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1                                              MBC and EPS, both increased ~1.5X and ~3X due to drying
2                                              MBC subtypes exhibit distinct upregulated profiles, incl
3                                              MBC-like WM harbored significantly more clonal CXCR4 mut
4                                              MBC-like WM hypomethylation was enriched in motifs belon
5                                              MBCs capable of neutralizing distinct subclasses of path
6  with IgG(2)(+) MBCs; and (6) with IgA(1)(+) MBCs.
7 witched MBCs without and; (5) with IgG(2)(+) MBCs; and (6) with IgA(1)(+) MBCs.
8                                          225 MBC samples were immunostained for HMG-CoAR and 124 were
9 was evaluated by immunohistochemistry in 289 MBC samples to assess their association.
10 ve CD27(+) MBCs with almost normal IgG(3)(+) MBCs; (3) absence of switched MBCs; and (4) presence of
11 nd against the bacteria tested, with a 0.37% MBC v/v for E. coli and 0.18% v/v for the other bacteria
12                             We assembled 446 MBCs on tissue microarrays and assessed clinicopathologi
13 on with inflammation and increased activated MBC frequencies in neonates.
14                                    Activated MBCs were also induced by TT booster immunization, indic
15 acious for the treatment of locally advanced/MBC for patients with bone, liver, lung, lymph node, and
16 64 pretreated patients with locally advanced/MBC from studies 301 and 305.
17 fficacious in patients with locally advanced/MBC, irrespective of the location of metastases at basel
18 oint to selection of relatively low-affinity MBCs as a mechanism to promote diversity.
19 ng burnout, which would be the result if all MBCs generated only terminal effector function.
20 constitutes a shared signaling node allowing MBC cells to simultaneously engage a diversity of growth
21    Although HIV-exposed neonates had altered MBC subset distributions, detection of tetanus-specific
22 ion between MBCs and naive B cells and among MBC subsets and how this leads to memory responses.
23 on and 1 shows bactericidal activity with an MBC of 6.25 mug/mL.
24       Together plant belowground biomass and MBC explained 99.4% of variation in mean soil respiratio
25               Total gaseous C loss, CUE, and MBC were greater in the slow (ramp) warming treatment.
26 positively correlated with increased DOC and MBC.
27 ruded samples showing high values of MIC and MBC as the microorganisms tested were multi-resistant is
28 In association, an interesting lower MIC and MBC values (2048 mg/L and 4096 mg/L respectively) were o
29 oliferation in the developing cerebellum and MBCs and they identify the SHH:YAP:YB1:IGF2 axis as a po
30 d 3-IPMA showed MICs values of 4096 mg/L and MBCs values of 8192 mg/L or higher against several food
31 er (Tfh) cell responses as well as LLPCs and MBCs.
32                   The evaluation of MICs and MBCs on 11 promysalin analogs, synthesized utilizing div
33  within the range of their in vitro MICs and MBCs.
34 icted to surface membrane (sm)IgA(+) PCs and MBCs, with 2 clear subgroups showing strongly decreased
35               Here we comprehensively assess MBC frequency and specificity alongside serum binding an
36 ly may not have known how to ask an atypical MBC to function.
37 neonates had greater proportions of atypical MBC compared with the other groups.
38 st that the increased proportion of atypical MBC phenotypes found in HIV-1-infected individuals resul
39 speculate that at least in malaria, atypical MBCs may not be exhausted but rather may be functional,
40  higher proportion of AMA1-specific atypical MBCs.
41 colonized the splenic MZ, revealing T-bet(+) MBC plasticity.
42                                     T-bet(+) MBCs could be subdivided into recirculating T-bet(lo) MB
43                                     T-bet(+) MBCs expressed MBC subset markers CD80 and PD-L2.
44                                Many T-bet(+) MBCs lacked CD11b or CD11c expression but had marginal z
45 nterconversion between T-bet(-) and T-bet(+) MBCs, and parabionts showed differential tissue residenc
46                         report that T-bet(+) MBCs, formed in response to a primary influenza infectio
47 nd intraparenchymal localization of T-bet(+) MBCs.
48 hat underlie differences in function between MBCs and naive B cells and among MBC subsets and how thi
49 y correlated with plant belowground biomass, MBC, soil temperature and soil moisture.
50 , revealing that the reaction engenders both MBC subsets with different immune effector function and,
51 finity for Fe(2)O(3), which was confirmed by MBC and in agreement with GV.
52 solved organic C (DOC), microbial biomass C (MBC) and C accumulation in the heavy soil fraction in so
53  C (SOC), soil total N, microbial biomass C (MBC), microbial biomass N (MBN), water-soluble organic C
54 f Origin (PDO) Mozzarella di Bufala Campana (MBC) cheese has promoted the development of simple, fast
55                Mozzarella di Bufala Campana (MBC) is a PDO cheese produced from whole buffalo milk in
56 al bone lesions in metastatic breast cancer (MBC) by (18)F-FDG PET instead of (99m)Tc bone scintigrap
57  2 (HER2)-negative metastatic breast cancer (MBC) in germline (g)BRCA1/2 mutation carriers.
58                          Male breast cancer (MBC) is a rare hormone-driven disease often associated w
59                    Metastatic breast cancer (MBC) is an extremely recalcitrant disease capable of byp
60                          Male breast cancer (MBC) is rare.
61 ring patients with metastatic breast cancer (MBC) is unknown; however, data suggest that intensive mo
62 es are unclear for metastatic breast cancer (MBC) patients diagnosed with hormone receptor-positive (
63   Opioid use among metastatic breast cancer (MBC) patients has not been well-studied.
64 h locally advanced/metastatic breast cancer (MBC) regardless of visceral or nonvisceral disease.
65 w risk factors for metastatic breast cancer (MBC) through epidemiologic studies, these risk factors h
66 rvival outcomes in metastatic breast cancer (MBC) using a new quantitative multiplex assay (cMethDNA)
67 2 (HER2)-positive, metastatic breast cancer (MBC) who previously received trastuzumab and a taxane.
68 ne metastases from metastatic breast cancer (MBC).
69 atus in women with metastatic breast cancer (MBC).
70 d ATM-Chk2 signalings in male breast cancer (MBC).
71 lating exosomes in metastatic breast cancer (MBC).
72 uired by >=40% of metastatic breast cancers (MBC) resistant to adjuvant aromatase inhibitor (AI) ther
73  total N (TN), and microbial biomass carbon (MBC) and WP rotations had higher inorganic N content tha
74 d biomass and soil microbial biomass carbon (MBC), while high-level N additions decreased them.
75                       High microbial carbon (MBC) demand, a proxy for energy demand (cost), during so
76                Metaplastic breast carcinoma (MBC) is a highly aggressive form of triple-negative canc
77 crease in MBC numbers; (2) defective CD27(+) MBCs with almost normal IgG(3)(+) MBCs; (3) absence of s
78 + T-cell cytokine production, memory B cell (MBC) activation, and recognition of non-vaccine strains)
79 These involve reengagement of memory B cell (MBC) clones, the diversity and specificity of which dete
80                     The early memory B cell (MBC) response was mediated by both classical immunoglobu
81 ittle is known about enduring memory B cell (MBC) responses to Zika virus (ZIKV) and their relationsh
82 Recent studies characterizing memory B cell (MBC)-derived MAbs have provided valuable insight into th
83 body-secreting cell (ASC) and memory B-cell (MBC) responses were enumerated in tonsils and blood.
84 or sustaining CGNP and medulloblastoma cell (MBC) proliferation.
85 roducing somatically mutated memory B cells (MBC) and long-lived plasma cells.
86 ter proportions of activated memory B cells (MBC) compared with United States neonates.
87                              Memory B cells (MBC) respond to secondary antigen challenge to protect a
88  can differentiate to become memory B cells (MBC), in which EBV persistence is established.
89 a cells and rapidly reactive memory B cells (MBC).
90 y-secreting cells (ASCs) and memory B cells (MBCs) after infection or vaccination.
91 t control differentiation of memory B cells (MBCs) and long-lived plasma cells (LLPCs).
92 or B-cell subsets, including memory B cells (MBCs) and plasma cells (PCs).
93                              Memory B cells (MBCs) are critical for the rapid development of protecti
94                              Memory B cells (MBCs) are essential for long-lived humoral immunity.
95                              Memory B cells (MBCs) are key determinants of the B cell response to inf
96                              Memory B cells (MBCs) are key for protection from reinfection.
97                              Memory B cells (MBCs) are long-lived and produce high-affinity, generall
98                              Memory B cells (MBCs) can respond to heterologous antigens either by mol
99                              Memory B cells (MBCs) expressing the transcription factor T-bet have bee
100  a subpopulation of atypical memory B cells (MBCs) greatly expands and these MBCs show attenuation of
101 ies of T-bet(+) and T-bet(-) memory B cells (MBCs) in the context of the influenza-specific immune re
102 ctive immunoglobulin M (IgM) memory B cells (MBCs) that express the transcription factor T-bet and ha
103 e assayed for antibodies and memory B cells (MBCs) to mumps, measles, and rubella.
104 he development of polyclonal memory B cells (MBCs) to the 4 DENV serotypes and ZIKV during DENV infec
105 ved plasma cells (LLPCs) and memory B cells (MBCs), cell types canonically generated during germinal
106    We comprehensively review memory B cells (MBCs), covering the definition of MBCs and their identit
107 creased counts of blood PCs, memory B cells (MBCs), or both expressing distinct IgA and IgG subclasse
108 f preexisting virus-specific memory B cells (MBCs).
109 atypical and total activated memory B cells (MBCs).
110 uencies and isotype of CD27+ memory B cells (MBCs).
111 pported by Mineral Binding Characterization (MBC) (TGA, ATR-FTIR and zeta Potential), while at the "m
112                                    Comparing MBC and TNBC protein profiles we show MBC-specific incre
113  MIC and minimal bactericidal concentration (MBC) determinations.
114 ature on minimum bactericidal concentration (MBC), vitamin C content, total polyphenols content and a
115 e their minimal bactericidal concentrations (MBC) against the spoilage food bacteria Escherichia coli
116                  Women with biopsy-confirmed MBC and not given trastuzumab for 2 mo or more underwent
117 amples of buffalo milk and the corresponding MBC samples collected in the reference area in winter an
118 gramming language code contained in the CRAN MBC package version 0.10-438.' The correct version state
119  (absent in 98%), with 6 different defective MBC (and clinical) profiles: (1) profound decrease in MB
120                 Reciprocally, Hhex-deficient MBCs exhibited increased Bcl6 expression and reduced exp
121 n factors regulating germinal centre-derived MBC development and function.
122 nd 10% of the participants had no detectable MBCs to mumps.
123 this exploratory analysis of newly diagnosed MBC patients, (18)F-FDG PET versus BS to assess bone les
124 ssessment of bone lesions in newly diagnosed MBC.
125 plus ceCT, for patients with newly diagnosed MBC.
126         Thus, T-bet expression distinguishes MBC subsets that have profoundly different homing, resid
127 ve treatment, chronic HIV infection disturbs MBCs by reducing numbers and altering functionality due
128 ctericidal activity compared to AgNO3 (i.e., MBC of 15ppm compared to 5ppm), and significantly lower
129                Thus, patients with mutant ER MBC might respond to standard-of-care fulvestrant or oth
130                                  In ERalpha+ MBC, only AR had prognostic significance, suggesting AR
131                      T-bet(+) MBCs expressed MBC subset markers CD80 and PD-L2.
132                                          Few MBC clones, generally derived from higher-affinity germl
133 efore, identifying critical risk factors for MBC continues to be a major research imperative, and one
134 ting the transcriptional circuitry governing MBC differentiation.
135                        Eligible patients had MBC with measurable disease and germline mutations in no
136 zation of first-line therapy among HR+/HER2+/MBC patients and (2) compare overall survival (OS) betwe
137 ially more effective care path for HR+/HER2+/MBC patients, signaling a need for randomized studies.
138 National Cancer Database patients (HR+/HER2+/MBC) who were treated between 2010 and 2015.
139 T-bet(lo) MBCs and spleen-resident T-bet(hi) MBCs.
140 f MBCs and their identities and subsets, how MBCs are generated, where they are localized, how they a
141                                        Human MBCs displayed similar features.
142 d IgG(+) MBC subsets and an unmutated IgD(+) MBC population.
143 ereas swIg(+) and atypical IgM(+) and IgD(+) MBCs were stable over time.
144 eloped a method to identify bona fide IgE(+) MBCs in humans, demonstrated their extreme rarity in cir
145                              H3-reactive IgG MBC expansion after infection included reactivity to hea
146 ated immunoglobulin M(+) (IgM(+)) and IgG(+) MBC subsets and an unmutated IgD(+) MBC population.
147        Thus, even in competition with IgG(+) MBCs, IgM(+) MBCs are rapid, plastic, early responders t
148 (+)) MBC populations; however, classical IgM MBCs waned rapidly, whereas swIg(+) and atypical IgM(+)
149                                       IgM(+) MBCs also gave rise to T cell-dependent IgM(+) and IgG(+
150 even in competition with IgG(+) MBCs, IgM(+) MBCs are rapid, plastic, early responders to a secondary
151 ally hypermutated Plasmodium-specific IgM(+) MBCs proliferated and gave rise to antibody-secreting ce
152 ial interaction mechanisms between immunity, MBC and the metastatic niche.
153  PET for all patients included in the IMPACT-MBC study (NCT01957332) at the University Medical Center
154                    Targetable alterations in MBC, including AR, CHI3L1, and ISG, arise following estr
155  compared with BS plus ceCT led to change in MBC management recommendations in 16% of patients (95% C
156 (BS) supports clinically relevant changes in MBC management.
157  characterization for treatment decisions in MBC.
158 clinical) profiles: (1) profound decrease in MBC numbers; (2) defective CD27(+) MBCs with almost norm
159 s study highlights the persistent defects in MBC from HIV-infected individuals and points to the PI3K
160 static niche were significantly different in MBC patients with respect to controls.
161 y highlights the nuanced role of immunity in MBC spread, progression and outcome.
162 ease in SOC and total soil N, an increase in MBC and WSOC, and a decrease in MBN and WSON.
163 ive children showed significant increases in MBC counts after LAIV vaccination.
164 wever, the transcription factors involved in MBC differentiation are poorly defined.
165 hex-induced transcription factor involved in MBC differentiation.
166  by EBV, thus favouring long-term latency in MBC and asymptomatic persistence.
167 s a strong predictor of survival outcomes in MBC and may have clinical usefulness in risk stratificat
168 ased proteomics we quantify 5798 proteins in MBC, TNBC, and normal breast from 27 patients.
169 lective reprogramming of enhancer regions in MBC-like WM and repressed and heterochromatic regions in
170 e therapeutic potential of targeting SHP2 in MBC.
171 eviously associated with shorter survival in MBC.
172 ection, uptake of (64)Cu-DOTA-trastuzumab in MBC is strongly associated with patient HER2 status and
173    To identify targetable vulnerabilities in MBC, we examined steroid hormone receptors and tumor-inf
174 hed early in life, but nevertheless includes MBC adaptation to the infecting virus.IMPORTANCE Rapid a
175 ion profile alike that of MBCs and increased MBC differentiation.
176  Our findings thus provide new insights into MBC transcriptional programs and epigenetic regulation,
177 minal center (GC) B cells differentiate into MBCs.
178 cells in the process of differentiating into MBCs.
179 ited bacterial inhibition (MIC) and killing (MBC) activities up to 65 folds higher than that of auran
180 indle MBC with mouse spindle (CCN6 knockout) MBC tumors reveals a shared spindle-specific signature o
181 nclude V-region mutation and result in liver MBC localization.
182 d be subdivided into recirculating T-bet(lo) MBCs and spleen-resident T-bet(hi) MBCs.
183            Application of the proposed MEBAS-MBC-GV approach to a broad range of soil/earthwork compo
184                                   By merging MBC-PDO samples with non-PDO samples of buffalo mozzarel
185                         We measured the MIC, MBC and MBIC of DMADDM and DMAHDM respectively.
186 imum inhibitory/biocidal concentrations (MIC/MBC), and disc diffusion assays against Meticillin-resis
187 ut antibiotic was low, confirmed by high MIC/MBC, and a no inhibition on agar lawns.
188 rice and the limited amount of buffalo milk, MBC is potentially subject to mislabelling.
189                 Rediversification of mutated MBCs is infrequent within secondary germinal centers (GC
190 h extreme use were hormone receptor-negative MBC (odds ratio [OR], 1.63; 95% CI, 1.27 to 2.08), histo
191  DNA methylation patterns, related to normal MBC and PC profiles, and reminiscent of other memory and
192 s of MBC and allowed identification of novel MBC subsets with distinct functions defined according to
193  had measurable disease, and 45% had de novo MBC.
194 ological subtypes and metastatic behavior of MBC are unknown.
195                       Despite the breadth of MBC expansion, the MBC response included an increase in
196  the cross-reactive response, the breadth of MBC responses against different serotypes was greater af
197 led postmenopausal women with a diagnosis of MBC and prior exposure to an aromatase inhibitor.
198 g-term management of pain after diagnosis of MBC will continue to be necessary for many patients.
199 escription within 1 year before diagnosis of MBC, and 20,416 (81.4%) had an opioid prescription withi
200 opioid usage patterns after the diagnosis of MBC.
201 cts the engagement of the large diversity of MBC clones generated by priming.
202 at both sites, and a substantial fraction of MBC are produced prior to GC formation.
203  cascade seems to be active in a fraction of MBC patients and may represent a negative prognostic fac
204 bitors synergistically blocked the growth of MBC cells.
205 ve antibody-based screen revealed markers of MBC and allowed identification of novel MBC subsets with
206       In summary, the principle phenotype of MBC was luminal A, ductal, grade 2.
207                            RNA-sequencing of MBC subsets from multiple tissues revealed a tissue-resi
208                            Recent studies of MBC development and function after protein immunization
209 y B cells (MBCs), covering the definition of MBCs and their identities and subsets, how MBCs are gene
210 on is associated with a limited induction of MBCs with effector potential.
211 provide experimental support for the role of MBCs in maintaining imprinting effects and suggest a mec
212 d to a gene expression profile alike that of MBCs and increased MBC differentiation.
213 erent forms of influenza antigen exposure on MBC populations has received little attention.
214 fferent forms of influenza virus exposure on MBC populations is therefore an important guide to the d
215 r than CT and bone scintigraphy in bone-only MBC.
216 l one for evaluating the authenticity of PDO MBC cheese products.
217 all, our study sheds light on the polyclonal MBC response to DENV and ZIKV in naive and DENV-preimmun
218        In this study, we analyzed polyclonal MBCs at the single-cell level from peripheral blood mono
219  epidermal growth factor receptor 2-positive MBC, human epidermal growth factor receptor 2-targeted t
220 nd D538G) in estrogen receptor (ER)-positive MBC and determine whether mutation is associated with in
221 e identified all patients with HER2-positive MBC who received T-DM1 after trastuzumab and pertuzumab
222 orts of trastuzumab-resistant, HER2-positive MBC, but one third of patients received therapy with T-D
223 al treatment for most women with HR-positive MBC.
224 h acutely induced cells from the preexisting MBC pool.
225 th FGF2, PDGF, and hGF and readily prevented MBC cell growth induced by these factors.
226 d was found to interact with Hhex to promote MBC development.
227 icant reduction of antimicrobial properties (MBC 50%) at 82 degrees C and 62 degrees C after 15 and 1
228 elop vaccines that induce broadly protective MBCs to rapidly mutating pathogens have not yet been suc
229 cits robust type-specific and cross-reactive MBC responses after primary and secondary DENV infection
230  virus infection also induced cross-reactive MBC responses recognizing ZIKV, particularly after secon
231 ot influence type-specific or cross-reactive MBC responses, although ZIKV has the highest cross-react
232 rall, our findings indicate that H3-reactive MBC expansion following H3N2 infection is consistent wit
233       Notably, expansion of H3 head-reactive MBC populations was particularly broad and reflected ori
234 Notably, we show that hemagglutinin-reactive MBC expansion reflects imprinting by early-life infectio
235  through expansion of hemagglutinin-reactive MBC populations that recognize head and stalk regions of
236 size and character of hemagglutinin-reactive MBC populations.
237                          DENV cross-reactive MBCs expanded by ZIKV infection decline in number and pr
238 oportion of type-specific and cross-reactive MBCs were comparable between primary and secondary DENV
239 stalk-reactive, as well as to head-reactive, MBCs.
240 in Hhex as a transcription factor regulating MBC differentiation.
241 tter understanding of the signals regulating MBC development and function are essential to overcome c
242   Overexpression of Bcl-2 was able to rescue MBC differentiation in Hhex-deficient cells.
243  multiple tissues revealed a tissue-resident MBC gene signature as well as gut- and spleen-specific s
244                 We defined a tissue-resident MBC phenotype that was predominant in the gut but absent
245 ure plasmablast and memory B cell responses (MBC) in APTB cases and healthy donor controls.
246 om a loss in the number of naive and resting MBCs rather than an increase in the number of atypical a
247 s results from the loss of naive and resting MBCs.
248                          The loss of resting MBCs and naive B cells was mirrored in a population of c
249 C expansion and PC formation and to restrict MBC differentiation.
250 paring MBC and TNBC protein profiles we show MBC-specific increases related to epithelial-to-mesenchy
251 tein immunization have uncovered significant MBC heterogeneity.
252 mIgA(+) PCs with mild versus severe smIgA(+) MBC defects and higher frequencies of nonrespiratory tra
253 showed defects in both smIgA(+) and smIgG(+) MBCs and PCs.
254 s explaining 63.4% of the variation and soil MBC explaining the remaining 36%.
255 ing reduced AA content, even as overall soil MBC increased (~35%).
256 itor, PTEN, for identifying antigen-specific MBC from HIV-infected individuals compared to healthy co
257 tion "imprints" for strong H3 stalk-specific MBC expansion.
258 ese data identify potential subtype specific MBC biomarkers and therapeutic targets.
259 distributions, detection of tetanus-specific MBC from cord blood, indicative of fetal priming with te
260 IKV infection elicits a robust type-specific MBC response, and the majority of late convalescent anti
261                                DIII-specific MBCs were contained mostly within the plasma-cell-biased
262  The frequency of circulating mumps-specific MBCs was 5 to 10 times lower than measles and rubella, a
263        Long-lived murine Plasmodium-specific MBCs consisted of three populations: somatically hypermu
264 Comparison of the proteomes of human spindle MBC with mouse spindle (CCN6 knockout) MBC tumors reveal
265 cells adopt multiple fates upon stimulation, MBCs are more restricted in their responses.
266 r, in the case of secondary infections, such MBC-based approaches fail to distinguish acutely induced
267 MBCs and IgG(+) or IgA(+) class-switched (sw)MBCs from humans of different age, sex and race.
268 27(+)) and switched immunoglobulin (swIg(+)) MBC populations; however, classical IgM MBCs waned rapid
269 (4) presence of both unswitched and switched MBCs without and; (5) with IgG(2)(+) MBCs; and (6) with
270 rmal IgG(3)(+) MBCs; (3) absence of switched MBCs; and (4) presence of both unswitched and switched M
271 illar MBC responses correlated with systemic MBC and serological responses.
272 g BrdU pulse-labeling studies, we found that MBC formation preceded the formation of LLPCs in an adop
273 body variable gene expression indicates that MBCs emerge through unbiased selection from NBCs.
274    Despite the breadth of MBC expansion, the MBC response included an increase in affinity for the H3
275 ZIKV induces greater cross-reactivity in the MBC pool than in serum antibodies.
276 y when non-PDO cheeses were made outside the MBC reference area.
277               Evolving work reveals that the MBC compartment in mice and humans consists of distinct
278 distinct from ASCs and were committed to the MBC lineage.
279 kills drug susceptible A. baumannii with the MBC of 2.0 mug/mL and an MDR A. baumannii with the MBC o
280  2.0 mug/mL and an MDR A. baumannii with the MBC of 3.13 mug/mL.
281 ory B cells (MBCs) greatly expands and these MBCs show attenuation of B cell receptor signaling, loss
282                       The expansion of these MBCs is also associated with inefficient control of infe
283         Engineering immunogens to avoid this MBC diversity may facilitate flavivirus-type-specific va
284 and the ratio of TT-specific plasmablasts to MBCs in the APTB cases was 7:1.
285                                    Tonsillar MBC responses correlated with systemic MBC and serologic
286 o the infecting serotype dominated the total MBC response.
287 t in ER-positive aromatase inhibitor-treated MBC.
288 , especially against Salmonella typhimurium (MBC = 0.44 mg/mL).
289 naive B cells (NBC), IgD(+) unswitched (unsw)MBCs and IgG(+) or IgA(+) class-switched (sw)MBCs from h
290  were found by any imaging modality, virtual MBC management recommendations were made by a multidisci
291 tients from 189 centers in 24 countries with MBC to exemestane plus placebo or exemestane plus everol
292 we identified female patients diagnosed with MBC in 2006-2015.
293 e, privately insured patients diagnosed with MBC.
294  is an effective treatment for patients with MBC and gPALB2 or sBRCA1/2 mutations, significantly expa
295  assessed olaparib response in patients with MBC with somatic (s)BRCA1/2 mutations or g/s mutations i
296 are database was used to identify women with MBC diagnosed from 2002 to 2011 who underwent disease mo
297                              Most women with MBC require opioid analgesia within the first month afte
298 pproximately one third of elderly women with MBC were extreme users of disease-monitoring tests.
299 with exemestane to postmenopausal women with MBC whose disease progresses while receiving nonsteroida
300    In multivariable models, among women with MBC, a high versus low CMI at week 4 was independently a
301 ] and radiographic imaging) among women with MBC.

 
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