ライフサイエンスコーパス: HER2-amplified breast cancer

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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 this three-drug regimen for the treatment of HER2-amplified breast cancer brain metastases.

9 We developed a mouse model of HER2-amplified breast cancer brain metastasis using an o

10 ted the sensitive versus resistant states in HER2-amplified breast cancer cell responses to the HER2-

11 g frame screen to identify genes that rescue HER2-amplified breast cancer cells from HER2 inhibition

12 Increasing evidence suggests that HER2-amplified breast cancer cells use HER3/ErbB3 to dri

13 iently transfected HEK293T cells but also in HER2-amplified breast cancer cells.

14 (HER2)-targeting agents for the treatment of HER2-amplified breast cancer has dramatically improved o

15 Approximately 35% of HER2-amplified breast cancers have coamplification of th

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

17 have enhanced activity in PIK3CA mutant and HER2 amplified breast cancers in which PI3K inhibition d

18 This is best exemplified in the subset of HER2-amplified breast cancers, in which an increasing nu

19 ctivated Akt signaling is well documented in HER2-amplified breast cancer models, but the significanc

20 nal antibody currently used for treatment of HER2-amplified breast cancer patients.

21 ng drives Akt-dependent tumor progression in HER2-amplified breast cancers, rationalizing clinical in

22 Responses were noted in patients with HER2-amplified breast cancer resistant to trastuzumab, H

23 pectedly, we found that in PIK3CA mutant and HER2 amplified breast cancers sensitive to PI3K inhibito

24 s tumorigenesis, cell growth and survival in HER2-amplified breast cancer through transcriptional reg

25 ation of HER3, but not EGFR, was observed in HER2-amplified breast cancer tissues.

26 ects of PI3K inhibition in PIK3CA mutant and HER2 amplified breast cancers using PI3K inhibitors curr

27 In contrast to HER2-amplified breast cancers, we found that PI3K-mTOR i

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