ライフサイエンスコーパス: HER2

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

6 ivo antitumor activity in mouse Her2(2+) and Her2(1+) xenograft models.

7 e linear quadratic survival curve of MCF7 /: HER2-18 cells exposed to gamma-rays.

8 The surviving fraction of MCF7 /: HER2-18 cells treated with (64)Cu-labeled trastuzumab (0

9 MCF7/HER2-18 cells were exposed in vitro to (64)Cu-labeled tr

10 s potent in vivo antitumor activity in mouse Her2(2+) and Her2(1+) xenograft models.

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

15 Eleven women were HER2+ (8 immunohistochemistry 3+; 3 immunohistochemistry

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

22 A sequencing to predict the efficacy of anti-HER2 agents.

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

25 Targeted therapies for ER+/PR+ and HER2-amplified breast cancers have improved patient surv

26 Using SERS nanoparticles that target HER2 and CD44 in breast cancer cells, we demonstrate lab

27 Drug treatment experiments targeting HER2 and components of the PI3K pathway supported proteo

28 reast cancer patients, especially those with HER2 and ER negative tumors, who will receive one of the

29 ty assays to study the functional effects of HER2 and HER3 inhibition and reactivation.

30 or size, grade, hormone receptors, and ERBB2/HER2 and Ki67 status.

31 High levels of ERBB2/HER2 and low levels of ESR1 were associated with pCR in

32 isms of resistance to combined inhibition of HER2 and PI3K.

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-

36 ent SUVmax (<SUVmax>pt) was compared between HER2+ and HER2- patients.

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

43 d its catalytically active homologs EGFR and HER2 are essential for their signaling.

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

49 an important role in promoting the growth of HER2 + BC by cross-talking with the HER2 signaling.

50 plore the involvement of AR on the growth of HER2 + BC cells (HCC1954 and SKBR3).

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

53 tical performance in comparison with current HER2 biosensors.

54 r 2 (HER2)-positive breast cancers with dual HER2 blockade resulted in increased pathologic complete

55 Insertion mutations in EGFR and HER2 both occur at analogous positions in exon 20.

56 ER2-derived peptide vaccines administered to HER2(+) breast cancer patients in the adjuvant setting s

57 ad no effect on constitutive ERK activity in HER2(+) breast carcinoma cells.

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

60 Thus, EGFR or HER2 can catalyse rigidity sensing after associating wit

61 epidermal growth factor receptor 2 protein (HER2) cancer biomarker as a model analyte.

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

64 Further evaluation of HER2-CAR VSTs in a phase 2b study is warranted as a sing

65 activity compared with treatment with either HER2.CAR T cells alone or HER2.CAR T cells plus Onc.Ad.

66 However, combining CAd-VECPDL1 with HER2.CAR T cells enhanced antitumor activity compared wi

67 atment with either HER2.CAR T cells alone or HER2.CAR T cells plus Onc.Ad.

68 ling among the resistant models and parental HER2(+) cells.

69 Further, MUC13-HER2 co-localization also holds true in PDAC tissues wit

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

73 Knockdown and overexpression lines of HER2 confirmed the role of HER2, which encodes an oxidor

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

77 Since the signal peptide of HER2 directed mCherry to the mitochondria, we targeted t

78 setting) and with progression on two or more HER2-directed regimens in the advanced setting.

79 tient variability was greater for HER2+ than HER2- disease (P < 0.005 and 0.001, respectively, on day

80 The HER2 distribution was hardly influenced by trastuzumab f

81 rCa signatures, PAM50 assignments, and ERBB2/HER2 DNA-level gains.

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

84 irection of changes were not the same in the HER2-driven mammary carcinomas.

85 and mutation of MED1 to evaluate its role in HER2-driven tumorigenesis.

86 HER2-negative tumors acquired a luminal B or HER2-E profile during metastatic progression, likely ref

87 of cases luminal A and B tumors converted to HER2-E tumors.

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

95 Her2 (ERBB2) is one of the most established therapeutic

96 the role of CD73 on the activity of the anti-HER2/ErbB2 monoclonal antibody (mAb) trastuzumab.

97 In immunocompetent mouse models of HER2/ErbB2-driven breast cancer, CD73 expression by tumo

98 ine kinase receptors, EGFR/ErbB1/HER1, ErbB2/HER2, ErbB3/HER3, and ErbB4/HER4, which trigger intracel

99 ed drug resistance in drug-sensitive EGFR or HER2 exon 20 insertion models.

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

102 d Cys(59)-ADAPT6 were internalized slowly by HER2-expressing cancer cells.

103 le patients, including six patients with low HER2-expressing tumours, ten patients achieved an object

104 durable antitumour immune responses against HER2-expressing tumours.

105 Inhibiting HER2 expression in bone tumor xenografts reduced prolife

106 ng enhancer and is inversely correlated with HER2 expression in breast cancer samples.

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

109 Knocking down NHERF1 reduces PMCA2 and HER2 expression, inhibits HER2 signaling, dissociates HE

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

112 the HER2 3' gene body, which we have termed HER2 gene body enhancer (HGE).

113 as well as the overlap between the HER2+ and HER2- groups, suggests a role for (64)Cu-DOTA-trastuzuma

114 Overexpression of HER2 has been reported in around 25% of human breast can

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

119 ot be accessible to biopsy and assessment of HER2 heterogeneity.

120 enesis, based on coamplification of MED1 and HER2 in certain breast cancers.

121 munosensor can be applied for the testing of HER2 in clinical samples of breast cancer patients.

122 howed excellent selectivity for detection of HER2 in complex matrix of human serum samples.

123 PMCA2 and the tyrosine kinase receptor ErbB2/HER2 in normal mammary epithelial cells and breast cance

124 mprehensive guidelines for the assessment of HER2 in patients with GEA.

125 The detection limit for HER2 in serum is lower than 100fM.

126 broad implications for the roles of EGFR and HER2 in the absence of EGF both for normal and cancerous

127 m the stromal and immune microenvironment in HER2+ invasive breast cancer.

128 These results indicate that HER2 is involved in transducing the perception of E-2-he

129 ERBB2 (erb-b2 receptor tyrosine kinase 2 or HER2) is currently the only biomarker established for se

130 However, we observed no differences in HER2 levels and signaling among the resistant models and

131 tastasis-specific amplification of the ERBB2/HER2 locus.

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

137 DCs exhibit potent activity, particularly in HER2 models.

138 Using map-based cloning we positioned the her2 mutation to the At5g63620 locus, resulting in a phe

139 tic enrichment of the activating V777L ERBB2/HER2 mutation.

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

143 In hormone receptor-positive/HER2-negative (n = 318) disease, BCSS was 100% in patien

144 ine-resistant, hormone receptor-positive and HER2-negative advanced breast cancer.

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

147 firmed metastatic hormone receptor-positive, HER2-negative breast cancer.

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

152 Three of these 7 cases were ERBB2/HER2-negative out of 13 ERBB2/HER2-negative in the prima

153 e oncogenic contributions of EVI1 in ER- and HER2-negative subsets of breast cancer.

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

157 In female MMTV-HER2/neu transgenic mice, we found that ERalpha and ERbe

158 d many of these observations in an inducible Her2/Neu-driven breast cancer model and in syngeneic pan

159 ation of Pik3r1 accelerates a mouse model of HER2/neu-driven breast cancer.

160 human triple-negative (MDA-MB-231) and mouse Her2/Neu-overexpressing (MCNeuA) breast cancers.

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

165 Of the three HER2 overexpressing cell lines in this panel, SKBr3 and

166 stem composed of two cell lines representing HER2 overexpressing esophageal adenocarcinomas (EACs) an

167 ly approved liposomal doxorubicin (Doxil) in HER2-overexpressing BT474 tumor xenograft models.

168 reastfeeding was not associated with risk of HER2-overexpressing type, but protective for all other s

169 or human epidermal growth factor receptor 2 (HER2) overexpression.

170 The variability within and among HER2+ patients, as well as the overlap between the HER2+

171 6.8 g/mL for HER 2+ and 3.7 and 4.3 g/mL for HER2- patients (P < 0.005 either day).

172 (<SUVmax>pt) was compared between HER2+ and HER2- patients.

173 We previously showed that HER2(+)/PIK3CA(H1047R) transgenic mammary tumors are res

174 -resistant tumors were generated by treating HER2(+)/PIK3CA(H1047R) tumor-bearing mice long term with

175 However, it is unclear how AR functions in HER2 positive (+) BC.

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

181 Patients were classified as HER2-positive (HER2+) or -negative (HER2-) based on fluo

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

184 s choice in previously treated patients with HER2-positive advanced breast cancer.

185 emtansine in patients previously treated for HER2-positive advanced gastric cancer (unresectable, loc

186 Eligible patients had HER2-positive advanced gastric cancer and progressed dur

187 standard of care for first-line treatment of HER2-positive advanced gastric cancer, there is no estab

188 ent as initial therapy for all patients with HER2-positive advanced GEA.

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

196 h calorie restriction (CR) may limit risk of HER2-positive breast cancer.

197 cally recurrent, unresectable, or metastatic HER2-positive breast cancer.

198 tuzumab-based adjuvant therapy in women with HER2-positive breast cancer.

199 ene ERBB2)-targeted therapy in patients with HER2-positive breast cancer.

200 NHERF1 expression is increased in HER2-positive breast cancers and correlates with HER2-po

201 ontributes to an enhanced HER2 expression in HER2-positive breast cancers with HER2 gene amplificatio

202 ple-negative breast carcinoma but not in the HER2-positive breast carcinoma subset.

203 ndromic) duplication of genomic segments, in HER2-positive breast tumors.

204 Five-year BCSS was > 95% in HER2-positive disease independent of chemotherapy respon

205 ith UBC were screened, and 232 with HER1- or HER2-positive disease were randomly assigned.

206 quent resection of a brain metastasis proved HER2-positive disease, confirming that the (89)Zr-pertuz

207 ptor (ER)-positive disease but less clear in HER2-positive disease.

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

211 erapy, improves outcomes among patients with HER2-positive early breast cancer.

212 ant NeoALTTO trial randomized 455 women with HER2-positive early-stage breast cancer to trastuzumab,

213 ence trastuzumab in neoadjuvant treatment of HER2-positive early-stage breast cancer.

214 administered to 10 patients with metastatic HER2-positive EGA.

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

217 zumab avidity was a true-positive result for HER2-positive malignancy.

218 were evaluated for the ability to visualize HER2-positive metastases.

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

222 Six patients with HER2-positive metastatic breast cancer were enrolled and

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 (

225 Conclusion Triple-negative or HER2-positive tumors showing absence of late enhancement

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

229 of T-DM1 versus trastuzumab with ET in early HER2-positive/HR-positive breast cancer.

230 Conclusion The ADAPT HER2-positive/HR-positive trial demonstrates that neoadj

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

234 cetylated histone 3 lysine 9 (H3K9ac) at the HER2 promoter region.

235 enhances the transcriptional activity of the HER2 promoters.

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

238 cines and trastuzumab, the mAb targeting the HER2 protein.

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

241 inst tumour-cell populations that lacked the HER2 receptor.

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

245 n T-DM1-resistant cells from patient-derived HER2(+) samples.

246 Using a human-Her2 self-antigen mouse model, we report here that alpha

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

250 rowth of HER2 + BC by cross-talking with the HER2 signaling.

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

253 b in MBC is strongly associated with patient HER2 status and is indicative of binding to HER2.

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

258 estrogen receptor, progesterone receptor, or HER2 status.

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

262 er that defines patient eligibility for anti-HER2 targeted therapies in breast cancer.

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

266 tients had received no prior chemotherapy or HER2-targeted therapy in the metastatic setting.

267 sation, stratified by world region, previous HER2-targeted therapy, and previous gastrectomy.

268 ts with advanced GEA, who are candidates for HER2-targeted therapy, should be assessed for HER2 statu

269 n overexpression indicate a poor response to HER2-targeted therapy.

270 e or the proportion of patients eligible for HER2-targeted therapy.

271 sed for HER2 status before the initiation of HER2-targeted therapy.

272 HER2-targeted treatments have improved outcomes in patie

273 plicating Src as a mediator of resistance to HER2-targeting agents.

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

276 d guideline with recommendations for optimal HER2 testing in patients with GEA.

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

282 for their association with response to anti-HER2 therapy and long-term outcome.

283 ) vs a small molecule-based (lapatinib) anti-HER2 therapy.

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

286 Male FVB/N-Tg(MMTVneu)202Mul/J (Her2) transgenic mice were bred to female MNX mice havin

287 ivalent bispecific IgGs composed of the anti-HER2 trastuzumab moiety paired with affinity-modulated V

288 In vitro, increased HER2 uptake by DC increased cross-presentation of E75, t

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

291 The expression of ERBB2/HER2 was the most significant predictor of pCR, followed

292 iol terminated DNA aptamer with affinity for HER2 was used to prepare the bio-recognition layer via s

293 ADCs targeting HER2 were prepared and demonstrated to be highly potent

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

300 Among these, a Her2 x CD3 bispecific antibody (BsAb) was constructed by

301 Moreover, the Her2 x CD3 BsAb shows potent in vivo antitumor activity