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1 intracranial control following resection of brain metastasis.
2 compared with WBRT in patients with resected brain metastasis.
3 nase in vitro cell invasion and experimental brain metastasis.
4 knowledge of the initial events that lead to brain metastasis.
5 with breast cancer, 362 developed subsequent brain metastasis.
6 and independently associated with subsequent brain metastasis.
7 m could prove valuable for the inhibition of brain metastasis.
8 s, which served as a proxy for an orthotopic brain metastasis.
9 n contrast, ST6GALNAC5 specifically mediates brain metastasis.
10 is of melanoma cells, consequently promoting brain metastasis.
11 al cues at the BBB affects the mechanisms of brain metastasis.
12 cases, 5/5 meningioma cases and 3/3 cases of brain metastasis.
13 s and treatment response in CNS lymphoma and brain metastasis.
14 be uniquely suited to the local treatment of brain metastasis.
15 ival for patients with a single unresectable brain metastasis.
16 ages in 23 patients disclosed no evidence of brain metastasis.
17 nt immune response can eliminate established brain metastasis.
18 tial for study of the biology and therapy of brain metastasis.
19 r mechanisms of angiogenesis in experimental brain metastasis.
20 ich significantly decreased the incidence of brain metastasis.
21 y correlated with angiogenesis and growth of brain metastasis.
22 t during metastatic evolution is crucial for brain metastasis.
23 an experimental mouse model of breast cancer brain metastasis.
24 pe in the brain, the astrocyte, in promoting brain metastasis.
25 ese drugs could be used to treat established brain metastasis.
26 RCC with vascular invasion, liver, lung and brain metastasis.
27 therapy can inhibit growth of breast cancer brain metastasis.
28 anged non-small-cell lung cancer (NSCLC) and brain metastasis.
29 n and recruitment of myeloid cell to promote brain metastasis.
30 tic target or serve as a prognostic tool for brain metastasis.
31 eural effusion and pericardial effusion; and brain metastasis.
32 able therapeutic platform to target melanoma brain metastasis.
33 enges in the development of therapeutics for brain metastasis.
34 d MET attenuation decreased the incidence of brain metastasis.
35 rvention of MMP-2-dependent diseases such as brain metastasis.
36 t patients with breast cancer suffering from brain metastasis.
37 presents a potential target for treatment of brain metastasis.
38 R2 signaling for HER2-positive breast cancer brain metastasis.
39 hanistic and therapeutic studies of melanoma brain metastasis.
40 Additional imaging showed no brain metastasis.
41 ted vessels in two separate murine models of brain metastasis.
43 is a novel prognostic marker for lung and/or brain metastasis and a predictive marker for the respons
44 ions in the USA and Canada with one resected brain metastasis and a resection cavity less than 5.0 cm
45 cer: peripheral blood, the primary tumour, a brain metastasis and a xenograft derived from the primar
46 terface in 26 patients during resection of a brain metastasis and assessed mean diffusivity and fract
47 ment for patients with a single unresectable brain metastasis and considered for patients with two or
48 we developed a model to study human melanoma brain metastasis and found that Stat3 activity was incre
50 ical metabolic condition required to sustain brain metastasis and suggest that targeting gluconeogene
51 ary but not sufficient for the production of brain metastasis and that the inhibition of VEGF represe
53 re also associated with development of NSCLC brain metastasis and were selectively enriched in brain
54 asis (BCBM) may allow for early diagnosis of brain metastasis and/or help for treatment choice and it
55 mately 50% of patients with melanoma develop brain metastasis, and currently there are no beneficial
56 metabolism is a key element in breast cancer brain metastasis, and raise the possibility of targeting
58 iologic and therapeutic advances in melanoma brain metastasis are hampered by the paucity of reproduc
62 ain metastases and data from an experimental brain metastasis assay, both indicative of a functional
63 blished a human breast cancer cell model for brain metastasis based on circulating tumor cells from a
64 anding of CTCs associated with breast cancer brain metastasis (BCBM) is necessary for early identific
65 TCs derived from breast cancer patients with brain metastasis (BCBM) may allow for early diagnosis of
66 ts had at least one untreated or progressive brain metastasis between 5 and 20 mm in diameter without
70 cally in the intracardially induced model of brain metastasis but with lower sensitivity because of s
71 als cellular events during the initiation of brain metastasis by breast cancer cells and documents th
72 onal in LUAD and show that astrocytes oppose brain metastasis by mediating the downregulation of TRPA
74 rostate cancer cell line, originating from a brain metastasis, carries a truncating mutation of EPHB2
75 of brain metastasis (P = 0.02) and a shorter brain metastasis-free survival in lymph node-negative pa
76 uced MMP9 were significantly correlated with brain metastasis-free survival of breast cancer patients
77 FET) PET for differentiating local recurrent brain metastasis from radiation necrosis after radiation
82 ritical role for Src activation in promoting brain metastasis in a preclinical model of breast cancer
84 as been implicated as an important driver of brain metastasis in breast cancer, but the critical targ
85 transplantable model of spontaneous melanoma brain metastasis in immunocompetent mice and developed m
87 bust tool that is able to predict subsequent brain metastasis in patients with breast cancer with non
89 ived cells showed an increased potential for brain metastasis in vivo and exhibited a unique protein
90 metabolic pathway decreased the incidence of brain metastasis in vivo Taken together, our results sho
98 bility to be more inclusive of patients with brain metastasis is justified in many cases and may spee
99 survival time of breast cancer patients with brain metastasis is less than 6 months, and even a small
107 inflammatory response has been documented in brain metastasis, its contribution to cancer progression
108 d quantify volumetric and spatial aspects of brain metastasis landscapes, including diverse tumor mor
110 tic phenotype with the unusual occurrence of brain metastasis, making it an important target for diag
111 hese data suggest that the glial response to brain metastasis may provide a sensitive biomarker of tu
112 adiosurgery group for patients with a single brain metastasis (median survival time 6.5 vs 4.9 months
113 these results indicate a novel mechanism of brain metastasis mediated by EVs that triggers the destr
118 stemic delivery of OV, we developed melanoma brain metastasis models in immunocompromised and immunoc
123 rats with HER2-positive cells derived from a brain metastasis of a breast cancer patient (MDA-MB-361)
124 suggest that miR-509 has a critical role in brain metastasis of breast cancer by modulating the RhoC
125 metastatic cancer cell-derived EVs promoted brain metastasis of breast cancer cell lines and are pre
126 In contrast, the calculated pore size of a brain metastasis of breast cancer was approximately 10-f
128 l possesses the unique capability to examine brain metastasis of human lung, breast and melanoma cell
129 on with a dominant-negative Stat3 suppressed brain metastasis of human melanoma cells in animal model
132 R2 signaling for HER2-positive breast cancer brain metastasis.Oncogene advance online publication, 24
134 and < .001, respectively), whereas a single brain metastasis or initial treatment with SRS versus WB
135 ode status, along with a higher incidence of brain metastasis (P = 0.02) and a shorter brain metastas
139 of the 2 patients, subsequent resection of a brain metastasis proved HER2-positive disease, confirmin
140 time-activity curve can differentiate local brain metastasis recurrence from radionecrosis with high
147 gression, and death caused by progression of brain metastasis, seemed to be improved compared with hi
148 eviously, we reported a protein signature of brain metastasis showing increased ability of brain meta
149 f activated Stat3 is also increased in human brain metastasis specimens when compared with that in th
151 ancer (NSCLC) to try to improve incidence of brain metastasis, survival, and eventually quality of li
152 In this work, we developed a robust model of brain metastasis that empowers quantitative tracking of
154 w discusses recent advances in breast cancer brain metastasis therapy and potential approaches for su
155 d validated in a cohort of 128 patients with brain metastasis treated at the Cross Cancer Institute (
156 mouse model of HER2-amplified breast cancer brain metastasis using an orthotopic xenograft of BT474
159 for the correct identification of recurrent brain metastasis were evaluated by receiver-operating-ch
161 th a constitutively activated Stat3 enhanced brain metastasis, whereas blockade of Stat3 activation b
162 -713 in the intracerebrally induced model of brain metastasis, which was significantly greater than t
163 enriched patient population at high risk for brain metastasis will facilitate the design of trials ai
164 eir kind that provide insight into targeting brain metastasis with stem-cell mediated delivery of pro
165 ent (observation group, 46 patients) for the brain metastasis, with median follow-up of 48 weeks and
166 rvival in two murine models of breast cancer brain metastasis, without any apparent local or systemic
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