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1 asia; NEL_INST: 11 patients, 33 lesions, all brain metastases).
2 in patients with HER2-positive breast cancer brain metastases.
3 (TLR) 9 agonist, CpG-C, is effective against brain metastases.
4 t to improve the treatment and prevention of brain metastases.
5 e to antiangiogenic treatment in gliomas and brain metastases.
6 here is a high risk of developing additional brain metastases.
7 ory accuracy in predicting the tumor type of brain metastases.
8 (62%) patients in the full analysis set had brain metastases.
9 velopment of gene and cell therapies against brain metastases.
10 ve longer and thus are at increased risk for brain metastases.
11 ted 20% of patients with cancer will develop brain metastases.
12 inib has not been studied in active melanoma brain metastases.
13 patients with EGFR-mutant NSCLC who develop brain metastases.
14 r improve outcomes in patients with melanoma brain metastases.
15 atus, extracranial metastases, and number of brain metastases.
16 months from the time of initial treatment of brain metastases.
17 with non-small-cell lung cancer (NSCLC) and brain metastases.
18 free survival were measured from the date of brain metastases.
19 alternative therapies for the management of brain metastases.
20 patients with newly diagnosed and untreated brain metastases.
21 in patients with BRAF(V600)-mutant melanoma brain metastases.
22 alteration data for patients with NSCLC and brain metastases.
23 brain radiotherapy (WBRT) each year to treat brain metastases.
24 with cancer hospitalized with a diagnosis of brain metastases.
25 2006 and 2014 with NSCLC and newly diagnosed brain metastases.
26 ls in the murine brain and in human melanoma brain metastases.
27 ry for a response to the antibodies in these brain metastases.
28 le which was CNS penetrant in order to treat brain metastases.
29 py in patients with untreated or progressive brain metastases.
30 -life endpoints into trials of patients with brain metastases.
31 or retrospective study focusing on melanoma brain metastases.
32 secondary ALK kinase domain mutations and/or brain metastases.
33 r cohort and refine it integrating number of brain metastases.
34 for use in clinical trials of treatment for brain metastases.
35 what metabolic changes benefit breast cancer brain metastases.
36 ligand (123)I-DPA-713 for early detection of brain metastases.
37 tral radiological review of individuals with brain metastases.
38 rst-line treatment for gliomas and recurrent brain metastases.
39 us toward new perspectives in understanding brain metastases.
40 acardially into female BALB/c mice to induce brain metastases.
41 tastatic breast cancer eventually developing brain metastases.
42 rt tumor and confirmed partial resolution of brain metastases.
43 s in a rodent model of breast adenocarcinoma brain metastases.
44 physiology, both for primary gliomas and for brain metastases.
45 ormance status of 2, and 18% of patients had brain metastases.
46 trategies for primary brain malignancies and brain metastases.
47 trast to (18)F-FDG PET, immuno-PET disclosed brain metastases.
48 ugs against primary brain tumours as well as brain metastases.
49 monotherapy for HER2-positive breast cancer brain metastases.
50 f pembrolizumab to treat small, asymptomatic brain metastases.
51 is safe in selected patients with untreated brain metastases.
52 tumor burden and reduced the average size of brain metastases.
53 mptoms and signs related to mass effect from brain metastases.
54 ry, ALK-positive NSCLC, including those with brain metastases.
55 ohort study of 293 patients with cancer with brain metastases (104 with therapeutic enoxaparin and 18
56 through 2014 with NSCLC and newly diagnosed brain metastases (1521 adenocarcinoma and 665 nonadenoca
57 ed 52 patients with untreated or progressive brain metastases (18 with melanoma, 34 with NSCLC), and
59 and HER2-negative primary breast cancers and brain metastases, (89)Zr-pertuzumab PET/CT suggested tha
62 mainstay of treatment for many patients with brain metastases, a growing number of systemic options a
63 vailable treatment options for patients with brain metastases, a multidisciplinary approach is strong
65 inst refractory, HER2-positive breast cancer brain metastases, adding additional evidence that the ef
66 tastatic breast cancer, including those with brain metastases, adding tucatinib to trastuzumab and ca
67 ter local treatment of one to three melanoma brain metastases, adjuvant WBRT does not provide clinica
68 aim to characterize patients with cancer and brain metastases admitted to hospitals nationwide and id
69 proximately 3% of patients hospitalized with brain metastases also had a diagnosis of ICH, which was
70 ndings suggest that for patients with 1 to 3 brain metastases amenable to radiosurgery, SRS alone may
71 f the brain because of the high incidence of brain metastases among patients with HER2-positive advan
73 f 94 patients with retrospectively confirmed brain metastases and at least one post-baseline MRI or C
74 ts in neurological outcome for patients with brain metastases and could potentially be tested in othe
76 nstitutions with EGFR-mutant NSCLC developed brain metastases and met inclusion criteria for the stud
78 nt of metastatic melanoma are active against brain metastases and offer new opportunities to improve
79 he treatment and management of patients with brain metastases and provide speculation on future resea
80 reclinical model of breast cancer-associated brain metastases and support continued investigation int
81 signaling in the promotion of breast cancer brain metastases and support the prognostic and therapeu
82 trate that somatic alterations contribute to brain metastases and that genomic sequencing of a suffic
83 models are critical to study the biology of brain metastases and to identify effective therapeutic a
84 wo patients who had 83 previously irradiated brain metastases and who underwent (18)F-FDOPA PET becau
85 ts who have received prior therapy for their brain metastases and whose CNS disease is radiographical
86 ample, 66% had primary brain tumors, 27% had brain metastases, and 8% underwent prophylactic cranial
87 comprised patients with previously untreated brain metastases, and cohort B comprised patients whose
88 arise evidence for the treatment of melanoma brain metastases, and discuss the rationale and evidence
89 yroid dysfunction or diabetes, had no active brain metastases, and had not received previous immune c
90 of 0 to 1, adequate organ function, treated brain metastases, and no recent vascular events or bleed
91 Performance Status (KPS), gender, status of brain metastases, and the status of primary lung cancer.
96 as peripheral metastases, but patients with brain metastases are generally excluded because of the l
101 as options for VTE treatment; patients with brain metastases are now addressed in the VTE treatment
106 (70% [53-83]) of 40 patients with measurable brain metastases as assessed by the independent review c
107 nt or adjuvant chemotherapy, and presence of brain metastases as per investigator's assessment at scr
108 fied analyses based on prior cancer therapy, brain metastases at baseline, and sex showed similar tre
110 t of patients with follow-up had progressive brain metastases at death, and repeated interventions fo
111 ed to identify predictors of the presence of brain metastases at diagnosis and factors associated wit
112 estimates of the incidence and prognosis of brain metastases at diagnosis of breast cancer are lacki
114 atients with ROS1 fusion-positive NSCLC have brain metastases at the diagnosis of advanced disease.
118 the years 2010 through 2012 had synchronous brain metastases at the time of diagnosis, and Medicare
119 etastases, defined as new and/or progressive brain metastases at the time of study entry; and those w
120 he incidence and prognosis for patients with brain metastases at time of diagnosis of breast cancer.
122 afts (PDXs) of HER2-expressing breast cancer brain metastases (BCBM), and their use for the identific
123 ed with increased incidence of breast cancer brain metastases (BCBM), but the mechanisms underlying t
129 lapsed (BCR) and their paired (n = 40 pairs) brain metastases (BM) using the NanoString(TM) nCounter(
132 eceptor 2 (HER2)-positive breast cancer with brain metastases (BMs) showed statistically significant
134 cluding low-grade and high-grade gliomas and brain metastases (BrMs) originating from diverse extracr
135 PDGFB protein expression was prognostic for brain metastases, but not metastases to other sites.
136 gnetic resonance imaging (MRI) to screen for brain metastases, but rather should have a low threshold
137 hage is frequently observed in patients with brain metastases, but that therapeutic anticoagulation d
138 ents with BRAF(V600)-mutant melanoma without brain metastases, but the median duration of response wa
139 frequently in patients with cancer who have brain metastases, but there is limited evidence supporti
141 rogression-free survival among patients with brain metastases, confirmed objective response rate, and
142 st cancer, the incidence of life-threatening brain metastases continues to increase in some of these
144 lly stable at study entry; those with active brain metastases, defined as new and/or progressive brai
145 e key populations: those with treated/stable brain metastases, defined as patients who have received
146 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
151 r day) in four patient cohorts with melanoma brain metastases enrolled from 32 hospitals and institut
152 xpanding treatment options for patients with brain metastases, enrolment in clinical trials is essent
153 anticoagulation carefully for patients with brain metastases, especially those with melanoma and kid
156 stigated in patients with breast cancer with brain metastases for their ability to reduce CSFTC count
157 the emergence of resistance mutations and of brain metastases frequently causes relapse in patients.
161 nti-miR10b into mice bearing lung, bone, and brain metastases from breast cancer resulted in selectiv
162 ntiangiogenic therapies, but its activity on brain metastases from ccRCC remains unknown, because the
164 FR and ALK inhibitors have shown activity on brain metastases from EGFR and ALK mutant non-small-cell
165 New inhibitors are being investigated in brain metastases from ER-positive or triple-negative bre
169 tor pembrolizumab in patients with untreated brain metastases from melanoma or non-small-cell lung ca
170 ) and dexamethasone are widely used to treat brain metastases from non-small cell lung cancer (NSCLC)
171 rain radiotherapy required to treat multiple brain metastases from non-small-cell lung cancer when hi
173 e analysis included radiomic features of 658 brain metastases from T1-weighted contrast material-enha
175 ecially feared complication in patients with brain metastases given the potential for significant mor
176 ble analysis of the breast-GPA and number of brain metastases (> three v </= three), both were indepe
177 gible patients were those with HER2-positive brain metastases (>/= 1 cm in longest dimension) who exp
179 Historically, the prognosis of patients with brain metastases has been poor; however, with new therap
180 f the biology and molecular underpinnings of brain metastases has greatly improved, resulting in more
188 n of extracranial disease control, number of brain metastases, histology, maximal resection cavity di
189 RAF(V600)-mutant metastatic melanoma without brain metastases; however, the activity of dabrafenib pl
190 primary breast tumors, and in patients with brain metastases, hypoxic signaling within CTCs predicts
194 in patients with HER2-positive breast cancer brain metastases in a multicenter, phase II open-label t
195 ith MRI radiomic image features of different brain metastases in a multiclass machine learning approa
198 ons regarding the inclusion of patients with brain metastases in clinical trials, as part of a broade
202 inhibitors (TKIs) are treatment options for brain metastases in patients with EGFR-mutant non-small-
205 rradiation not only reduces the incidence of brain metastases in patients with SCLC and with non-meta
208 s required to optimally manage patients with brain metastases, including consideration of radiation t
209 potential pathways to target ALK-rearranged brain metastases, including next generation ALK inhibito
210 val (OS) in patients with breast cancer with brain metastases, including the breast graded prognostic
211 Furthermore, overexpression of YTHDF3 in brain metastases is attributed to increased gene copy nu
212 We conclude that the T-cell response to brain metastases is not a surrogate of local tumor invas
213 eatment led to regression of EML4-ALK-driven brain metastases, leading to prolonged mouse survival, i
214 egulation of SERPINB1, a protein elevated in brain metastases, led to a reduction in brain metastasis
215 that are focused on other tumors, including brain metastases, leptomeningeal metastases, spine tumor
216 racking; (3) outcome prediction in epilepsy, brain metastases, lumbar spinal stenosis, lumbar disc he
220 examined specific eligibility criteria (ie, brain metastases, minimum age, HIV infection, and organ
221 may benefit NSCLC patients with synchronous brain metastases more than it does patients without intr
223 organoids could be established directly from brain metastases not typically amenable to in vitro cult
224 ALK-positive non-small-cell lung cancer with brain metastases now have the potential to achieve a pro
225 velop brain metastases, with the majority of brain metastases occurring in those with lung, breast an
226 uzumab most likely fails in the treatment of brain metastases of breast cancer because of poor CNS pe
227 ormal breast tissues and stromal cultures of brain metastases of breast cancer had similar effects as
229 in tumours, which face similar challenges to brain metastases of extracranial origin, and vice versa.
230 expression of PDGFRbeta(D849V) also promoted brain metastases of mammary tumor cells expressing high
231 REP1 accumulation in a large number of human brain metastases of various solid tumors, including NSCL
232 45,225 hospitalizations were associated with brain metastases, of which 4,145 (2.85%) had a concurren
233 Patients were excluded if they had active brain metastases or active autoimmune disease requiring
235 The Quality of Life after Treatment for Brain Metastases (QUARTZ) study is a non-inferiority, ph
236 s of search terms and synonyms for melanoma, brain metastases, radiation, chemotherapy, immunotherapy
237 The Response Assessment in Neuro-Oncology Brain Metastases (RANO-BM) working group is an internati
238 he 6-month and 12-month freedom from distant brain metastases rates were 74.1% and 68.8%, respectivel
239 our newly improved models of patient-derived brain metastases recapitulate the histologic, molecular,
240 derstanding the molecular characteristics of brain metastases relative to the primary tumour so that
245 3-mediated astrocyte reactivity in rats with brain metastases restored cerebrovascular function, as s
246 radiation to the surgical cavity of resected brain metastases results in low rates of local failure.
247 , CSFTC) of nine breast cancer patients with brain metastases revealed dynamic changes in tumor cell
248 ical to distinguish recurrent or progressive brain metastases (RPBM) from late or delayed radiation i
249 s Patients with treated or clinically stable brain metastases should be routinely included in trials
251 had complete resection of one, two, or three brain metastases significantly lowers local recurrence c
252 s in understanding the mechanisms that drive brain metastases so that they can be targeted with preve
253 ld enable substantially earlier detection of brain metastases than the current clinical approach of g
254 gle-shot detector models detected nearly all brain metastases that were 6 mm or larger with limited f
255 s is the first description of a patient with brain metastases that were characterised by restricted d
257 ger following the diagnosis and treatment of brain metastases, there has been rising concern about tr
258 of evidence of targeted therapy in melanoma brain metastases through an evaluation of dabrafenib plu
259 ailable specimens of matched fresh breast-to-brain metastases tissue and derived cells from patients
260 ng cancer (NSCLC) or melanoma with untreated brain metastases to determine the activity of PD-1 block
261 phase III trial enrolled adult patients with brain metastases to HA-WBRT plus memantine or WBRT plus
262 ung cancer (NSCLC) patients with synchronous brain metastases to identify predictors of the decision
263 ge was conferred by the ability of breast-to-brain metastases to take up and catabolize GABA into suc
265 status [0 vs 1-2] and presence or absence of brain metastases) to oral ceritinib 750 mg per day faste
266 astuzumab emtansine, who had or did not have brain metastases, to receive either tucatinib or placebo
270 f orthotopic mouse models of patient-derived brain metastases via an improved intracarotid injection
274 ratified by EGFR mutation type and status of brain metastases, was done centrally using a validated n
275 To identify genomic alterations that promote brain metastases, we performed whole-exome sequencing of
277 and no history of TKIs before development of brain metastases were associated with improved survival
284 tions in North America, patients with 1 to 3 brain metastases were randomized to receive SRS or SRS p
285 had local treatment of one to three melanoma brain metastases were randomly assigned to WBRT or obser
287 izumab treatment, histology, and presence of brain metastases, were allocated (by computer-generated
288 specific role in spinal cord compression and brain metastases, where improved analgesia is a secondar
291 formance status who plan to receive WBRT for brain metastases with no metastases in the HA region.
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
298 20% of all patients with cancer will develop brain metastases, with the majority of brain metastases