 ell-resembling expression profile in distant metastatic lesions as revealed by the analysis of metast
101 omas in situ, 107 invasive primaries, and 38 metastatic lesions), as well as 11 human melanoma cell l
102 ability of the cancer cell to develop into a metastatic lesion at that distant site.
103 evidence of recurrent BAC in the lungs or of metastatic lesions at any site.
104 tein originally found to be overexpressed in metastatic lesions but absent in the matched primary tum
105 cancer, SPARC immunoreactivity is highest in metastatic lesions but distinct contributions of tumoral
106 nhibition does not affect MAM recruitment to metastatic lesions but regulates a set of inflammatory r
107  at a high frequency in melanocytic nevi and metastatic lesions, but recent data have revealed much l
108 take is observed in normal bone by 24 hr and metastatic lesions by 3-7 days.
109  suggest that SSeCKS suppresses formation of metastatic lesions by inhibiting VEGF expression and by
110 ed reduction of gp100 expression in the same metastatic lesion compared with prevaccination.
111 pressing HP1Hsalpha in seven of nine distant metastatic lesions compared with normal mammary and prim
112 nt for measuring PD-L1 status in primary and metastatic lesions could be important for optimizing dru
113                                  Analysis of metastatic lesions demonstrated that concomitant loss of
114  The growth of disseminated tumor cells into metastatic lesions depends on the establishment of a fav
115 d tomography (CT) in terms of organ-specific metastatic lesion detection and radiation dose in patien
116  the leading cause of cancer-related deaths; metastatic lesions develop from disseminated cancer cell
117 ize, microenvironment or other features of a metastatic lesion dictate its behaviour or determine the
118 d treatment by early detection of primary or metastatic lesions, differentiating benign from malignan
119     Further, cells obtained from bone marrow metastatic lesions displayed self-renewal capability in
120          On the contrary, breast cancer bone metastatic lesions do select for high levels of NOG expr
121 alterations that could be masked in advanced metastatic lesions due to their inherently high genetic
122                                Assessment of metastatic lesions during anti-PD-1 therapy demonstrated
123 nt tumor recurrence and the establishment of metastatic lesions, either during chemotherapy or after
124      A small proportion of tumors (20-30% of metastatic lesions) escape the apoptotic response and re
125 unohistochemistry analysis in PC tissues and metastatic lesions established an association between NC
126 advanced castrate-resistant prostate cancer, metastatic lesions exhibited an increased CD14(+)/CD206(
127 al of primary tumor is curative; however, if metastatic lesions exist and are not responsive to treat
128  showed that the prostatic tumors as well as metastatic lesions expressed high levels of MUC18, indic
129 om primary breast tumors and also from brain metastatic lesions followed by microRNA profiling analys
130  in known driver genes were present in every metastatic lesion for each patient studied.
131 oliferative outbreak of dormant BC cells and metastatic lesion formation; however, SFK inhibition did
132 high-grade PanIN, 79% of primary, and 83% of metastatic lesions from human pancreatic tissue samples
133                                     Multiple metastatic lesions from individual patients were analyze
134                         RNA from primary and metastatic lesions from patients with melanoma was hybri
135 effects, and we verified their expression in metastatic lesions from patients with melanoma.
136 aging, the heterogeneous expression of FR in metastatic lesions from the same patient, and the inabil
137 nd treatment of prostate adenocarcinoma, the metastatic lesions from this tumor are incurable.
138 tracranial neoplasms, including meningiomas, metastatic lesions, glioblastomas multiforme, and low-gr
139                   Substantial regressions of metastatic lesions have been observed in up to 70% of pa
140  MUC5AC is overexpressed in both primary and metastatic lesions; however, its functional role is not
141 ction resulted in suppression of primary and metastatic lesions, i.t. replication and necrosis, vecto
142 onstrated by immunohistochemical analysis of metastatic lesions, IFN-gamma enzyme-linked immunosorben
143 icity profile and regression of at least one metastatic lesion in 12 of 30 patients.
144 ic tumor cell line SUIT-2 was derived from a metastatic lesion in the liver of a patient with pancrea
145 east cancer and with at least one measurable metastatic lesion in the liver that was treated with 3 c
146                                 Seventy-four metastatic lesions in 10 women and 18 men (mean age, 61.
147               Results There were 242 distant metastatic lesions in 30 patients, 18 breast cancers in
148 ary adenocarcinoma of the lung with numerous metastatic lesions in both cerebral and cerebellar hemis
149 ners have increased detection of primary and metastatic lesions in both tumor types with [18F]deoxygl
150 disease settings and during the formation of metastatic lesions in cancer-bearing mice.
151 T-guided biopsy of (18)F-FDG-avid primary or metastatic lesions in different locations consented to p
152  on paraffin-embedded pancreatic tissues and metastatic lesions in liver, lungs, and lymph nodes.
153 al-like breast carcinoma that readily formed metastatic lesions in lungs of mice.
154 ion was relatively higher in prostate cancer metastatic lesions in lymph node, lung, and bone/bone ma
155 arison with the corresponding EBER1-positive metastatic lesions in lymph nodes (10 cases) and EBV-inf
156  patterns at the invasive front of pulmonary metastatic lesions in murine and human patient samples.
157 nt of residual tumor in resection margins or metastatic lesions in patients with ccRCC.
158 ls resulted in the production of microscopic metastatic lesions in the brain parenchyma, without a de
159                                  Only 61% of metastatic lesions in the brain were identified at PET.
160             Whole-body optical images showed metastatic lesions in the brain, liver, and bone of B16F
161 e, growth of the primary colon tumor and its metastatic lesions in the liver and skeleton.
162 ke indices for residual primary tumor or any metastatic lesions in the liver, bone, lung, or lymph no
163 ssion of AQPs 1 and 5 was maintained even in metastatic lesions in the liver.
164 n chromosome 16 were injected, the number of metastatic lesions in the lung was significantly reduced
165 etaRIIDN-BM mice showed a virtual absence of metastatic lesions in the lung.
166      At 4 weeks after F5M2 cell inoculation, metastatic lesions in the lungs were detectable using CX
167 fspring and specifically exhibit macroscopic metastatic lesions in the lungs.
168                                 Treatment of metastatic lesions in the orbit and ocular adnexa is usu
169 stically reduced the incidence and growth of metastatic lesions in vitro or in vivo, respectively.
170 y induced EMT but also enabled cells to form metastatic lesions in vivo.
171 on of organ-confined tumors and emergence of metastatic lesions in young mice.
172  mean age, 54 years) with one or two painful metastatic lesions involving bone, with a score of 4 or
173 dicates that the fraction of bone containing metastatic lesions is a strong prognostic indicator of s
174 tributing to the establishment and growth of metastatic lesions is crucial for the development of nov
175 opment of quick and simple methods to detect metastatic lesions is in high demand.
176 naling in prostate cancer cells within boney metastatic lesions is not clearly understood.
177  however, deriving this information from the metastatic lesions is not feasible until after resection
178 f the somatic genetic alterations found in a metastatic lesion isolated at first relapse.
179 ocated to the cytoplasm, whereas in PDAC and metastatic lesions, its expression is significantly dimi
180 suggest that discordance between primary and metastatic lesions leads to detrimental outcome.
181 e largest lymph node (N), and of the largest metastatic lesion (M); SUVmax; SUVmean; size-incorporate
182 imal models and to the concern that multiple metastatic lesions may be more resistant to immunotherap
183 ations present in each patient's primary and metastatic lesions (mean, 75%).
184 ary site of origin for an independent set of metastatic lesions (n = 50), resected from brain, lung,
185      The LNCaP cell line, established from a metastatic lesion of human prostatic adenocarcinoma, car
186 hat AKT is activated in both the thyroid and metastatic lesions of a mouse model of follicular thyroi
187 tly up-regulated in primary brain tumors and metastatic lesions of brain homing cancers, we show that
188 l diagnostic test for detecting recurrent or metastatic lesions of breast carcinoma.
189 foci in patients with suspected recurrent or metastatic lesions of breast carcinoma.
190 oma cell lines were isolated from primary or metastatic lesions of patients described as having "earl
191 ional imaging modalities in the detection of metastatic lesions of SDHB-associated PGL.
192                                        Since metastatic lesions of solid tumors are the major cause o
193 s in normal human skin and blood compared to metastatic lesions of subjects with progressive stage IV
194 oma continues to account for the majority of metastatic lesions of the orbit and ocular adnexa.
195 essed and activated in anatomically distinct metastatic lesions of the same patient is not known.
196 is also highly expressed in both primary and metastatic lesions of TRAMP mice.
197                                    Growth of metastatic lesions of WT, syngeneic melanoma cells in th
198 asis is less than 6 months, and even a small metastatic lesion often causes severe neurological disab
199 y explain in part the heterogeneous fates of metastatic lesions often observed in the clinic post-the
200 curative intent, three or fewer extracranial metastatic lesions on choline positron emission tomograp
201                     In two patients, obvious metastatic lesions on functional imaging were missed by
202  prior malignancy, who were asymptomatic for metastatic lesions on initial clinical examination, and
203 re, two out of the eight ras/p21-/- mice had metastatic lesions, one in its lungs, the other in its a
204 rtery of mice, K-1735 melanoma cells produce metastatic lesions only in the brain parenchyma, whereas
205 cells of B16 x K-1735 melanoma cells produce metastatic lesions only in the leptomeninges and ventric
206 f 2000 cGy or more could be delivered to the metastatic lesion or lesions, therapeutic radioiodine wa
207 imultaneous decrease and increase in size of metastatic lesions or appearance of new ones.
208  levels, both within primary (p < 0.001) and metastatic lesion (p = 0.010).
209  peritoneum) (P = 0.170), and primary versus metastatic lesion (P = 0.561).
210 n both the primary tumors (P >/= 0.0198) and metastatic lesions (P >/= 0.0067), respectively, by chi(
211                               In contrast to metastatic lesions, primary melanomas did not host folli
212 e generated from a fine needle aspirate of a metastatic lesion progressing after initial response to
213 and bone degradation and also contributes to metastatic lesions reinitiation.
214 ably, cytoplasmic expression was elevated in metastatic lesions relative to primary tumors (P = 0.03)
215 umor is curable by conventional methods, but metastatic lesions remain refractile to current treatmen
216 cadherin profiles on peritoneal anchoring of metastatic lesions remains poorly understood.
217 use for resistance to treatment in 20-30% of metastatic lesions remains to be identified.
218  ability of cancer cells to establish lethal metastatic lesions requires the survival and expansion o
219                                              Metastatic lesions resected after vaccination showed T l
220  cells of the immune system in all patients, metastatic lesions resected after vaccination were dense
221                                     Although metastatic lesions resected before vaccination were mini
222 asive ductal carcinomas and their autologous metastatic lesions revealed an inverse correlation for t
223 etermine the primary subclone from which the metastatic lesion(s) originated.
224 le, in part, for the osteoblastic changes in metastatic lesions secondary to prostate cancer.
225 tested using in situ hybridization on 30 pre-metastatic lesions, showing intratumoral concentration o
226 could assess HER2 status in both primary and metastatic lesions simultaneously, could be a valuable t
227 s an improvement of at least 50% in previous metastatic lesions subjectively or a change from prior d
228 ighly expressed in primary tumors but not in metastatic lesions, suggesting that ARID1A can be lost a
229 ression in human cancers was higher in liver metastatic lesions than in primary lesions.
230 l-time primary tumor growth and formation of metastatic lesions that developed in the spleen, bowel,
231 ic MMTVneu mice spontaneously develop BC and metastatic lesions that overexpress cyclin D1 and VPAC1
232          Mean pretreatment DUR values in the metastatic lesions that responded did not differ signifi
233                                              Metastatic lesions that were resected after vaccination
234 es dormant D2.0R cells to form proliferative metastatic lesions through beta1-integrin signaling.
235 ta strongly support the need for biopsies of metastatic lesions to accurately determine patient progn
236  precision medicine to longitudinally sample metastatic lesions to capture the evolving constellation
237 ltrating leukocytes (TILs) and CD3+ cells in metastatic lesions to search for a molecular basis for t
238         The infused cells must accumulate in metastatic lesions to suppress growth; however, this pro
239 The aim of this study is to analyze cases of metastatic lesions to the gingiva compared with cases me
240  reduced formation of prostate-tumor derived metastatic lesions to the lungs in an in vivo spontaneou
241 ween 1916 and 2011 was searched for cases of metastatic lesions to the oral mucosa; only cases metast
242                         For solid tumors and metastatic lesions, tumor vascularity is a critical fact
243 creased in the developing adenoma through to metastatic lesions, understanding the function of the BA
244 or burden indices of total fluoride skeletal metastatic lesion uptake (TLF10) and total volume of flu
245  active uPA in small soft-tissue and osseous metastatic lesions using a cardiac dissemination prostat
246  melanoma cell lines derived from primary or metastatic lesions using the monoclonal antibodies HECD-
247 ent in Me9923 cells that were derived from a metastatic lesion was also found in the Me9923P cell lin
248                       SUVmax for the largest metastatic lesion was the only variable independently as
249    Importantly, the development of pulmonary metastatic lesions was also reduced.
250            The expression of IL-13Ralpha2 in metastatic lesions was found to be increased compared wi
251 onal TRF2 null primary tumors, the number of metastatic lesions was similar to control cancers.
252                       While dissemination of metastatic lesions was widespread in old bigenic mice we
253 ensity of prostate cancer cells to form bone metastatic lesions, we investigated whether the alphavbe
254 Nine mice with visible, palpable, or unknown metastatic lesions were entered into the protocol.
255 as, 84 primary colorectal carcinomas, and 13 metastatic lesions were evaluated immunohistochemically
256                                 Thirty-eight metastatic lesions were seen at MR imaging; 23 (61%) of
257 ts with known independent primary tumors and metastatic lesions were used for lineage test developmen
258                                          All metastatic lesions, when compared to the pre-treatment t
259 MP mice and was elevated in the accompanying metastatic lesions, whereas prostatic IGF-I mRNA remaine
260 scans (in nine patients) identified multiple metastatic lesions, whereas the thallium scans were inte
261 pful in differentiation of the origin of the metastatic lesion with known SEL features.
262 y regimens, who exhibited regression of some metastatic lesions with concomitant progression of other
263 ect detection of reporter gene expression in metastatic lesions within sentinel lymph nodes.
264 rived from V12S35 Ras-tumors formed numerous metastatic lesions within the lung.

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