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1 le which was CNS penetrant in order to treat brain metastases.
2 py in patients with untreated or progressive brain metastases.
3 ted 20% of patients with cancer will develop brain metastases.
4 -life endpoints into trials of patients with brain metastases.
5 or retrospective study focusing on melanoma brain metastases.
6 secondary ALK kinase domain mutations and/or brain metastases.
7 r cohort and refine it integrating number of brain metastases.
8 for use in clinical trials of treatment for brain metastases.
9 what metabolic changes benefit breast cancer brain metastases.
10 ligand (123)I-DPA-713 for early detection of brain metastases.
11 tral radiological review of individuals with brain metastases.
12 rst-line treatment for gliomas and recurrent brain metastases.
13 us toward new perspectives in understanding brain metastases.
14 acardially into female BALB/c mice to induce brain metastases.
15 tastatic breast cancer eventually developing brain metastases.
16 rt tumor and confirmed partial resolution of brain metastases.
17 s in a rodent model of breast adenocarcinoma brain metastases.
18 of life are major concerns for patients with brain metastases.
19 rove the targeting of immune cell therapy of brain metastases.
20 ived from human cell lines or from patients' brain metastases.
21 inib has not been studied in active melanoma brain metastases.
22 Antitumour activity was also recorded in brain metastases.
23 was not associated with an increased risk of brain metastases.
24 cell lines for their ability to develop into brain metastases.
25 patients with EGFR-mutant NSCLC who develop brain metastases.
26 (GPA), a prognostic index for patients with brain metastases.
27 arnofsky performance score and the number of brain metastases.
28 r improve outcomes in patients with melanoma brain metastases.
29 d stratify clinical trials for patients with brain metastases.
30 ubbles can improve outcomes in breast cancer brain metastases.
31 he treatment of HER2-amplified breast cancer brain metastases.
32 y of this drug specifically in patients with brain metastases.
33 Two patients had previously treated brain metastases.
34 se with melanoma and untreated, asymptomatic brain metastases.
35 ificantly to the management of patients with brain metastases.
36 ary tumor growth and abrogating formation of brain metastases.
37 ndependence after surgery or radiosurgery of brain metastases.
38 estigational approaches in the management of brain metastases.
39 n and treatment of symptomatic breast cancer brain metastases.
40 despite increasing the invasive histology of brain metastases.
41 tracranial disease of 14 patients with known brain metastases.
42 n patients with NSCLC and previously treated brain metastases.
43 and memory in patients with newly diagnosed brain metastases.
44 trastuzumab or those who have HER2-negative brain metastases.
45 ose with squamous cell histology and treated brain metastases.
46 ) and HER-2, in patients with HER-2-positive brain metastases.
47 and whether the trial excluded patients with brain metastases.
48 re accumulating for targeted agents to treat brain metastases.
49 ghly refractory patients with HER-2-positive brain metastases.
50 -2 and EGFR was also observed in a subset of brain metastases.
51 atus, extracranial metastases, and number of brain metastases.
52 months from the time of initial treatment of brain metastases.
53 with non-small-cell lung cancer (NSCLC) and brain metastases.
54 free survival were measured from the date of brain metastases.
55 alternative therapies for the management of brain metastases.
56 patients with newly diagnosed and untreated brain metastases.
57 in patients with BRAF(V600)-mutant melanoma brain metastases.
58 alteration data for patients with NSCLC and brain metastases.
59 brain radiotherapy (WBRT) each year to treat brain metastases.
60 2006 and 2014 with NSCLC and newly diagnosed brain metastases.
61 ve longer and thus are at increased risk for brain metastases.
62 ls in the murine brain and in human melanoma brain metastases.
63 ry for a response to the antibodies in these brain metastases.
64 : the development of central nervous system (brain) metastases.
65 ohort study of 293 patients with cancer with brain metastases (104 with therapeutic enoxaparin and 18
66 through 2014 with NSCLC and newly diagnosed brain metastases (1521 adenocarcinoma and 665 nonadenoca
67 ed 52 patients with untreated or progressive brain metastases (18 with melanoma, 34 with NSCLC), and
69 s 17% (n=603), with subgroup ORR as follows: brain metastases (26 of 213 [12%]), ECOG performance sta
70 s population included 321 (7%) patients with brain metastases, 582 (13%) with Eastern Cooperative Onc
71 and HER2-negative primary breast cancers and brain metastases, (89)Zr-pertuzumab PET/CT suggested tha
73 tor 2 (HER-2)-positive breast cancer develop brain metastases; a subset progress in the CNS despite s
74 diosurgery or surgery of a limited number of brain metastases, adjuvant WBRT reduces intracranial rel
75 ndings suggest that for patients with 1 to 3 brain metastases amenable to radiosurgery, SRS alone may
76 f the brain because of the high incidence of brain metastases among patients with HER2-positive advan
78 f 94 patients with retrospectively confirmed brain metastases and at least one post-baseline MRI or C
79 Her-2 expression trends from resected human brain metastases and data from an experimental brain met
81 nstitutions with EGFR-mutant NSCLC developed brain metastases and met inclusion criteria for the stud
83 nt of metastatic melanoma are active against brain metastases and offer new opportunities to improve
84 GR cells had significantly more experimental brain metastases and shorter overall survival than did m
85 tes in the subclinical perivascular stage of brain metastases and show that they are inhibitable by p
86 s, we review the state of clinical trials of brain metastases and suggest a consensus recommendation
87 he inclusion of these endpoints in trials of brain metastases and the methods by which these measures
88 lity in decreasing the rapid growth of solid brain metastases and vasogenic edema in patients with ad
89 wo patients who had 83 previously irradiated brain metastases and who underwent (18)F-FDOPA PET becau
90 ts who have received prior therapy for their brain metastases and whose CNS disease is radiographical
91 ample, 66% had primary brain tumors, 27% had brain metastases, and 8% underwent prophylactic cranial
92 arise evidence for the treatment of melanoma brain metastases, and discuss the rationale and evidence
93 yroid dysfunction or diabetes, had no active brain metastases, and had not received previous immune c
94 1 is up-regulated on vessels associated with brain metastases, and if so, whether VCAM-1-targeted MRI
95 of 0 to 1, adequate organ function, treated brain metastases, and no recent vascular events or bleed
99 noma, expression of HLA*A0201, an absence of brain metastases, and suitability for high-dose interleu
100 Performance Status (KPS), gender, status of brain metastases, and the status of primary lung cancer.
112 PCI significantly reduced the probability of brain metastases as first site of failure (7.8% at 5 yea
113 nt or adjuvant chemotherapy, and presence of brain metastases as per investigator's assessment at scr
115 t of patients with follow-up had progressive brain metastases at death, and repeated interventions fo
116 ed to identify predictors of the presence of brain metastases at diagnosis and factors associated wit
117 estimates of the incidence and prognosis of brain metastases at diagnosis of breast cancer are lacki
122 etastases, defined as new and/or progressive brain metastases at the time of study entry; and those w
123 he incidence and prognosis for patients with brain metastases at time of diagnosis of breast cancer.
124 afts (PDXs) of HER2-expressing breast cancer brain metastases (BCBM), and their use for the identific
131 gnetic resonance imaging (MRI) to screen for brain metastases, but rather should have a low threshold
132 hage is frequently observed in patients with brain metastases, but that therapeutic anticoagulation d
133 ents with BRAF(V600)-mutant melanoma without brain metastases, but the median duration of response wa
134 frequently in patients with cancer who have brain metastases, but there is limited evidence supporti
138 tissue and was lower in patient tissue from brain metastases compared to same-patient primary tumour
139 ce of extracranial metastases, and number of brain metastases, confirming the original Lung-GPA.
140 st cancer, the incidence of life-threatening brain metastases continues to increase in some of these
141 Ib or IV; chemotherapy naive; no symptomatic brain metastases; deemed unsuitable for chemotherapy bec
142 lly stable at study entry; those with active brain metastases, defined as new and/or progressive brai
143 e key populations: those with treated/stable brain metastases, defined as patients who have received
144 ved drugs, sunitinib and dasatinib, prohibit brain metastases derived from breast cancer, addressing
145 actors found in 1833 patients with NSCLC and brain metastases diagnosed between 1985 and 2005: patien
148 HER2-positive breast cancer with progressive brain metastases during or after treatment with trastuzu
150 r day) in four patient cohorts with melanoma brain metastases enrolled from 32 hospitals and institut
153 stigated in patients with breast cancer with brain metastases for their ability to reduce CSFTC count
154 brain imaging can identify clinically silent brain metastases; frequency of detection might have incr
155 the emergence of resistance mutations and of brain metastases frequently causes relapse in patients.
159 ular morphologic changes during treatment of brain metastases from breast cancer and if serial quanti
161 nti-miR10b into mice bearing lung, bone, and brain metastases from breast cancer resulted in selectiv
163 (+) astrocytes were also identified in human brain metastases from eight craniotomy specimens and in
164 we show that outgrowth of large experimental brain metastases from human 231-BR or murine 4T1-BR brea
167 tor pembrolizumab in patients with untreated brain metastases from melanoma or non-small-cell lung ca
168 ) and dexamethasone are widely used to treat brain metastases from non-small cell lung cancer (NSCLC)
169 rain radiotherapy required to treat multiple brain metastases from non-small-cell lung cancer when hi
170 rgery or radiosurgery of a limited number of brain metastases from solid tumors may negatively impact
171 2009, we enrolled patients with melanoma and brain metastases from ten US centres who were older than
173 ble analysis of the breast-GPA and number of brain metastases (> three v </= three), both were indepe
174 gible patients were those with HER2-positive brain metastases (>/= 1 cm in longest dimension) who exp
176 Historically, the prognosis of patients with brain metastases has been poor; however, with new therap
182 trials in cancer, patients with symptomatic brain metastases have commonly been excluded from partic
183 with non-small-cell lung cancer (NSCLC) and brain metastases have previously been excluded from tria
184 hes to estimating prognosis of patients with brain metastases highlight the importance of tailoring t
185 sitive association between disease stage and brain metastases highlights a patient subset that may po
186 n of extracranial disease control, number of brain metastases, histology, maximal resection cavity di
187 RAF(V600)-mutant metastatic melanoma without brain metastases; however, the activity of dabrafenib pl
190 in patients with HER2-positive breast cancer brain metastases in a multicenter, phase II open-label t
192 ons regarding the inclusion of patients with brain metastases in clinical trials, as part of a broade
196 inhibitors (TKIs) are treatment options for brain metastases in patients with EGFR-mutant non-small-
199 rradiation not only reduces the incidence of brain metastases in patients with SCLC and with non-meta
200 rgery or radiosurgery of a limited number of brain metastases in patients with stable solid tumors.
201 wo-part series, we review clinical trials of brain metastases in relation to measures of clinical ben
203 sequences of detection of new or progressive brain metastases in trials mainly exploring the extra-CN
205 potential pathways to target ALK-rearranged brain metastases, including next generation ALK inhibito
206 val (OS) in patients with breast cancer with brain metastases, including the breast graded prognostic
208 We conclude that the T-cell response to brain metastases is not a surrogate of local tumor invas
210 eatment led to regression of EML4-ALK-driven brain metastases, leading to prolonged mouse survival, i
211 that are focused on other tumors, including brain metastases, leptomeningeal metastases, spine tumor
212 racking; (3) outcome prediction in epilepsy, brain metastases, lumbar spinal stenosis, lumbar disc he
216 that a subset of patients with asymptomatic brain metastases might be appropriately entered into pha
218 examined specific eligibility criteria (ie, brain metastases, minimum age, HIV infection, and organ
221 In patients with melanoma and untreated brain metastases, nine of ten patients had reductions in
222 organoids could be established directly from brain metastases not typically amenable to in vitro cult
223 ALK-positive non-small-cell lung cancer with brain metastases now have the potential to achieve a pro
225 uzumab most likely fails in the treatment of brain metastases of breast cancer because of poor CNS pe
226 or (PEDF) is downregulated in resected human brain metastases of breast cancer compared with primary
227 ormal breast tissues and stromal cultures of brain metastases of breast cancer had similar effects as
230 REP1 accumulation in a large number of human brain metastases of various solid tumors, including NSCL
232 Patients were excluded if they had active brain metastases or active autoimmune disease requiring
233 ate treatment is influenced by the number of brain metastases, overall patient performance status and
234 in some patients with advanced melanoma and brain metastases, particularly when metastases are small
237 ed the outgrowth of established experimental brain metastases, prolonging the survival of metastases-
238 The Quality of Life after Treatment for Brain Metastases (QUARTZ) study is a non-inferiority, ph
240 s of search terms and synonyms for melanoma, brain metastases, radiation, chemotherapy, immunotherapy
241 The Response Assessment in Neuro-Oncology Brain Metastases (RANO-BM) working group is an internati
242 for the correct identification of recurrent brain metastases reached 78% using TBR(max) (area under
243 metastasis and were selectively enriched in brain metastases relative to paired primary lung tumors.
247 igh-risk primary BC subgroups for developing brain metastases, represented by genetic alterations in
249 , CSFTC) of nine breast cancer patients with brain metastases revealed dynamic changes in tumor cell
250 ical to distinguish recurrent or progressive brain metastases (RPBM) from late or delayed radiation i
251 erlotinib in patients with NSCLC and treated brain metastases seems to be safe and is associated with
252 s Patients with treated or clinically stable brain metastases should be routinely included in trials
254 es whether patients with a limited number of brain metastases should undergo whole brain radiation th
255 cal review of trials specifically addressing brain metastases shows key issues that could prevent acc
256 had complete resection of one, two, or three brain metastases significantly lowers local recurrence c
258 ld enable substantially earlier detection of brain metastases than the current clinical approach of g
260 s is the first description of a patient with brain metastases that were characterised by restricted d
262 ger following the diagnosis and treatment of brain metastases, there has been rising concern about tr
263 of evidence of targeted therapy in melanoma brain metastases through an evaluation of dabrafenib plu
264 ailable specimens of matched fresh breast-to-brain metastases tissue and derived cells from patients
265 ge was conferred by the ability of breast-to-brain metastases to take up and catabolize GABA into suc
267 status [0 vs 1-2] and presence or absence of brain metastases) to oral ceritinib 750 mg per day faste
268 gnificantly larger fraction of breast cancer brain metastases tumor tissue compared with samples from
269 abase of 3,940 patients with newly diagnosed brain metastases underwent univariate and multivariate a
276 ratified by EGFR mutation type and status of brain metastases, was done centrally using a validated n
278 and no history of TKIs before development of brain metastases were associated with improved survival
281 (EGFR) mRNA levels in a cohort of 12 frozen brain metastases were increased up to 5- and 9-fold, res
282 s (n = 40) on MRI after radiation therapy of brain metastases were investigated with dynamic (18)F-FE
284 tions in North America, patients with 1 to 3 brain metastases were randomized to receive SRS or SRS p
285 Patients with one to three newly diagnosed brain metastases were randomly assigned using a standard
288 bsequent growth of bone metastases, although brain metastases were subject to rebound growth after th
289 izumab treatment, histology, and presence of brain metastases, were allocated (by computer-generated
290 specific role in spinal cord compression and brain metastases, where improved analgesia is a secondar
292 s a single-arm phase II study of HA-WBRT for brain metastases with prespecified comparison with a his
293 and had a complete resection of one to three brain metastases (with a maximum diameter of the resecti
294 BRAF(V600E)-positive, asymptomatic melanoma brain metastases, with no previous local brain therapy,
295 F(V600D/K/R)-positive, asymptomatic melanoma brain metastases, with or without previous local brain t
296 (V600D/E/K/R)-positive, symptomatic melanoma brain metastases, with or without previous local brain t
297 BRAF(V600E)-positive, asymptomatic melanoma brain metastases, with previous local brain therapy, and
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