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1 one receptor (PR) content, and HER2 content (human epidermal growth factor receptor 2).
2 rombin, human prostate specific antigen, and human epidermal growth factor receptor 2.
3 strogen receptor, progesterone receptor, and human epidermal growth factor receptor 2.
4 ne receptor and those that were negative for human epidermal growth factor receptor 2.
5 estrogen receptor, progesterone receptor, or human epidermal growth factor receptor 2.
6 r receptors, including estrogen receptor and human epidermal growth factor receptor-2.
7 tigen binding fragment (Fab) targeting HER2 (human epidermal growth factor receptor 2), allowing site
9 ike epidermal growth factor receptor (EGFR), human epidermal growth factor receptor 2, anaplastic lym
10 bility and increases the expression of HER2 (human epidermal growth factor receptor 2) and E-cadherin
11 ogen receptor, progesterone receptor, Ki-67, human epidermal growth factor receptor 2, and Elston gra
12 investigated targets in this disease include human epidermal growth factor receptor 2, angiogenesis,
13 rapamycin inhibitors, drugs targeted to the human epidermal growth factor receptor 2, BRAF-mutation
14 of the hormone receptor positive (MCF7) and Human Epidermal Growth Factor Receptor 2/c- Erythroblast
16 ypes of breast cancer (luminal A, luminal B, human epidermal growth factor receptor 2 [currently know
17 ntified AI-unresponsive nonluminal subtypes (human epidermal growth factor receptor 2 enriched or bas
18 ic molecular subtypes: luminal A, luminal B, human epidermal growth factor receptor 2 enriched, and b
19 zing four main intrinsic molecular subtypes: human epidermal growth factor receptor 2-enriched, basal
20 type 5-mediated delivery of a transgene in a human epidermal growth factor receptor 2-, epidermal gro
21 library an aptamer specifically recognizing human epidermal growth factor receptor 2 (ErbB-2/HER2),
22 atio, 3.80; 95% CI, 2.46-5.87; P < .001) and human epidermal growth factor receptor 2 (ERBB2 [formerl
24 ased treatment for patients with early-stage human epidermal growth factor receptor 2 (ERBB2, formerl
25 automated MxIF scoring of a single section, human epidermal growth factor receptor 2, estrogen recep
26 strogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 expression.
27 autologous cellular immunotherapy targeting human epidermal growth factor receptor 2, for which he w
28 mmended further changes to the evaluation of human epidermal growth factor receptor 2 gene (HER2) amp
29 ndritic and epithelial cells, 205 kDa)-HER2 (human epidermal growth factor receptor 2) had significan
31 the control of the cyclooxygenase-2 (Cox-2), human epidermal growth factor receptor 2 (Her-2), and su
32 s epithelial cell adhesion molecule (EpCAM), human epidermal growth factor receptor-2 (HER-2), and pr
34 Ps are antibody functionalized to target the human epidermal growth factor receptor 2 (HER2 neu) prot
35 d to patients with hormone receptor-negative/human epidermal growth factor receptor 2 (HER2) -negativ
36 ational phase III trial, 1,144 patients with human epidermal growth factor receptor 2 (HER2) -negativ
37 t therapy in hormone receptor (HR) -positive/human epidermal growth factor receptor 2 (HER2) -negativ
38 global nor estrogen receptor (ER) -positive/human epidermal growth factor receptor 2 (HER2) -negativ
39 ecitabine for locally advanced or metastatic human epidermal growth factor receptor 2 (HER2) -negativ
40 as associated with improved DFS in luminal B/human epidermal growth factor receptor 2 (HER2) -negativ
41 bability in estrogen receptor (ER) -negative/human epidermal growth factor receptor 2 (HER2) -negativ
42 ne as second-line treatment of patients with human epidermal growth factor receptor 2 (HER2) -negativ
43 kg) with docetaxel as first-line therapy for human epidermal growth factor receptor 2 (HER2) -negativ
44 decision making for premenopausal women with human epidermal growth factor receptor 2 (HER2) -negativ
45 P) as first-line treatment for patients with human epidermal growth factor receptor 2 (HER2) -overexp
46 ab, has demonstrated substantial activity in human epidermal growth factor receptor 2 (HER2) -positiv
47 rastuzumab in patients with small (</= 2 cm) human epidermal growth factor receptor 2 (HER2) -positiv
49 ing trastuzumab in patients with early-stage human epidermal growth factor receptor 2 (HER2) -positiv
50 ple-negative BC (TNBC) tumors and those with human epidermal growth factor receptor 2 (HER2) -positiv
51 umab with observation in 5,102 patients with human epidermal growth factor receptor 2 (HER2) -positiv
52 tuzumab (arm C) in the phase III early-stage human epidermal growth factor receptor 2 (HER2) -positiv
53 irst-line bevacizumab-containing therapy for human epidermal growth factor receptor 2 (HER2) -positiv
54 n single-arm studies enrolling patients with human epidermal growth factor receptor 2 (HER2) -positiv
55 l benefit rate (CBR) of 50% in patients with human epidermal growth factor receptor 2 (HER2) -positiv
56 option for patients with heavily pretreated human epidermal growth factor receptor 2 (HER2) -positiv
58 trastuzumab plus lapatinib in patients with human epidermal growth factor receptor 2 (HER2) -positiv
60 Lapatinib is effective in the treatment of human epidermal growth factor receptor 2 (HER2) -positiv
61 ositive, progesterone receptor-positive, and human epidermal growth factor receptor 2 (HER2) -positiv
62 ne (X) as first-line combination therapy for human epidermal growth factor receptor 2 (HER2) -positiv
63 of trastuzumab to adjuvant chemotherapy for human epidermal growth factor receptor 2 (HER2) -positiv
64 3CA) correlates with response to neoadjuvant human epidermal growth factor receptor 2 (HER2) -targete
65 characterized the safety and efficacy of two human epidermal growth factor receptor 2 (HER2) -targete
66 bines the cytotoxic activity of DM1 with the human epidermal growth factor receptor 2 (HER2) -targete
69 erone receptor expression as well as lack of human epidermal growth factor receptor 2 (HER2) amplific
70 In hormone-negative breast cancers lacking human epidermal growth factor receptor 2 (HER2) amplific
72 ation by key breast cancer oncogenes such as human epidermal growth factor receptor 2 (HER2) and disc
73 n of epidermal growth factor receptor (EGFR)/human epidermal growth factor receptor 2 (HER2) and HER2
74 sion of NOTCH 2, 3 and 4, JAG2, HES1, GATA3, human epidermal growth factor receptor 2 (HER2) and HER3
75 and other members of the ErbB family, namely human epidermal growth factor receptor 2 (HER2) and huma
76 is of exosomes derived from cells expressing human epidermal growth factor receptor 2 (HER2) and pros
78 e antitumor properties of the humanized anti-human epidermal growth factor receptor 2 (HER2) antibody
80 o investigate whether hormonal receptors and human epidermal growth factor receptor 2 (HER2) change t
81 highlighted the importance of an appropriate human epidermal growth factor receptor 2 (HER2) evaluati
84 wer histologic grade (P < .001), and lack of human epidermal growth factor receptor 2 (HER2) expressi
85 ishing tumors or metastases that overexpress human epidermal growth factor receptor 2 (HER2) from tho
86 humanized monoclonal antibody that inhibits human epidermal growth factor receptor 2 (HER2) heterodi
88 epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2) in cance
90 epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2) inhibito
96 ring alterations in hormone receptors and/or human epidermal growth factor receptor 2 (HER2) may be r
99 tive tumors (luminal A HR = 0.55, luminal B [human epidermal growth factor receptor 2 (HER2) negative
100 ly identified higher rates of PR positivity, human epidermal growth factor receptor 2 (HER2) negativi
102 sterone receptor expression and negative for human epidermal growth factor receptor 2 (HER2) overexpr
104 s including estrogen receptor (ER) positive, human epidermal growth factor receptor 2 (HER2) positive
105 re defined as triple negative (TN; n = 310), human epidermal growth factor receptor 2 (HER2) positive
106 hormone receptor (HR) negative, and 31% were human epidermal growth factor receptor 2 (HER2) positive
107 cal (IHC) profile, tumors were classified as human epidermal growth factor receptor 2 (HER2) positive
108 ensitivity of the device for the analysis of human epidermal growth factor receptor 2 (HER2) protein
110 HC)-based, histopathologic classification of human epidermal growth factor receptor 2 (HER2) status i
112 prior studies have adequately controlled for human epidermal growth factor receptor 2 (HER2) status o
113 n the estrogen (ER), progesterone (PgR), and human epidermal growth factor receptor 2 (HER2) status o
115 receptor (ER), progesterone receptor (PgR), human epidermal growth factor receptor 2 (HER2) status,
116 subtype defined by hormone receptor (HR) and human epidermal growth factor receptor 2 (HER2) status,
117 to eight biomarker subtypes on the basis of human epidermal growth factor receptor 2 (HER2) status,
118 ging finding, progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2) status,
119 istology, hormone receptor (HmR) status, and human epidermal growth factor receptor 2 (HER2) status.
120 es on the basis of hormone receptor (HR) and human epidermal growth factor receptor 2 (HER2) status.
122 dy been adopted in some tumor types, such as human epidermal growth factor receptor 2 (HER2) testing
123 of American Pathologists recommendations for human epidermal growth factor receptor 2 (HER2) testing
124 Food and Drug Administration (FDA) approved human epidermal growth factor receptor 2 (HER2) testing
127 the epidermal growth factor receptor (EGFR)/human epidermal growth factor receptor 2 (HER2) tyrosine
128 ith early breast cancer testing positive for human epidermal growth factor receptor 2 (HER2) who were
130 microarrays containing luminal A, luminal B, human epidermal growth factor receptor 2 (HER2)(+)/ER(-)
131 antibody against the extracellular domain of human epidermal growth factor receptor 2 (HER2), 3 other
132 tasensor for the detection and estimation of human epidermal growth factor receptor 2 (HER2), a bioma
133 cal assessment of ER, progesterone receptor, human epidermal growth factor receptor 2 (HER2), and Ki6
134 gen receptor/progesterone receptor (ER/PgR), human epidermal growth factor receptor 2 (HER2), and men
136 of estrogen receptor, progesterone receptor, human epidermal growth factor receptor 2 (HER2), cytoker
137 zed monoclonal antibody targeted against the human epidermal growth factor receptor 2 (HER2), for adu
138 ks differ by ER, progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2), grade,
139 btypes on the basis of status with regard to human epidermal growth factor receptor 2 (HER2), hormone
140 ion of a well-known breast cancer biomarker, human epidermal growth factor receptor 2 (HER2), in a bo
141 stases in expression of hormone receptors or human epidermal growth factor receptor 2 (HER2), one RCT
142 etastatic breast cancer that is positive for human epidermal growth factor receptor 2 (HER2), progres
143 locking epidermal growth factor receptor and human epidermal growth factor receptor 2 (HER2), to the
144 We previously reported the eradication of human epidermal growth factor receptor 2 (HER2)- amplifi
145 electively decreased its activity toward the human epidermal growth factor receptor 2 (HER2)- pY(1196
146 patients with estrogen receptor-positive and human epidermal growth factor receptor 2 (HER2)-negative
147 ostat or placebo in women with stage II/III, human epidermal growth factor receptor 2 (HER2)-negative
148 considering estrogen receptor (ER)-positive/human epidermal growth factor receptor 2 (HER2)-negative
149 If a patient has hormone receptor-positive, human epidermal growth factor receptor 2 (HER2)-negative
150 has shown clinical efficacy in patients with human epidermal growth factor receptor 2 (HER2)-negative
151 sponse in the breast in women with operable, human epidermal growth factor receptor 2 (HER2)-negative
152 th advanced oestrogen-receptor (ER)-positive/human epidermal growth factor receptor 2 (HER2)-negative
153 ; the majority had hormone receptor-positive/human epidermal growth factor receptor 2 (HER2)-negative
154 ients with oestrogen-receptor (ER)-positive, human epidermal growth factor receptor 2 (HER2)-negative
155 minal A-like tumors, 70.5% of luminal B-like human epidermal growth factor receptor 2 (HER2)-negative
156 agnosed operable estrogen receptor-positive, human epidermal growth factor receptor 2 (HER2)-negative
157 y of a potent antimicrotubule agent, DM1, to human epidermal growth factor receptor 2 (HER2)-overexpr
158 These patients were more likely to have human epidermal growth factor receptor 2 (HER2)-positive
159 a greater proportion of triple-negative and human epidermal growth factor receptor 2 (HER2)-positive
160 ILs) is associated with improved outcomes in human epidermal growth factor receptor 2 (HER2)-positive
164 subtype was triple-negative in 170 (24.5%), human epidermal growth factor receptor 2 (HER2)-positive
165 pathologic complete response (pCR) rates in human epidermal growth factor receptor 2 (HER2)-positive
166 timisation) enrolled 455 women with invasive human epidermal growth factor receptor 2 (HER2)-positive
167 eceptor- and progesterone receptor-negative, human epidermal growth factor receptor 2 (HER2)-positive
168 patients with hormone receptor (HR)-negative human epidermal growth factor receptor 2 (HER2)-positive
169 tial role in the management of patients with human epidermal growth factor receptor 2 (HER2)-positive
171 respectively).Five-year BCSS was highest in human epidermal growth factor receptor 2 (HER2)-positive
172 uzumab and chemotherapy for the treatment of human epidermal growth factor receptor 2 (HER2)-positive
173 improves clinical outcomes in patients with human epidermal growth factor receptor 2 (HER2)-positive
174 ntly approved for treatment in patients with human epidermal growth factor receptor 2 (HER2)-positive
175 ncer including adjuvant targeted therapy for human epidermal growth factor receptor 2 (HER2)-positive
176 immune signatures identifying patients with human epidermal growth factor receptor 2 (HER2)-positive
177 d Affibody molecule for in vivo diagnosis of human epidermal growth factor receptor 2 (HER2)-positive
178 Evidence-based treatments for metastatic, human epidermal growth factor receptor 2 (HER2)-positive
179 onent of adjuvant therapy for stage I to III human epidermal growth factor receptor 2 (HER2)-positive
180 ortance: In neoadjuvant trials, treatment of human epidermal growth factor receptor 2 (HER2)-positive
182 mically fused a recombinant sialidase to the human epidermal growth factor receptor 2 (HER2)-specific
183 an antibody-drug conjugate incorporating the human epidermal growth factor receptor 2 (HER2)-targeted
184 nd dosimetry of (89)Zr-pertuzumab PET/CT for human epidermal growth factor receptor 2 (HER2)-targeted
185 tive was to determine whether imaging with a human epidermal growth factor receptor 2 (HER2)-targeted
193 s or mammary tumors derived from conditional human epidermal growth factor receptor 2 (Her2)/neu tran
194 apy consisting of concurrent trastuzumab and human epidermal growth factor receptor 2 (HER2)/neu-spec
195 en approved: lapatinib, directed against the human epidermal growth factor receptor 2 (HER2); and bev
196 a viral oncogene homolog 2 [ERBB2] [formerly human epidermal growth factor receptor 2 (HER2)]) is con
197 growth factor receptor (EGFR; ErbB1), ErbB2 [human epidermal growth factor receptor 2 (HER2)], and [h
198 may predict the efficacy of chemotherapy and human epidermal growth factor receptor 2 (HER2, encoded
199 E75, recognizes our model cancer marker, the Human Epidermal growth factor Receptor 2 (HER2/neu) pept
200 atable short hairpin (sh)RNA cooperates with human epidermal growth factor receptor 2 (HER2/neu), lea
201 epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2/neu), res
202 Trastuzumab, a monoclonal antibody targeting human epidermal growth factor receptor 2 (HER2; also kno
205 or (PR) negative and lacked amplification of human epidermal growth factor receptor 2 (HER2; ie, HER2
206 f trastuzumab with observation in women with human epidermal growth factor receptor-2 (HER2) -positiv
209 nsformation and tumorigenesis induced by the human epidermal growth factor receptor-2 (HER2) oncogene
211 ceptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor-2 (HER2) status,
212 pothesized that the tyrosine kinase receptor human epidermal growth factor receptor-2 (HER2) would be
213 ce to trastuzumab, an antibody targeting the human epidermal growth factor receptor-2 (HER2), which i
214 s obstacle in the treatment of patients with human epidermal growth factor receptor-2 (HER2)-amplifie
215 ne mechanism of resistance to trastuzumab in human epidermal growth factor receptor-2 (HER2)-positive
218 associations between tumor characteristics (human epidermal growth factor receptor 2 [HER2] protein
219 mplification or overexpression of the ERBB2 (human epidermal growth factor receptor 2 [HER2]) proto-o
220 ical biomarker for invasive breast cancer is human epidermal growth factor receptor 2 [(HER2), also k
221 progesterone receptor are not expressed, and human epidermal growth factor-receptor 2 is not amplifie
222 pe binding site can be grafted onto the anti-human epidermal growth factor receptor 2 mAb trastuzumab
223 xM1 overexpression confers resistance to the human epidermal growth factor receptor 2 monoclonal anti
224 been largely restricted to agents targeting human epidermal growth factor receptor-2 (mutated or ove
226 e (80%), progesterone receptor negative, and human epidermal growth factor receptor 2 negative (0 by
227 e to early depict estrogen receptor-positive/human epidermal growth factor receptor 2-negative (ER+/H
228 ial advantages in hormone receptor-positive, human epidermal growth factor receptor 2-negative advanc
229 m PlanB (intermediate and high-risk, locally human epidermal growth factor receptor 2-negative BC).
230 in patients with estrogen receptor-positive, human epidermal growth factor receptor 2-negative breast
231 ens improved IDFS in patients with high-risk human epidermal growth factor receptor 2-negative breast
232 ometastases, estrogen receptor-positive, and human epidermal growth factor receptor 2-negative breast
233 eptor- and/or progesterone receptor-positive human epidermal growth factor receptor 2-negative cases
234 ne for first-line treatment of patients with human epidermal growth factor receptor 2-negative metast
238 patients who had estrogen-receptor-positive, human epidermal growth factor receptor 2-negative, and e
239 receptor/progesterone receptor-negative and human epidermal growth factor receptor-2-negative breast
240 1,468 women with estrogen receptor-positive, human epidermal growth factor receptor-2-negative, stage
242 strogen receptor, progesterone receptor, and human epidermal growth factor receptor-2/neu negative).
243 otype of NF639 breast cancer cells driven by human epidermal growth factor receptor-2/neu, which sign
244 For hormone receptor-positive, human epidermal growth factor receptor 2-nonoverexpressi
245 de, negative status of estrogen receptor and human epidermal growth factor receptor 2, number of meta
246 primary toxicity of trastuzumab therapy for human epidermal growth factor receptor 2-overexpressing
247 Exogenous WNT3A promoted tumor growth in one human epidermal growth factor receptor 2-overexpressing
248 re testing vaccines and agents targeting the human epidermal growth factor receptor 2, p53, and Hsp27
249 r negative (OR, 4.05; 95% CI, 2.24 to 7.25), human epidermal growth factor receptor 2 positive (OR, 5
250 l A, luminal B, triple negative, basal-like, human epidermal growth factor receptor 2 positive, cyclo
252 ), progesterone receptor positive (PR+), and human epidermal growth factor receptor-2 positive (HER2+
253 nguished between estrogen receptor positive, human epidermal growth factor receptor-2 positive, and t
254 FR2, NRP1, VEGFR3, NRP2) in the basal, HER2 (human epidermal growth factor receptor 2) positive, lumi
255 lly subdivided as hormone receptor-positive, human epidermal growth factor receptor 2-positive (HER2(
257 rably among breast cancer subtypes, with the human epidermal growth factor receptor 2-positive (HER2+
258 e of distinct molecular subgroups, except in human epidermal growth factor receptor 2-positive (HER2+
259 tive tumors (21% v 6%; P = .08), but not for human epidermal growth factor receptor 2-positive (lumin
261 and optimal treatments for older women with human epidermal growth factor receptor 2-positive breast
263 of trastuzumab to adjuvant chemotherapy for human epidermal growth factor receptor 2-positive breast
264 therapy in resected stages I to III invasive human epidermal growth factor receptor 2-positive breast
265 e standard of care for adjuvant treatment of human epidermal growth factor receptor 2-positive breast
266 ing evaluated in clinical trials for imaging human epidermal growth factor receptor 2-positive cancer
267 mab for adjuvant treatment of node-positive, human epidermal growth factor receptor 2-positive early-
269 se of lapatinib and trastuzumab is active in human epidermal growth factor receptor 2-positive MBC.
270 es as first site of relapse in patients with human epidermal growth factor receptor 2-positive metast
271 ve to lapatinib alone in heavily pretreated, human epidermal growth factor receptor 2-positive metast
272 with the relationship in triple-negative and human epidermal growth factor receptor 2-positive subtyp
273 e of response to RT, although, in our study, human epidermal growth factor receptor 2-positive tumors
274 clear tGIV/cytoplasmic pYGIV was observed in human epidermal growth factor receptor 2-positive tumors
275 ubtypes-including hormone receptor-positive, human epidermal growth factor receptor 2-positive, and t
276 ed, placebo-controlled trial of lapatinib in human epidermal growth factor receptor 2-positive, early
277 2, for which he was eligible on the basis of human epidermal growth factor receptor 2 positivity (>/=
278 e estrogen/progesterone receptor status, and human epidermal growth factor receptor 2 positivity (all
279 core and clinical characteristics, including human epidermal growth factor receptor 2 positivity, est
280 hemical aptamer-based assay for detection of human epidermal growth factor receptor 2 protein (HER2)
281 and PR status (EP), or combined ER, PR, and human epidermal growth factor receptor 2 status (M).
282 ologic subtype, estrogen receptor status and human epidermal growth factor receptor 2 status (method
283 e immunohistochemistry test for diagnosis of human epidermal growth factor receptor 2 status in breas
284 utic regimens based on estrogen receptor and human epidermal growth factor receptor 2 status was also
285 utic regimens based on estrogen receptor and human epidermal growth factor receptor 2 status was also
286 chemistry) early breast cancer any nodal and human epidermal growth factor receptor 2 status, were ra
290 e, estrogen or progesterone receptor status, human epidermal growth factor receptor-2 status, node st
291 95% CI, 1.0 to 1.8) but not among those with human epidermal growth factor receptor 2 subtypes (HR, 1
292 ermal growth factor receptor 2-positive MBC, human epidermal growth factor receptor 2-targeted therap
293 to the well-known estrogen receptor (ER) and human epidermal growth factor receptor 2, the androgen r
294 n to estrogen and progesterone receptors and human epidermal growth factor receptor 2, the panel foun
295 itor of the nerve growth factor receptor and human epidermal growth factor receptor 2 (TrkA/HER2) sig
297 by subtype (luminal A like, luminal B like, human epidermal growth factor receptor 2 type, and tripl
298 arities were observed for triple-negative or human epidermal growth factor receptor 2-type tumors.
299 strogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 was found to gu
300 and progesterone receptors and negative for human epidermal growth factor receptor 2, with associate
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