ライフサイエンスコーパス: HER2

1 recognizes RasGAP-binding sites on EGFR and HER2.

2 ance mutations in CDK4, CDK6, ERK2, EGFR and HER2.

3 gainst wild-type Her2 and its mutant variant Her2-A775_G776insYVMA.

4 with the combination of an Fc-optimised anti-HER2 agent (margetuximab) along with anti-PD-1 checkpoin

5 Human epidermal growth factor receptor 2 (HER2)-amplified breast cancers are treated using targete

6 activity of targeted therapies against rare HER2 and AKT1 mutations, confirming these mutations coul

7 Dual HER2 and CDK7 inhibition induced tumor regression in two

8 Neither GES nor NPC learned that HER2 and ER are direct risk factors.

9 MBIL learned that HER2 and ER interact to directly affect 5 year metastasi

10 ew of important mutations affecting EGFR and Her2 and highlight their influence on the kinase domain

11 The aptasensor showed specificity to HER2 and integrin alphavbeta6 positive, cell culture-der

12 We validate intrathecal delivery of EPHA2, HER2 and interleukin 13 receptor alpha2 chimeric antigen

13 identify three cell-surface targets, EPHA2, HER2 and interleukin 13 receptor alpha2, expressed on me

14 pounds, which were applied against wild-type Her2 and its mutant variant Her2-A775_G776insYVMA.

15 her reduction in response to DOX (P < 0.05); HER2 and Ki67 levels were also attenuated.

16 stance and confirm its impact in BRAF, EGFR, HER2 and MEK1.

17 /AKT/MTOR pathway, despite inhibition of the HER2 and the RAS-ERK pathways in tumor cells.

18 t a reactive cysteine in the binding site of Her2 and were further optimized by means of structure-ba

19 in cN0 patients, especially in ER+HER2+, ER-HER2+, and triple negative subtypes.

20 , BAP1, ARID1B, ELF3, PBRM1, PRKACA, PRKACB, HER2, and BRAF.

21 onal kinase activity of CDK7 is regulated by HER2, and by the receptor tyrosine kinases activated in

22 or cancer patients that are not sensitive to HER2 antagonists.

23 activity of a megamolecule mimic of an anti-HER2 antibody.

24 EGFR (epidermal growth factor receptor) and Her2 are among the prominent mutated oncogenic drivers o

25 nd human epidermal growth factor receptor 2 (HER2) are involved in tumor resistance to RTK-targeted t

26 of human epidermal growth factor receptor 2 (HER2) are observed in 15-20% of breast cancers (HER2+ br

27 nd human epidermal growth factor receptor-2 (HER2) are the three crucial biomarkers for the clinical

28 nd human epidermal growth factor receptor 2 (HER2), are absent is known to express the most aggressiv

29 cells showed that this drug did not inhibit HER2 as reported, but directly inhibits mitochondrial re

30 several key features of human luminal B HR(+)HER2(-) BC, including limited immune infiltration and po

31 a significantly longer OS was observed with HER2 blockade (hazard ratio, 0.58; 95% CI, 0.34 to 0.97)

32 Accordingly, HER2 blockers, but not c-MET inhibitors, are paradoxical

33 subset of SCCs that are uniquely amenable to HER2 blocking therapies.

34 l2(low)p-p38(low)E-cadherin(low) in the MMTV-Her2 breast cancer model.

35 1 inhibitors synergistically target TNBC and HER2 breast cancer since these two pathways are concurre

36 ssion in the murine NeuNT model of amplified-HER2 breast cancer.

37 te subtype-specific differences in amplified-HER2 breast cancer.

38 ical model to predict tumor response for two HER2 + breast cancer patients treated with the same ther

39 epidermal growth factor receptor 2 positive (HER2 +) breast cancer, HER2 + patients do not always res

40 HER2 kinase-targeted therapy in a subset of HER2(+) breast cancer cell lines and allow cancer cells

41 een Indigenous American genetic ancestry and HER2(+) breast cancer suggests that the high incidence o

42 2-targeted therapies, patients with advanced HER2(+) breast cancer ultimately develop drug resistance

43 d chromosome 11q13.3 (encompassing CCND1) in HER2(+) breast cancer.

44 targeting early metastatic dissemination in Her2(+) breast cancer.

45 be used as a monotherapy in the treatment of HER2(+) breast cancer.

46 are currently required for the treatment of HER2(+) breast cancer.

47 a significant benefit in patients with ER(+)/HER2(-) breast cancer.

48 inhibitors of AKT and HER2 was conducted in HER2+ breast cancer cell lines with or without PIK3CA mu

49 e-agent anti-HER2 treatment in PIK3CA-mutant HER2+ breast cancer cell lines.

50 e-agent anti-HER2 therapies in patients with HER2+ breast cancer.

51 HLA-G6, as a possible new marker for pCR in HER2+ breast cancer.

52 ficantly improved prognosis of patients with HER2+ breast cancer.

53 2) are observed in 15-20% of breast cancers (HER2+ breast cancers), and anti-HER2 therapies have sign

54 We identified patients with stage I-III ER+/HER2- breast cancer.

55 epidermal growth factor receptor 2-negative (HER2-) breast cancer and is used to inform recommendatio

56 marker (mutations or amplifications) (TP53, HER2, c-myc, GATA6, PIK3CA and KRAS) and ITGAV expressio

57 o effect on the proliferation of luminal and HER2+ cancer cells and normal breast cells.

58 Three cycles of HER2 CAR T cells given after lymphodepleting chemotherap

59 ieved after one cycle of lymphodepletion and HER2 CAR T cells.

60 ow metastatic rhabdomyosarcoma to autologous HER2 CAR T cells.

61 ve to TAK1 inhibitor compared to luminal and HER2(+) cell lines.

62 Owing to the high expression levels of HER2, combination therapies are currently required for t

63 lls, transform into nanofibrils that disrupt HER2 dimerization and subsequent downstream signalling e

64 Here, we investigate the role of MYC in HER2+ disease, examining the relationship between HER2 e

65 Its affinity for the model system HER2-DIVMP was found in a nanomolar range.

66 tor and anti-EGFR drugs in prostate and EGFR/HER2-driven tumor models, respectively, identifying a re

67 CRISPR-mediated CD47 and HER2 dual knockouts not only inhibit clonogenicity but a

68 es have differential sensitivity to clinical HER2/EGFR-targeted therapeutics, but small-molecule acti

69 al A primary breast tumors that give rise to HER2-enriched (HER2E) subtype metastases, but remain cli

70 lymphocytes (continuous variable), subtype (HER2-enriched and basal-like vs rest), and 13 genes comp

71 ortened time to develop BCBM and enriched in HER2-enriched and triple-negative breast cancers.

72 an women, we show an increased prevalence of HER2-enriched molecular subtypes and higher prevalence o

73 pendent, good prognostic factor, whereas the HER2-enriched signature, which was associated with a hig

74 eletion (NDL) mouse mammary carcinoma model (Her2(+), ER/PR negative).

75 with ypN0 in cN0 patients, especially in ER+HER2+, ER-HER2+, and triple negative subtypes.

76 g, human epidermal growth factor receptor 2 (HER2/ERBB2) in vesicles derived from mammalian cell memb

77 ll as potentially druggable mutations (e.g., HER2/ERBB2).

78 tumors match existing subtypes of amplified-HER2, estrogen receptor-negative human tumors by molecul

79 displayed sub-nanomolar cytotoxicity against HER2-expressing cancer cells, while showing no activity

80 CD47 is upregulated preferentially in HER2-expressing cells, and blocking CD47 or HER2 reduces

81 disease, examining the relationship between HER2 expression and MYC phosphorylation in HER2+ patient

82 These FCF analogs also suppress HER2 expression at a concentration lower than that of FC

83 lation-specific genetic variant(s) affecting HER2 expression in breast cancer.

84 assessed the number of HER2 gene copies and HER2 expression in cancer cells using the fluorescent in

85 wever, spatial and temporal heterogeneity of HER2 expression may prevent identification of optimal pa

86 man epidermal growth factor receptor type 2 (HER2) expression may help to stratify breast and gastroe

87 nd human epidermal growth factor receptor 2 (HER2) expression, is associated with heightened metastat

88 ced by Ad/E2TM or naked pE2TM, both encoding HER2 extracellular and transmembrane domains.

89 Amplification of HER2 gene (ERBB2) and overexpression of HER2 protein on

90 HER2 gene CNV was also assessed in formalin-fixed paraff

91 Furthermore, we assessed the number of HER2 gene copies and HER2 expression in cancer cells usi

92 ve significantly more often a high number of HER2 gene copies in liquid biopsy (p = 0.04).

93 We found that the HER2 gene copy number in liquid biopsy was higher in GC

94 that patients with a high copy number of the HER2 gene in the tumor tissue assessed by qPCR (but not

95 However, hyper-crosslinking of HER2 has been shown to override the receptor's native be

96 Activation of the HER2/HER3 axis by cancer-associated fibroblast-secreted

97 involves reprogramming of the kinome through HER2/HER3 signaling via the activation of multiple tyros

98 Anti-HER2 IgG was induced by Ad/E2TM or naked pE2TM, both enc

99 er NK cell depletion, and they produced less HER2 IgG, demonstrating positive regulatory function of

100 adherin-11 was downregulated (P < 0.001) and HER2 increased (P < 0.05).

101 or tyrosine kinases activated in response to HER2 inhibition, as well as by the downstream SHP2 and P

102 can maintain this pathway in the context of HER2 inhibition.

103 Combination therapy of a HER2 inhibitor and an AKT inhibitor, as well as other PI

104 se of THZ1 displayed potent synergy with the HER2 inhibitor lapatinib in HER2iR BC cells in vitro.

105 targets cyclin-dependent kinase 7 (CDK7) in HER2 inhibitor-resistant (HER2iR) breast cancer.

106 We show that both HER2 inhibitor-sensitive (HER2iS) and HER2iR breast canc

107 a human epidermal growth factor receptor 2 (HER2) inhibitor approved by the FDA for HER2-positive br

108 to human epidermal growth factor receptor 2 (HER2) inhibitors involves reprogramming of the kinome th

109 e that in early lesion breast cancer models, Her2 inhibits p38 by inducing Skp2 through Akt-mediated

110 de 2 and one grade 3; and one grade 2 ER/PR+ HER2- invasive lobular carcinoma (ILC).

111 hat trigger endocytosis upon ligand binding, HER2 is an internalization-resistant receptor.

112 Dual blockade of CD47 and HER2 is suggested to eliminate resistant cancer cells in

113 Human epidermal growth factor receptor 2 (HER2) is overexpressed in >20% of breast cancers.

114 HER2 kinase as a well-established target for breast canc

115 cells to proliferate in the presence of the HER2 kinase inhibitor lapatinib.

116 ould have superior efficacy versus selective HER2 kinase inhibitors.

117 roblasts counteract the cytotoxic effects of HER2 kinase-targeted therapy in a subset of HER2(+) brea

118 HER2 levels measured using two clinically validated anti

119 hnCD16-iNK cells, combined with anti-HER2 mAb, also mediated improved survival in an ovarian

120 N-terminal to the substrate pTyr in EGFR and HER2 mediate specific binding by the SHP2 active site, l

121 These findings identify Her2-mediated suppression of the p38-MK2-Hsp27 pathway a

122 Estrogen, proliferation, invasion, and HER2 module scores from RS were used to characterize the

123 Primary and acquired neratinib resistance in HER2-mutant breast cancer patient-derived xenografts (PD

124 We developed neratinib-resistant HER2-mutant cancer cells by gradual dose escalation.

125 nt 500 mg); cohort B comprised patients with HER2 mutations (treated with oral neratinib 240 mg, and

126 ies were taken at diagnosis in patients with HER2+ (n = 28), luminal B-like (n = 49) and triple-negat

127 E) subtype metastases, but remain clinically HER2 negative (cHER2-).

128 ve/human epidermal growth factor receptor 2 (HER2)-negative analysis population included 4,891 women

129 II human epidermal growth factor receptor 2 (HER2)-negative breast cancer.

130 ve/human epidermal growth factor receptor 2 (HER2)-negative cases without chemotherapy treatment were

131 nd human epidermal growth factor receptor 2 (HER2)-negative metastatic breast cancer represents a maj

132 nd human epidermal growth factor receptor 2 (HER2)-negative metastatic breast cancer who had received

133 R+/human epidermal growth factor receptor 2 (HER2)-negative metastatic breast cancer with prior clini

134 ntinued before progression, in patients with HER2-negative advanced breast cancer and a germline BRCA

135 Overall, 202 untreated patients with HER2-negative AEGC and a Zubrod performance status of 0-

136 5% CI) = 2.00 (1.17-3.45), P-trend < 0.001), HER2-negative BC (multivariable OR for the highest categ

137 Premenopausal women with HR-positive/HER2-negative breast cancer and high recurrence risk, as

138 BRCA carriers with cT1-3 (>= 1.5 cm), cN0-3 HER2-negative breast cancer were randomly assigned to pr

139 ogically or cytologically confirmed advanced HER2-negative breast cancer, an Eastern Cooperative Onco

140 wo had pathologic findings that demonstrated HER2-negative disease, and one had a fine-needle aspirat

141 y-six percent had estrogen receptor-positive HER2-negative disease.

142 ric cancer (GC) are needed, particularly for HER2-negative GC, which represents the majority of cases

143 tly associated with poor clinical outcome in HER2-negative GC.

144 line treatment of hormone receptor-positive, HER2-negative metastatic breast cancer.

145 , 55 years +/- 11 [standard deviation]) with HER2-negative primary breast cancer were enrolled.

146 cting HER2-positive metastases in women with HER2-negative primary breast cancer.

147 epict HER2-positive metastases in women with HER2-negative primary breast cancer.

148 Within the POAI-treated HER2-negative subpopulation, 5-year recurrence risk in w

149 ent discrimination between HER2-positive and HER2-negative tumors as early as 2 h after injection (tu

150 lly sensitive theranostic imaging method for HER2-negative, CEA-positive metastatic breast cancer pat

151 h and histologically confirmed, progressive, HER2-negative, metastatic breast cancer were enrolled fr

152 x1 can act as an oncogene and cooperate with HER2/neu to enhance breast cancer initiation and metasta

153 progesterone receptor-positive (ER/PR+) and HER2/neu-negative (HER2-), one grade 2 and one grade 3;

154 on clinical T/N stage, tumor grade, ER, PR, HER2, number of metastatic sites, and presence of bone-o

155 under aqueous conditions but, on binding to HER2 on cancer cells, transform into nanofibrils that di

156 strate that the effect of p38 suppression by Her2 on early dissemination is mediated by MK2 and heat

157 0.89 AUC (ER), 0.81 AUC (PR), and 0.79 AUC (Her2) on a large, independent test set (n = 2531).

158 plex hybrid glycans, especially for KRAS and HER2 oncogenes.

159 tor-positive (ER/PR+) and HER2/neu-negative (HER2-), one grade 2 and one grade 3; and one grade 2 ER/

160 sents a significant challenge for exploiting HER2 overexpression for improved tumor killing.

161 n HER2 expression and MYC phosphorylation in HER2+ patient tumors and characterizing the functional e

162 receptor 2 positive (HER2 +) breast cancer, HER2 + patients do not always respond to therapy.

163 warranted to assess its prognostic value for HER2+ patients and develop novel prediction model for la

164 tool for predict long-term survival in HoR+/HER2- patients.

165 ican women have reported a high incidence of HER2 positive (+) tumors; however, the factors contribut

166 re human epidermal growth factor receptor 2 (HER2) positive.

167 th human epidermal growth factor receptor 2 (HER2)-positive breast cancer with brain metastases (BMs)

168 II human epidermal growth factor receptor 2 (HER2)-positive breast cancer with residual invasive dise

169 th human epidermal growth factor receptor 2 (HER2)-positive metastatic breast cancer who have disease

170 0 or 1 and centrally confirmed, measurable, HER2-positive advanced breast cancer previously treated

171 We aimed to test this combination in HER2-positive advanced breast cancer that had progressed

172 or older, who had hormone receptor-positive, HER2-positive advanced breast cancer with unresectable,

173 bpopulation of patients with PD-L1-positive, HER2-positive advanced breast cancer.

174 resulted in excellent discrimination between HER2-positive and HER2-negative tumors as early as 2 h a

175 NCT00769470), participants with early-stage HER2-positive breast cancer (N = 128) were recruited fro

176 Triple-negative breast cancer (TNBC) and HER2-positive breast cancer are particularly aggressive

177 r of intracranial responses in patients with HER2-positive breast cancer brain metastases.

178 itumor activity against BMs in patients with HER2-positive breast cancer in a randomized, controlled

179 atients with newly diagnosed, node-positive, HER2-positive breast cancer or, if node negative, with a

180 r 2 (HER2) inhibitor approved by the FDA for HER2-positive breast cancer treatment; however, it has n

181 In mice engrafted with HER2-positive breast cancer tumors, coinjection of MCs i

182 he second cohort, 3 patients with metastatic HER2-positive breast cancer were included.

183 d five women with untreated stage II and III HER2-positive breast cancer were randomly assigned to re

184 score identifies patients with early-stage, HER2-positive breast cancer who might be candidates for

185 In patients with HER2-positive breast cancer with BMs, the addition of tu

186 Patients with HER2-positive breast cancer with pathologic invasive res

187 current therapeutic landscape of early stage HER2-positive breast cancer, focusing on strategies for

188 n situ (DCIS) from patients with luminal and HER2-positive breast cancer.

189 igher estimated pCR rates in HR-negative and HER2-positive breast cancer.

190 have improved the survival of patients with HER2-positive breast cancer.

191 on and de-escalation treatment strategies in HER2-positive breast cancer.

192 val outcome in patients with newly diagnosed HER2-positive breast cancer.

193 r-pertuzumab PET/CT that were suspicious for HER2-positive disease.

194 pertuzumab plus trastuzumab in patients with HER2-positive early breast cancer in the neoadjuvant-adj

195 ntibody) in previously treated patients with HER2-positive gastro-oesophageal adenocarcinoma.

196 favorable toxicity profile and its uptake in HER2-positive lesions, this radiopharmaceutical can offe

197 ed therapies are successful in patients with HER2-positive malignancies; however, spatial and tempora

198 zirconium 89 ((89)Zr)-pertuzumab can depict HER2-positive metastases in women with HER2-negative pri

199 ertuzumab PET/CT was successful in detecting HER2-positive metastases in women with HER2-negative pri

200 ertuzumab-avid foci that were suspicious for HER2-positive metastases were tissue sampled and examine

201 Of these six women, three had biopsy-proven HER2-positive metastases, two had pathologic findings th

202 We randomly assigned patients with HER2-positive metastatic breast cancer previously treate

203 In heavily pretreated patients with HER2-positive metastatic breast cancer, including those

204 d therapy has changed the natural history of HER2-positive metastatic breast cancer, with the dual bl

205 y improves overall survival in patients with HER2-positive metastatic gastric cancer.

206 h trastuzumab and chemotherapy in first-line HER2-positive metastatic oesophagogastric (gastric, oeso

207 h trastuzumab and chemotherapy in first-line HER2-positive metastatic oesophagogastric cancer is unde

208 d chemotherapy and has promising activity in HER2-positive metastatic oesophagogastric cancer.

209 rial in patients aged 18 years or older with HER2-positive metastatic oesophagogastric cancer.

210 to treat gastric cancer include trastuzumab (HER2-positive patients first line), ramucirumab (anti-an

211 sion, and tumor vasculature of both TNBC and HER2-positive trastuzumab-refractory breast cancer.

212 ically inhibited in vitro growth of TNBC and HER2-positive trastuzumab-resistant BT474-TtzmR cells.

213 To increase HER2-positive tumor cell selective drug delivery, we opt

214 HER2-positive tumors have treatment options but often ac

215 The tumor-to-contralateral breast ratios for HER2-positive tumors were significantly (P < 0.05) highe

216 ligible patients were 18 years or older, had HER2-positive, metastatic breast cancer, had not receive

217 Oncology Group performance status of 0 or 1, HER2-positive, operable, locally advanced, or inflammato

218 nresectable, locally advanced or metastatic, HER2-positive, PD-L1-unselected gastro-oesophageal adeno

219 Nevertheless, for HER2+ postmenopausal patients, the model has less effect

220 7-mediated anti-phagocytosis conjugated with HER2-prompted proliferation.

221 We were able to measure HER2 protein levels using 0.5 ug/sample total protein ly

222 b, and trastuzumab to monitor MET, EGFR, and HER2 protein levels, respectively, during treatment with

223 n of HER2 gene (ERBB2) and overexpression of HER2 protein on cancer cells are found in 10-26% of gast

224 The HER2 receptor is overexpressed on numerous cancers, maki

225 growth inhibition was achieved by Dox-loaded HER2 receptor targeted nanoparticles, TNP(HER2pep), over

226 HER2 receptors expression were markedly reduced in 5-FU-

227 HER2-expressing cells, and blocking CD47 or HER2 reduces both receptors with diminished clonogenicit

228 Suppression of p38 and MK2 by Her2 reduces MK2-mediated Hsp27 phosphorylation, and unp

229 Analysis of a HER2 S310F-mutant PDX suggests that an antibody drug con

230 erein we present structural optimization for HER2-selective targeting.

231 inhibits SHP2 activity in vitro and EGFR and HER2 signaling in cells, suggesting inhibition of SHP2 p

232 In EGFR (HER1) and EGFR2 (HER2) signaling, SHP2 increases the half-life of activat

233 Still, immune sera inhibited HER2+ SKBR3 cell survival in a dose-dependent fashion.

234 The early disseminating cells are Her2(+)Skp2(high)Tpl2(low)p-p38(low)E-cadherin(low) in t

235 Next, the possibility of using A9 as HER2- specific probe for the nuclear medicine imaging wa

236 iodistribution, dosimetry, and safety of the HER2-specific (99m)Tc-ADAPT6.

237 nts enabled the determination of ER, PR, and Her2 status from whole slide H&E images with 0.89 AUC (E

238 e used as an auxiliary method to analysis of HER2 status in tumor tissue in gastric or esophagogastri

239 ion and explore the impact of menopausal and HER2 status on CTS5 model.

240 tor status, progesterone receptor status, or HER2 status were excluded.

241 apy, lymph node status, hormone receptor and HER2 status, age, and geographical region.

242 story, morphology, ER status, PR status, and HER2 status, and (neo)adjuvant therapy.

243 Additional divisions were made based on HER2 status, PR status, cT stage, tumor grade, and prese

244 examined by pathologic analysis to document HER2 status.

245 low Tpl2 expression are associated with the Her2(+) status; Tpl2 expression positively correlates wi

246 .87), cN1 (OR 0.03, 95% CI 0.02-0.04) and ER+HER2- subtype (OR 0.30, 95% CI 0.20-0.44), and increased

247 Whilst HER2-subtype and enriched immune score are associated wi

248 as decreased in breast cancer of luminal and HER2 subtypes and inversely correlated with patients' pr

249 t cancer suggests that the high incidence of HER2(+) subtypes in Latinas might be due to population a

250 is undetectable in luminal A, luminal B, and HER2+ subtypes, as well as in normal breast cells with w

251 on Human epidermal growth factor receptor 2 (HER2)-targeted imaging with zirconium 89-pertuzumab PET/

252 nd Human epidermal growth factor receptor 2 (HER2)-targeted therapies are successful in patients with

253 In this Review, we summarize the available HER2-targeted agents and associated mechanisms of resist

254 ease progression after therapy with multiple HER2-targeted agents have limited treatment options.

255 ting treatment by either combining different HER2-targeted agents or extending the duration of HER2-t

256 f the immune microenvironment in response to HER2-targeted agents.

257 urpose To determine whether imaging with the HER2-targeted PET tracer zirconium 89 ((89)Zr)-pertuzuma

258 HER2-targeted therapies (lapatinib, neratinib, tucatinib

259 and who had previously received at least two HER2-targeted therapies for advanced disease.

260 Advances in HER2-targeted therapies have improved the survival of pa

261 Despite the implementation of multiple HER2-targeted therapies, patients with advanced HER2(+)

262 ment options but often acquire resistance to HER2-targeted therapy after initial response.

263 pre-treatment (N = 110), after one cycle of HER2-targeted therapy alone (N = 89), and at time of sur

264 HER2-targeted therapy has changed the natural history of

265 occurring during neoadjuvant treatment with HER2-targeted therapy plus chemotherapy in 5% or more of

266 after standard preoperative chemotherapy and HER2-targeted therapy should be offered 14 cycles of adj

267 Four cycles of HER2-targeted therapy were administered concurrently wit

268 fter completing neoadjuvant chemotherapy and HER2-targeted therapy were allocated to adjuvant trastuz

269 res increased in all arms after one cycle of HER2-targeted therapy, decreasing again by the time of s

270 patinib (L; N = 36), or both (TL; N = 58) as HER2-targeted therapy, with each participant given one c

271 targeted agents or extending the duration of HER2-targeted therapy.

272 forecast treatment response with and without HER2-targeted therapy.

273 ome activation associated with resistance to HER2-targeted therapy.

274 ination group); neither death was related to HER2-targeted therapy.

275 le human epidermal growth factor receptor 2 (HER2) -targeting drugs added to neoadjuvant chemotherapy

276 In CALGB 40601, dual HER2-targeting resulted in significant RFS and OS benefi

277 ast and gastroesophageal cancer patients for HER2-targeting therapies.

278 as an imaging probe to stratify patients for HER2-targeting therapy in areas where PET imaging is not

279 We suggested that HER2 testing in liquid biopsy could be used as an auxili

280 ast cancers (HER2+ breast cancers), and anti-HER2 therapies have significantly improved prognosis of

281 imitations associated with single-agent anti-HER2 therapies in patients with HER2+ breast cancer.

282 One resistance mechanism to anti-HER2 therapies is constitutive activation of the phospho

283 pant given one cycle of this designated anti-HER2 therapy alone followed by six cycles of standard co

284 s to early assessment of sensitivity to anti-HER2 therapy and shed light on the role of the immune mi

285 HER2 therapy sensitivity is restored in the fibroblast c

286 combination chemotherapy with the same anti-HER2 therapy.

287 (B6xA/J)F1 and (B6xNOD)F1 HER2 transgenic mice received Ad/E2TM after NK cell depl

288 The response of DO F1 HER2 transgenic mice was remarkably variable.

289 imitations associated with single-agent anti-HER2 treatment in PIK3CA-mutant HER2+ breast cancer cell

290 n multivariate models, the odds of having an HER2(+) tumor increased by a factor of 1.20 with every 1

291 tified that PAX2 inhibits cell growth of ER+/HER2- tumor cells in a dose-dependent manner.

292 Results suggest that the high prevalence of HER2(+) tumors in Latinas could be due in part to the pr

293 The biologic half-life of (131)I-GMIB-anti-HER2-VHH1 in healthy subjects was about 8 h.

294 tumor-imaging potential of (131)I-GMIB-anti-HER2-VHH1 in healthy volunteers and breast cancer patien

295 ncer showed focal uptake of (131)I-GMIB-anti-HER2-VHH1 in metastatic lesions.

296 The biodistribution of (131)I-GMIB-anti-HER2-VHH1 was assessed using whole-body (anterior and po

297 administered (38 +/- 9 MBq) (131)I-GMIB-anti-HER2-VHH1.

298 py with small-molecule inhibitors of AKT and HER2 was conducted in HER2+ breast cancer cell lines wit

299 To date, small-molecule inhibitors targeting Her2 which can be used in clinical routine are lacking,

300 has also been shown to affect HIF-1alpha and HER2, which are both known to play a crucial role in can

301 This mimic binds HER2 with comparable avidity to trastuzumab, has similar

302 ts that an antibody drug conjugate targeting HER2 would have superior efficacy versus selective HER2