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1 in the placebo group (sepsis, pneumonia, and metastatic breast cancer).
2 chemotherapeutic agent for the patients with metastatic breast cancer.
3 sured immunohistochemically in patients with metastatic breast cancer.
4 t PLD2 as a potential therapeutic target for metastatic breast cancer.
5 s from 170 patients with locally relapsed or metastatic breast cancer.
6 crine-refractory, estrogen receptor-positive metastatic breast cancer.
7 es in clinical and translational research in metastatic breast cancer.
8 than two previous lines of chemotherapy for metastatic breast cancer.
9 tients with hormonal therapy-resistant (HTR) metastatic breast cancer.
10 efore CT in most participants with bone-only metastatic breast cancer.
11 on of distant metastases in a mouse model of metastatic breast cancer.
12 , phase 3 equivalence study in patients with metastatic breast cancer.
13 genic effect of WAT progenitors on local and metastatic breast cancer.
14 e receptor-negative, HER2-negative recurrent metastatic breast cancer.
15 ights into a better understanding of distant metastatic breast cancer.
16 (mTOR) are currently used to treat advanced metastatic breast cancer.
17 and opportunities for precision treatment of metastatic breast cancer.
18 s without prior treatment for ERBB2-positive metastatic breast cancer.
19 sistance in estrogen receptor-positive (ER+) metastatic breast cancer.
20 the role of bone-modifying agents (BMAs) in metastatic breast cancer.
21 curement; and redesign of clinical trials in metastatic breast cancer.
22 ical activity in patients with HER2-positive metastatic breast cancer.
23 th or without pertuzumab in US patients with metastatic breast cancer.
24 py may be a promising treatment strategy for metastatic breast cancer.
25 n of this enzyme as a therapeutic target for metastatic breast cancer.
26 ormone receptor-positive locally advanced or metastatic breast cancer.
27 nce is crucial for treatment optimisation in metastatic breast cancer.
28 lyzed lesions affects response assessment in metastatic breast cancer.
29 resistance is a key therapeutic challenge in metastatic breast cancer.
30 relbine for such patients with HER2-positive metastatic breast cancer.
31 vasation, and metastasis in a mouse model of metastatic breast cancer.
32 ubtype and outcome in first-line HR-positive metastatic breast cancer.
33 as a therapeutic approach for patients with metastatic breast cancer.
34 wth factor receptor 2 (HER2) -overexpressing metastatic breast cancer.
35 th fulvestrant plus placebo in patients with metastatic breast cancer.
36 ase overall survival in a xenograft model of metastatic breast cancer.
37 response assessment with (18)F-FDG PET/CT in metastatic breast cancer.
38 or benefit in hormone receptor (HR)-positive metastatic breast cancer.
39 o 30% of women eventually relapse and die of metastatic breast cancer.
40 inhibitor (AI) therapy in patients with ER+ metastatic breast cancer.
41 nemia in patients receiving chemotherapy for metastatic breast cancer.
42 the 12 relapses seen, 2 were due to distant metastatic breast cancer.
43 iR-31) has been shown to be overexpressed in metastatic breast cancer.
44 cy of mTORC1, CDK4/6, and PARP inhibitors in metastatic breast cancer.
45 an individual's predilection for developing metastatic breast cancer.
46 reported in the literature for patients with metastatic breast cancer.
47 nt CTC as a clinically relevant biomarker in metastatic breast cancer.
48 as a strategy to treat solid tumors such as metastatic breast cancer.
49 ith previously treated, locally recurrent or metastatic breast cancer.
50 d the landscape of therapy for patients with metastatic breast cancer.
51 s of metastatic disease in a murine model of metastatic breast cancer.
52 al concern in the treatment of HER2-positive metastatic breast cancer.
53 50 postmenopausal women who later developed metastatic breast cancer.
54 hed in the peripheral blood of patients with metastatic breast cancer.
55 taxel in unresectable, locally recurrent, or metastatic breast cancer.
56 f trastuzumab in patients with HER2-positive metastatic breast cancer.
57 of hormone receptor-positive, HER2-negative metastatic breast cancer.
58 entiality of RNA metabolism that impinges on metastatic breast cancer.
59 at promise in the diagnosis and treatment of metastatic breast cancer.
60 eceptor-positive, HER2-negative, advanced or metastatic breast cancer.
61 and docetaxel in patients with HER2-positive metastatic breast cancer.
62 with germline BRCA1-mutated or BRCA2-mutated metastatic breast cancer.
63 erve as an attractive therapeutic target for metastatic breast cancer.
64 erapy and molecularly targeted therapies for metastatic breast cancer.
65 targets for treating endocrine-resistant and metastatic breast cancer.
66 uency of six known driver genes increases in metastatic breast cancer.
67 in hormone receptor-positive, HER2-negative, metastatic breast cancer.
68 ated efficacy in patients with BRCA-positive metastatic breast cancer.
69 int blockers in mice with primary as well as metastatic breast cancer.
70 ith hormone-receptor-positive, HER2-negative metastatic breast cancer.
71 ondrial membrane augments progression toward metastatic breast cancer.
72 CDK4/6 inhibitors for treating patients with metastatic breast cancer.
73 eceptor-positive (ER(+)) endocrine-resistant metastatic breast cancer.
74 re more frequently observed in HR(+)/HER2(-) metastatic breast cancers.
75 f eliminating ERalpha expression in advanced metastatic breast cancers.
76 as an effective target for the treatment of metastatic breast cancers.
77 ld offer a therapeutic target for aggressive metastatic breast cancers.
78 the landscape of somatic alterations in 617 metastatic breast cancers.
79 n several cancer cell lines including murine metastatic breast cancer 4T1, murine glioblastoma GL261,
80 breast cancers from two patient cohorts (149 metastatic breast cancers, 63 untreated primary tumors,
81 sents a novel therapeutic strategy to combat metastatic breast cancer, a disease that has had no redu
82 tcome in patients with ERBB2 (HER2)-positive metastatic breast cancer; a clinically effective biosimi
83 t in Hormone Receptor-Positive HER2-Negative Metastatic Breast Cancer After Endocrine Failure) trial,
85 host-intrinsic factor mediating evolution of metastatic breast cancer allows for development of inter
86 efficacy in estrogen receptor (ER)-positive metastatic breast cancer, although their cytostatic effe
87 mising potential as an effective therapy for metastatic breast cancer and a broader patient populatio
89 She had been diagnosed 10 years earlier with metastatic breast cancer and hadn't been sure she wanted
90 study provides insights into the biology of metastatic breast cancer and identifies clinically usefu
92 vestigate the effects of age at diagnosis on metastatic breast cancer and patients' prognosis, we col
93 trate the utility of ARM in the detection of metastatic breast cancer and the identification of prost
94 various mechanisms that shape the genome of metastatic breast cancer and the value of studying advan
95 Understanding the etiology of recurrent or metastatic breast cancer and underlying mechanisms is cr
96 1) mutations occur frequently in ER-positive metastatic breast cancer, and confer clinical resistance
97 cancer cell lines tested (two glioblastoma, metastatic breast cancer, and fibrosarcoma) migrated dir
98 n Csf1r+ myeloid cells associated with human metastatic breast cancer, and levels of these miRs in CD
99 emcitabine had shown significant activity in metastatic breast cancer, and there was evidence of a fa
100 n the placebo group; most deaths were due to metastatic breast cancer, and two were considered treatm
101 represents a potential therapeutic target in metastatic breast cancer, as its histone-binding capabil
102 sed to treat estrogen receptor (ER)-positive metastatic breast cancer (BC) in combination with endocr
104 evolution in a patient (index patient) with metastatic breast cancer bearing an activating PIK3CA (p
106 egrader (SERD), fulvestrant, is effective in metastatic breast cancer, but limited by poor pharmacoki
107 circulating tumour cell (CTC) line, MCF-7, a metastatic breast cancer by targeting epithelial cellula
108 investigate whether intrinsic properties of metastatic breast cancer cell growth can be regulated th
112 ation of two small EV sub-populations from a metastatic breast cancer cell line, with biochemical fea
113 rget miRs in total RNA (RNAt) extracted from metastatic breast cancer cell lines and human tissues.
115 tor (EGF)-mediated chemotaxis and CIL guides metastatic breast cancer cell motility, whereby cells be
116 e failure of producing E-cadherin protein in metastatic breast cancer cells after overexpressing E-ca
117 hich these procedures reduce the presence of metastatic breast cancer cells among the isolated follic
118 s where Runx2 is not detected, and absent in metastatic breast cancer cells and tissue biopsies that
119 ostaglandin E2 release could be abrogated in metastatic breast cancer cells by inhibition of iPLA2.
120 s simulations of the active cytoskeleton, on metastatic breast cancer cells embedded in a three-dimen
121 t al. now show that two tRNAs upregulated in metastatic breast cancer cells enhance stability and tra
124 tream of the HER2 driver oncogene in SUM-225 metastatic breast cancer cells from dynamic gene express
125 Moreover, we found that GIT1 depletion in metastatic breast cancer cells greatly reduced alpha5bet
127 of mice after injection of metastatic or non-metastatic breast cancer cells in 4T1.2 BALB/cJ and MDA-
129 model, that the plasticity of at least some metastatic breast cancer cells is dependent on the trans
130 and when PAK1 is depleted, brain tropism of metastatic breast cancer cells is significantly reduced,
131 Silencing OMA1 in vitro in patient-derived metastatic breast cancer cells isolated from the metasta
132 s to inhibit E-cadherin-mediated survival in metastatic breast cancer cells may have potential as a t
133 ning of naive mice with exosomes from highly metastatic breast cancer cells revealed the accumulation
134 y reduce plasma membrane PI(4,5)P2 levels in metastatic breast cancer cells through two independent m
135 that loss of CBFbeta inhibits the ability of metastatic breast cancer cells to invade bone cell cultu
138 in vivo in controlling multiple myelomas and metastatic breast cancer cells, in the latter case also
139 the PDZ-binding motif of Claudin-2 in liver metastatic breast cancer cells, including Afadin, Arhgap
140 gnificantly increase migratory properties in metastatic breast cancer cells, indicating that OMA1 pla
141 ial breast cells and patient-derived primary metastatic breast cancer cells, mesothelioma cells, and
142 ulations, and 3D chemotaxis assays on single metastatic breast cancer cells, we investigate the links
145 ytes in the bone marrow of 6/8 patients with metastatic breast cancer compared with age- and gender-m
146 improves clinical outcomes in patients with metastatic breast cancer compared with docetaxel treatme
147 ivation of PKCzeta signaling in invasive and metastatic breast cancers compared to non-invasive disea
148 ive, carcinoembryonic antigen (CEA)-positive metastatic breast cancer, compared with CT, bone MRI, an
151 ce to a class I PI3K inhibitor in a model of metastatic breast cancer driven by PI3K and MYC was asso
152 imes and the four markers mainly involved in metastatic breast cancer (EPCAM, CD47, CD44 and MET).
153 tients with previously treated HER2-positive metastatic breast cancer even in the presence of crossov
154 mal growth factor receptor 2 (HER2)-positive metastatic breast cancer eventually develop resistance t
156 r whether bone regions typically targeted by metastatic breast cancer feature distinct HA materials p
157 r the treatment of hormone-receptor-positive metastatic breast cancer following antiestrogen therapy.
158 eptor-positive, or both, locally advanced or metastatic breast cancer from 113 academic hospitals and
159 four initial cohorts: germline BRCA-mutated, metastatic breast cancer; germline BRCA-mutated, metasta
160 s were 18 years or older, had HER2-positive, metastatic breast cancer, had not received previous chem
161 Patients presenting with de novo stage IV metastatic breast cancer have a complex disease which is
162 Currently, antiangiogenic strategies in metastatic breast cancer have demonstrated modest improv
163 rns of genomic evolution between primary and metastatic breast cancer have not been studied in large
165 MM-302/trastuzumab therapy for HER2-positive metastatic breast cancer in a randomized phase II clinic
166 10 positively correlated with progression of metastatic breast cancer in clinical patient tumour samp
169 epidermal growth factor receptor 2-negative metastatic breast cancer in older women compared with yo
170 th stage-dependent targeting in mice bearing metastatic breast cancer in the bone, and carried out st
171 selective activation of hypoxic signaling by metastatic breast cancer in the brain may have therapeut
173 have shown little efficacy in patients with metastatic breast cancer, in part because of the low num
174 ficacy in MDA-MB-231 and 4T1 mouse models of metastatic breast cancer, including functional cures in
175 avily pretreated patients with HER2-positive metastatic breast cancer, including those with brain met
178 er-expressed in metastatic breast cancer yet metastatic breast cancer is generally resistant to anti-
184 of endocrine treatment for bone-predominant metastatic breast cancer, K(i) more reliably differentia
185 the combination of PANVAC with docetaxel in metastatic breast cancer may provide a clinical benefit.
186 ther assessment of potential bone lesions in metastatic breast cancer (MBC) by (18)F-FDG PET instead
187 mal growth factor receptor 2 (HER2)-negative metastatic breast cancer (MBC) in germline (g)BRCA1/2 mu
189 ptimal frequency of monitoring patients with metastatic breast cancer (MBC) is unknown; however, data
190 atment patterns and outcomes are unclear for metastatic breast cancer (MBC) patients diagnosed with h
192 gen receptor alpha (ESR1) mutations found in metastatic breast cancer (MBC) promote ligand-independen
193 vival (OS) in patients with locally advanced/metastatic breast cancer (MBC) regardless of visceral or
194 h we have established a few risk factors for metastatic breast cancer (MBC) through epidemiologic stu
195 tion markers to predict survival outcomes in metastatic breast cancer (MBC) using a new quantitative
196 al growth factor receptor 2 (HER2)-positive, metastatic breast cancer (MBC) who previously received t
203 e absence of ligand are acquired by >=40% of metastatic breast cancers (MBC) resistant to adjuvant ar
206 n, but patients with luminal A/HER2-negative metastatic breast cancer might be good candidates for le
207 ral tumor implantation technique in a murine metastatic breast cancer model (E0771) coupled with anti
208 nd that stable SDPR overexpression in highly metastatic breast cancer model cell lines inhibited pros
210 erations that were enriched in HR(+)/HER2(-) metastatic breast cancers, mutations in TP53, RB1 and NF
211 zed clinical trial enrolled 48 patients with metastatic breast cancer of all subtypes, without limita
212 ally, our investigations in the 4T1 model of metastatic breast cancer of the V-ATPase inhibitor archa
213 /EBPdelta expression is not abundant in most metastatic breast cancers, our data support a pro-tumori
217 aging method for HER2-negative, CEA-positive metastatic breast cancer patients and warrants further r
218 C expressing vimentin and TF in the blood of metastatic breast cancer patients consistent with our ob
221 e assayed in clinical trial samples from ER+ metastatic breast cancer patients randomized either to t
222 onal study of 102 postmenopausal, HR + HER2- metastatic breast cancer patients treated with everolimu
224 pes and liver metastasis on the prognosis of metastatic breast cancer patients who received combined
225 one metastases occur in approximately 70% of metastatic breast cancer patients, often leading to skel
226 e cells is present in the bone marrow of non-metastatic breast cancer patients, only part of which ar
232 inical efficacy of docetaxel and thiotepa on metastatic breast cancer patients; and metastatic sites
233 ountries, patients with locally recurrent or metastatic breast cancer previously treated with an anth
234 andomly assigned patients with HER2-positive metastatic breast cancer previously treated with trastuz
235 the treatment of patients with HER2-positive metastatic breast cancer previously treated with trastuz
236 2-positive unresectable, locally advanced or metastatic breast cancer previously treated with trastuz
239 ith hormone-receptor-positive, HER2-negative metastatic breast cancer, published between Jan 1, 2000,
240 al growth factor receptor 2 (HER2) -positive metastatic breast cancer, raising interest in evaluating
241 n of outcomes in patients with HER2-positive metastatic breast cancer randomized to an antibody-based
242 epidermal growth factor receptor 2-positive metastatic breast cancer receiving lapatinib-capecitabin
245 currently being used to treat HER2-positive metastatic breast cancer, relapsed or refractory Hodgkin
248 mal growth factor receptor 2 (HER2)-negative metastatic breast cancer represents a major milestone in
249 ected tissue biopsies from 442 patients with metastatic breast cancer reveals that, compared to prima
250 s more closely resemble the transcriptome of metastatic breast cancer samples compared to cell lines.
251 e closely resemble the different subtypes of metastatic breast cancer seen in the clinic and show tha
253 and plasma samples in a single patient with metastatic breast cancer shows that circulating tumour D
254 lood from healthy donors and from women with metastatic breast cancer stored under ambient conditions
256 therapy and lack of curative treatments for metastatic breast cancer suggest that current therapies
257 ults point to a new therapeutic strategy for metastatic breast cancers targeted to the mitochondrial
258 ith hormone-receptor-positive, HER2-negative metastatic breast cancer that had progressed on previous
259 ent hormone-receptor-positive, HER2-negative metastatic breast cancer that has progressed on previous
260 ledronic acid every 4 weeks in patients with metastatic breast cancer that involved the bone who had
262 C8A and RB1) were more frequently mutated in metastatic breast cancers that expressed hormone recepto
265 ntries and randomized 652 with HER2-positive metastatic breast cancer to receive trastuzumab or lapat
266 nal control for selected patients with early metastatic breast cancer treated with breast-conserving
267 Finally, in a pre-clinical murine model of metastatic breast cancer, treatment with Ambrisentan was
268 of Claudin-2 and/or Afadin expression in 206 metastatic breast cancer tumors revealed that high level
270 ith hormone-receptor-positive, HER2-negative metastatic breast cancer, upfront use of chemotherapy re
271 insic subtyping in hormone receptor-positive metastatic breast cancer warrants further investigation,
274 cally confirmed, progressive, HER2-negative, metastatic breast cancer were enrolled from 14 health ce
277 ials using (18)F-FES PET/CT in patients with metastatic breast cancer were performed at Memorial Sloa
279 iving first- or second-line chemotherapy for metastatic breast cancer, were randomly assigned to EPO
280 re remains highly relevant in the setting of metastatic breast cancer, where surgical decisions shoul
281 ng miR-17 has been linked to lung cancer and metastatic breast cancer, while its decrease has been fo
282 usal patients with hormone receptor-positive metastatic breast cancer who had been randomly assigned
283 atic biopsies from eight patients with ER(+) metastatic breast cancer who had developed resistance to
284 estrogen receptor-positive, locally advanced/metastatic breast cancer who had no previous therapy for
286 with HR-positive, HER2-negative recurrent or metastatic breast cancer who had not received previous s
287 led female patients with HER2-overexpressing metastatic breast cancer who had progressed on or follow
288 nt of choice for patients with HER2-positive metastatic breast cancer who had progressed on trastuzum
289 mal growth factor receptor 2 (HER2)-negative metastatic breast cancer who had received <=2 chemothera
290 mal growth factor receptor 2 (HER2)-positive metastatic breast cancer who have disease progression af
291 ormone receptor-positive locally advanced or metastatic breast cancer who have not received previous
292 s 3 + 3 dose-escalation study, patients with metastatic breast cancer who progressed on trastuzumab,
293 positive, HER2-negative, locally advanced or metastatic breast cancer, who had relapsed on or after e
294 ER2)-negative inoperable locally advanced or metastatic breast cancer whose disease had progressed on
295 for the treatment of locally advanced and/or metastatic breast cancer with germline BRCA1/2 deleterio
296 mal growth factor receptor 2 (HER2)-negative metastatic breast cancer with prior clinical benefit fro
297 ic strategy for the treatment of a subset of metastatic breast cancer with ZNF367 overexpression.
298 changed the natural history of HER2-positive metastatic breast cancer, with the dual blockade of pert
299 eceptor (EGFR) is commonly over-expressed in metastatic breast cancer yet metastatic breast cancer is