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1 rastuzumab in treating preclinical models of HER2-amplified breast cancer.
2 een implicated as key coreceptors that drive HER2-amplified breast cancer.
3 s patterns of gene expression in luminal and HER2-amplified breast cancer.
4 th human epidermal growth factor receptor-2 (HER2)-amplified breast cancer.
5 inically relevant than inhibition of EGFR in HER2-amplified breast cancer and also suggest that addin
6 erior efficacy in treating in vivo models of HER2-amplified breast cancer and support the development
7 er cells, including EGFR-mutant lung cancer, HER2-amplified breast cancer, and BCR-ABL leukemia.
8    Human epidermal growth factor receptor 2 (HER2)-amplified breast cancers are treated using targete
9 this three-drug regimen for the treatment of HER2-amplified breast cancer brain metastases.
10                We developed a mouse model of HER2-amplified breast cancer brain metastasis using an o
11  driving functions in the pathophysiology of HER2-amplified breast cancers, but this function is less
12 ve phosphorylation of HER3 are ubiquitous in HER2-amplified breast cancer cell lines, but much more v
13 ted the sensitive versus resistant states in HER2-amplified breast cancer cell responses to the HER2-
14 g frame screen to identify genes that rescue HER2-amplified breast cancer cells from HER2 inhibition
15            Increasing evidence suggests that HER2-amplified breast cancer cells use HER3/ErbB3 to dri
16 iently transfected HEK293T cells but also in HER2-amplified breast cancer cells.
17                        Inhibition of HER2 in HER2-amplified breast cancer has been remarkably success
18 (HER2)-targeting agents for the treatment of HER2-amplified breast cancer has dramatically improved o
19                         Approximately 35% of HER2-amplified breast cancers have coamplification of th
20           Targeted therapies for ER+/PR+ and HER2-amplified breast cancers have improved patient surv
21  have enhanced activity in PIK3CA mutant and HER2 amplified breast cancers in which PI3K inhibition d
22    This is best exemplified in the subset of HER2-amplified breast cancers, in which an increasing nu
23 ctivated Akt signaling is well documented in HER2-amplified breast cancer models, but the significanc
24 nal antibody currently used for treatment of HER2-amplified breast cancer patients.
25 ng drives Akt-dependent tumor progression in HER2-amplified breast cancers, rationalizing clinical in
26        Responses were noted in patients with HER2-amplified breast cancer resistant to trastuzumab, H
27 pectedly, we found that in PIK3CA mutant and HER2 amplified breast cancers sensitive to PI3K inhibito
28 s tumorigenesis, cell growth and survival in HER2-amplified breast cancer through transcriptional reg
29 ation of HER3, but not EGFR, was observed in HER2-amplified breast cancer tissues.
30 ects of PI3K inhibition in PIK3CA mutant and HER2 amplified breast cancers using PI3K inhibitors curr
31                               In contrast to HER2-amplified breast cancers, we found that PI3K-mTOR i
32             Through genomic profiling of 733 HER2-amplified breast cancers, we identify enrichment of