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1 actin, and human Cyclin D1, BRCA1, MT2A, and HER2.
2 lization, ubiquitination, and degradation of HER2.
3 R/PR), or amplification or overexpression of HER2.
4 HER2 status and is indicative of binding to HER2.
5 d KPL-4 (7 inactive) for the anti-HER2 ADCs (HER2 0 MCF7, all inactive) and 0.10-1.73 mug/mL (7 inact
11 he identification of a novel enhancer in the HER2 3' gene body, which we have termed HER2 gene body e
12 In vitro IC50 values were 11-48 ng/mL in HER2 3+ SK-BR-3 and KPL-4 (7 inactive) for the anti-HER2
13 lysis of patients strongly positive for HER1/HER2 (3+ on immunohistochemistry; n = 111), patients pos
14 chemistry 2+/FISH amplified), whereas 7 were HER2- (3 immunohistochemistry 2+/FISH nonamplified; 4 im
16 of human epidermal growth factor receptor 2 (HER2), a biomarker for breast cancer, in undiluted serum
17 d on deep learning that automatically scores HER2, a biomarker that defines patient eligibility for a
18 te comprised of a humanised antibody against HER2, a novel enzyme-cleavable linker, and a topoisomera
19 those of the basal subtype, suggesting that Her2 activity is also associated with subtype status.
20 SK-BR-3 and KPL-4 (7 inactive) for the anti-HER2 ADCs (HER2 0 MCF7, all inactive) and 0.10-1.73 mug/
21 human epidermal growth factor (hEGF) or anti-HER2 Affibody as targeting moieties, are developed to, r
23 subtype have a significantly higher rate of Her2 alterations than those of the basal subtype, sugges
24 BB2/HER2-positive with 1 BrM acquiring ERBB2/HER2 amplification and the other showing metastatic enri
28 reast cancer patients, especially those with HER2 and ER negative tumors, who will receive one of the
33 tion and germline SNP data of 627 ER(+), 207 HER2(+), and 191 triple-negative (TNBC) cancers from The
34 R)/human epidermal growth factor receptor 2 (HER2) and HER2/HER3 heterodimers and by down-regulating
35 patients, as well as the overlap between the HER2+ and HER2- groups, suggests a role for (64)Cu-DOTA-
37 hypothesis that combined inhibition of EGFR, HER2, and HER3 signalling with the tyrosine kinase inhib
38 las (TCGA) data was analyzed for HDAC, PI3K, HER2, and MAPK/RAS/RAF gene alterations from sarcoma TCG
39 rried out in an independent cohort of 43 ER+ HER2- and ER- HER2- primary breast tumors, confirming ma
40 shared among three subtypes, ER+ HER2-, ER- HER2-, and HER2+, many events on the exon level were sub
41 ansgenic mammary tumors are resistant to the HER2 antibodies trastuzumab and pertuzumab but respond t
42 ced CAR T-cell efficacy directed against the Her2 antigen in two different established solid tumor se
44 echanisms in the transcription regulation of HER2 are limited to the involvement of tri-methylated hi
45 ositive advanced breast cancer, and validate HER2 as a therapeutic target even after multiple lines o
46 t MUC13 functionally interacts and activates HER2 at p1248 in PDAC cells, leading to stimulation of H
47 three centers, we identified alterations of Her2 at the DNA, RNA and protein level, and demonstrate
48 ified as HER2-positive (HER2+) or -negative (HER2-) based on fluorescence in situ hybridization (FISH
51 The method was primarily evaluated using the HER2 binding antibodies Trastuzumab and Pertuzumab and t
52 also found that TFAP2C, a known regulator of HER2, binds to HGE and is required for its enhancer func
54 r 2 (HER2)-positive breast cancers with dual HER2 blockade resulted in increased pathologic complete
56 ER2-derived peptide vaccines administered to HER2(+) breast cancer patients in the adjuvant setting s
58 howed that trastuzumab facilitated uptake of HER2 by dendritic cells (DC), which was mediated by the
59 ndary mutations in EGFR (T790M or C797S) and HER2 (C805S) that mediated acquired drug resistance in d
62 thelial KRT14 expressing cells that separate HER2+ cancer cells from the stromal and immune microenvi
63 n and lower clonal heterogeneity in TNBC and HER2(+) cancers suggest an immune pruning effect and equ
65 activity compared with treatment with either HER2.CAR T cells alone or HER2.CAR T cells plus Onc.Ad.
70 ly, all of these phenotypic effects of MUC13-HER2 co-localization could be effectively compromised by
71 or with the potent antibody-cytotoxic, anti-HER2 compound trastuzumab emtansine (T-DM1) with or with
72 ipping signal of silver and the logarithm of HER2 concentrations was obtained in the range of 5.0 x 1
74 he human epidermal growth factor receptor-2 (HER2) contributes to an enhanced HER2 expression in HER2
75 rs over single-positive, non-target NCI-H358-HER2 CRISPR knock out tumors in nude mice bearing dual-f
76 l trials evaluating CD8(+) T cell-eliciting, HER2-derived peptide vaccines administered to HER2(+) br
79 tient variability was greater for HER2+ than HER2- disease (P < 0.005 and 0.001, respectively, on day
82 Our findings show that MED1 is critical for HER2-driven breast tumorigenesis, suggesting its candida
83 or-binding protein as a critical mediator of HER2-driven breast tumorigenesis, suggesting its candida
86 HER2-negative tumors acquired a luminal B or HER2-E profile during metastatic progression, likely ref
88 nd human epidermal growth factor receptor 2 (HER2, encoded by the gene ERBB2)-targeted therapy in pat
89 al variables and treatment arms, ERBB2/HER2, HER2-enriched subtype, ESR1, and Genomic Grade Index rem
90 st significant predictor of pCR, followed by HER2-enriched subtype, ESR1, treatment arm, ER immunohis
91 uminal B-like HER2-positive tumors, 21.3% of HER2-enriched tumors, and 7.8% of triple-negative tumors
92 -called intrinsic subtypes (luminal A and B, HER2-enriched, basal-like, and normal-like), which mostl
93 events were shared among three subtypes, ER+ HER2-, ER- HER2-, and HER2+, many events on the exon lev
94 vation of the EGF receptors EGFR (ErbB1) and HER2 (ErbB2) drives the progression of multiple cancer t
98 ine kinase receptors, EGFR/ErbB1/HER1, ErbB2/HER2, ErbB3/HER3, and ErbB4/HER4, which trigger intracel
100 nvestigated the effects of specific EGFR and HER2 exon 20 insertion mutations from NSCLC patients tha
101 he human epidermal growth factor receptor 2 (HER2) expressed by cancer cells and pro-phagocytosis sig
103 le patients, including six patients with low HER2-expressing tumours, ten patients achieved an object
107 receptor-2 (HER2) contributes to an enhanced HER2 expression in HER2-positive breast cancers with HER
108 of breast cancer, was mutually exclusive of HER2 expression, and correlated with aggressive features
110 ession, inhibits HER2 signaling, dissociates HER2 from HSP90, and causes the internalization, ubiquit
111 ression in HER2-positive breast cancers with HER2 gene amplification and HER2-low or HER2-negative br
113 as well as the overlap between the HER2+ and HER2- groups, suggests a role for (64)Cu-DOTA-trastuzuma
115 east and gastric cancer but agents targeting Her2 have not yet demonstrated anti-tumor activity in MI
116 ological variables and treatment arms, ERBB2/HER2, HER2-enriched subtype, ESR1, and Genomic Grade Ind
117 were incubated with NRG1-beta, a mediator of HER2-HER3 signaling, or A83-01, an inhibitor of transfor
118 pidermal growth factor receptor 2 (HER2) and HER2/HER3 heterodimers and by down-regulating EGFR via a
121 munosensor can be applied for the testing of HER2 in clinical samples of breast cancer patients.
123 PMCA2 and the tyrosine kinase receptor ErbB2/HER2 in normal mammary epithelial cells and breast cance
126 broad implications for the roles of EGFR and HER2 in the absence of EGF both for normal and cancerous
129 ERBB2 (erb-b2 receptor tyrosine kinase 2 or HER2) is currently the only biomarker established for se
132 ast cancers with HER2 gene amplification and HER2-low or HER2-negative breast cancers following radio
133 e breast cancer samples and individuals with HER2-low or HER2-negative breast cancers undergoing radi
134 chondrial genome (i.e., females crossed with Her2 males) showed significantly (P < 0.001) longer tumo
135 ng three subtypes, ER+ HER2-, ER- HER2-, and HER2+, many events on the exon level were subtype specif
136 ervational study of 102 postmenopausal, HR + HER2- metastatic breast cancer patients treated with eve
138 Using map-based cloning we positioned the her2 mutation to the At5g63620 locus, resulting in a phe
140 R1 (n = 102), and patients positive for only HER2 (n = 42) showed no significant benefit with lapatin
141 ke human epidermal growth factor receptor 2 (HER2)-negative tumors, 82.8% of luminal B-like HER2-posi
142 e, human epidermal growth factor receptor 2 (HER2)-negative, node-negative breast cancer, the MammaPr
145 n independent data set, 2 of 9 (22.2%) ERBB2/HER2-negative BrCa switched to ERBB2/HER2-positive with
146 linical implications for patients with ERBB2/HER2-negative breast cancer and support comprehensive pr
148 with HER2 gene amplification and HER2-low or HER2-negative breast cancers following radiotherapy or e
149 cer samples and individuals with HER2-low or HER2-negative breast cancers undergoing radiotherapy or
150 ntifying AGTR1 overexpression in a subset of HER2-negative breast cancers, and they provide a mechani
151 ses were ERBB2/HER2-negative out of 13 ERBB2/HER2-negative in the primary BrCa cohort and became immu
154 ained during metastatic progression, luminal/HER2-negative tumors acquired a luminal B or HER2-E prof
155 gically confirmed hormone-receptor-positive, HER2-negative, locally advanced or metastatic breast can
156 If a patient has hormone receptor-positive, HER2-negative, node-positive breast cancer, the MammaPri
158 d many of these observations in an inducible Her2/Neu-driven breast cancer model and in syngeneic pan
161 n the tumor cells led to decreased growth of Her2/Neu-overexpressing tumors in LDLR(-/)(-) and ApoE(-
162 of mammary tumorigenesis harboring the MMTV-HER2 oncogene and mutation of MED1 to evaluate its role
163 erb-b2 receptor tyrosine kinase 2 (ERBB2 or HER2), or vascular endothelial growth factor, including
164 Patients were classified as HER2-positive (HER2+) or -negative (HER2-) based on fluorescence in sit
166 stem composed of two cell lines representing HER2 overexpressing esophageal adenocarcinomas (EACs) an
168 reastfeeding was not associated with risk of HER2-overexpressing type, but protective for all other s
174 -resistant tumors were generated by treating HER2(+)/PIK3CA(H1047R) tumor-bearing mice long term with
176 anscript levels and distribution in cultured HER2 positive breast cancer cells and human breast tumor
177 e, human epidermal growth factor receptor 2 (HER2)-positive breast cancer was referred to a cardio-on
178 In human epidermal growth factor receptor 2 (HER2)-positive breast cancer, GSDMB gene amplification a
179 of human epidermal growth factor receptor 2 (HER2)-positive breast cancers with dual HER2 blockade re
180 tly improves outcome in patients with ERBB2 (HER2)-positive metastatic breast cancer; a clinically ef
182 (aged >/=18 years) with centrally confirmed HER2-positive advanced breast cancer previously treated
183 nagement of patients with previously treated HER2-positive advanced breast cancer, and validate HER2
185 emtansine in patients previously treated for HER2-positive advanced gastric cancer (unresectable, loc
187 standard of care for first-line treatment of HER2-positive advanced gastric cancer, there is no estab
189 performed, type of specimens, proportion of HER2-positive and equivocal patient cases, and number of
190 , 375 patients with early breast cancer with HER2-positive and HR-positive status (n = 463 screened)
191 18 years or older with stage I-IIIa operable HER2-positive breast cancer from 112 centres in 23 count
192 ents have improved outcomes in patients with HER2-positive breast cancer in the neoadjuvant, adjuvant
193 ic mechanisms in HER2 transcription, in both HER2-positive breast cancer samples and individuals with
194 3 trial to assess a neoadjuvant regimen for HER2-positive breast cancer that replaces traditional sy
195 quantities of TILs in patients with advanced HER2-positive breast cancer treated with either pertuzum
201 ontributes to an enhanced HER2 expression in HER2-positive breast cancers with HER2 gene amplificatio
206 quent resection of a brain metastasis proved HER2-positive disease, confirming that the (89)Zr-pertuz
208 tuzumab after chemotherapy for patients with HER2-positive early breast cancer significantly improves
209 ded, placebo-controlled trial, patients with HER2-positive early breast cancer were randomly assigned
210 phase 3 randomised trial of 5102 women with HER2-positive early breast cancer, who were enrolled fro
212 ant NeoALTTO trial randomized 455 women with HER2-positive early-stage breast cancer to trastuzumab,
215 irst report evaluating (89)Zr-trastuzumab in HER2-positive EGA; here, we evaluate the safety, pharmac
216 ildren's Hospital, patients with progressive HER2-positive glioblastoma were enrolled between July 25
219 indicated for the treatment of patients with HER2-positive metastatic breast cancer previously treate
220 the prediction of outcomes in patients with HER2-positive metastatic breast cancer randomized to an
221 ts from 21 countries and randomized 652 with HER2-positive metastatic breast cancer to receive trastu
223 ening imaging of the brain for patients with HER2-positive or triple-negative subtypes and extracrani
224 -positive breast cancers and correlates with HER2-positive status in human ductal carcinoma in situ (
226 R2)-negative tumors, 82.8% of luminal B-like HER2-positive tumors, 21.3% of HER2-enriched tumors, and
227 ) ERBB2/HER2-negative BrCa switched to ERBB2/HER2-positive with 1 BrM acquiring ERBB2/HER2 amplificat
228 mal growth factor receptor 2-overexpressing (HER2-positive) breast cancer is dose-independent cardiac
231 2,558 patient cases; 2,278 v 2,659 tumors), HER2 positivity remained constant (15.7% v 15.5%, respec
232 in breast cancer did not affect the overall HER2-positivity rate or the proportion of patients eligi
233 n independent cohort of 43 ER+ HER2- and ER- HER2- primary breast tumors, confirming many of the exon
236 glycosylation on the binding of Herceptin to HER2 protein in breast cancer and on the sensitivity of
237 the immunodominant epitope derived from the HER2 protein, an observation confirmed in two in vivo mo
239 g/mL concentrations of soluble or cell-bound HER2, proving this unique complementation system overcom
240 K1) to HER2, resulted in the blockade of the HER2-pY(1196)-PAK1-T(423) signaling pathway, thus increa
242 RNA and protein level, and demonstrate that Her2 relevance as a tumor driver likely may vary even wi
243 y (STEM) were used to quantitatively analyze HER2 responses upon drug binding, whereby many tens of w
244 serine/threonine-protein kinase 1 (PAK1) to HER2, resulted in the blockade of the HER2-pY(1196)-PAK1
247 rate that NHERF1 acts with PMCA2 to regulate HER2 signaling and membrane retention in breast cancers.
248 248 in PDAC cells, leading to stimulation of HER2 signaling cascade, including ERK1/2, FAK, AKT and P
249 reduces PMCA2 and HER2 expression, inhibits HER2 signaling, dissociates HER2 from HSP90, and causes
251 (BsAb) was constructed by inserting an anti-Her2 single-chain variable fragment (ScFv) into an anti-
252 nd/or PR positive vs ER and PR negative) and HER2 status (positive vs negative), TX+CEX was more effe
254 ER2-targeted therapy, should be assessed for HER2 status before the initiation of HER2-targeted thera
255 nical applications include assessment of the HER2 status of lesions that may not be accessible to bio
256 for patient subgroups defined by ER, PR, and HER2 status suggested additional associations of the NOT
257 mostly corresponded to hormone receptor and HER2 status, and further stratified luminal tumors based
259 of human epidermal growth factor receptor 2 (HER2) status in women with metastatic breast cancer (MBC
260 proportion of patient cases with unresolved HER2 statuses (equivocal by IHC and in situ hybridizatio
261 IC and CTC that metastasize to bone, whereas HER2 supports the growth of prostate cancer cells once t
263 should offer combination chemotherapy and an HER2-targeted agent as initial therapy for all patients
264 , dosimetry, biodistribution, and successful HER2-targeted imaging with (89)Zr-pertuzumab PET/CT.
265 diated by calreticulin, the mBiNE stimulated HER2-targeted phagocytosis and produced durable antitumo
268 ts with advanced GEA, who are candidates for HER2-targeted therapy, should be assessed for HER2 statu
274 of American Pathologists recommendations for HER2 testing in breast cancer did not affect the overall
275 To establish an evidence-based guideline for HER2 testing in patients with GEA, formalize the algorit
277 ithms for methods to improve the accuracy of HER2 testing while addressing which patients and tumor s
278 or human epidermal growth factor receptor 2 (HER2) testing in breast cancer on testing patterns and i
279 and interpatient variability was greater for HER2+ than HER2- disease (P < 0.005 and 0.001, respectiv
280 long with the receptor tyrosine kinase ERB2 (HER2), that define most mammary cancers, there are no ta
281 ally correlates with increased expression of HER2, the underlying mechanism remains poorly understood
284 enter included 527 consecutive patients with HER2+/TN (T1/T2 and N0/N1) cancer treated with NCT follo
285 ght on the roles of epigenetic mechanisms in HER2 transcription, in both HER2-positive breast cancer
287 ivalent bispecific IgGs composed of the anti-HER2 trastuzumab moiety paired with affinity-modulated V
289 at an NSCLC patient whose tumor harbored the HER2 V777_G778insGSP mutation and achieved a durable par
290 ximab and Trastuzumab, proximity of EGFR and HER2 was investigated before and after treatment of cell
292 iol terminated DNA aptamer with affinity for HER2 was used to prepare the bio-recognition layer via s
294 eceptors (EGFR) or to human EGF receptors 2 (HER2), which are overexpressed in several cancer cells.
295 pression lines of HER2 confirmed the role of HER2, which encodes an oxidoreductase, in the responsive
296 The most recurrent expression gain was ERBB2/HER2, which showed a greater than 2-fold expression incr
297 t pertuzumab (which inhibits dimerization of HER2 with HER3) or a specific antibody against HER3 (ant
298 cell lines with trastuzumab (an inhibitor of HER2), with or without pertuzumab (which inhibits dimeri
299 tein complex that includes PMCA2, HSP90, and HER2 within specific actin-rich and lipid raft-rich memb
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