about
A phase II trial to assess efficacy and safety of afatinib in extensively pretreated patients with HER2-negative metastatic breast cancerStructural and Functional Studies on the Interaction of Adenovirus Fiber Knobs and Desmoglein 2Therapeutic targets of triple-negative breast cancer: a reviewThe LINK-A lncRNA activates normoxic HIF1α signalling in triple-negative breast cancerCyanidin-3-o-glucoside directly binds to ERα36 and inhibits EGFR-positive triple-negative breast cancerConditional internalization of PEGylated nanomedicines by PEG engagers for triple negative breast cancer therapyhMAGEA2 promotes progression of breast cancer by regulating Akt and Erk1/2 pathways.Evolution of breast cancer therapeutics: Breast tumour kinase's role in breast cancer and hope for breast tumour kinase targeted therapyEMT and EGFR in CTCs cytokeratin negative non-metastatic breast cancerLinking signaling pathways to transcriptional programs in breast cancer.Is the future of personalized therapy in triple-negative breast cancer based on molecular subtype?Feasibility study of personalized peptide vaccination for metastatic recurrent triple-negative breast cancer patientsStandard of care and promising new agents for triple negative metastatic breast cancerToca-1 is suppressed by p53 to limit breast cancer cell invasion and tumor metastasis.Epidermal Growth Factor Receptor Expression in Triple Negative and Nontriple Negative Breast Carcinomas.The efficacy of betulinic acid in triple-negative breast cancer.Systematic Identification and Assessment of Therapeutic Targets for Breast Cancer Based on Genome-Wide RNA Interference TranscriptomesSHP2 acts both upstream and downstream of multiple receptor tyrosine kinases to promote basal-like and triple-negative breast cancer.Tamoxifen Action in ER-Negative Breast Cancer.Epithelial to mesenchymal transition promotes breast cancer progression via a fibronectin-dependent STAT3 signaling pathway.Features of triple-negative breast cancer: Analysis of 38,813 cases from the national cancer databaseThe potential role of nanotechnology in therapeutic approaches for triple negative breast cancer.Radiation-enhanced therapeutic targeting of galectin-1 enriched malignant stroma in triple negative breast cancer.Stress-induced EGF receptor signaling through STAT3 and tumor progression in triple-negative breast cancer.Comparison of a mouse and a novel human scFv-SNAP-auristatin F drug conjugate with potent activity against EGFR-overexpressing human solid tumor cells.Hypoxia-inducible factor prolyl hydroxylase 2 (PHD2) is a direct regulator of epidermal growth factor receptor (EGFR) signaling in breast cancer.Metalloprotease-dependent activation of EGFR modulates CD44+/CD24- populations in triple negative breast cancer cells through the MEK/ERK pathway.Potential therapeutic targets of triple-negative breast cancer based on its intrinsic subtype.Fatty acid synthase affects expression of ErbB receptors in epithelial to mesenchymal transition of breast cancer cells and invasive ductal carcinoma.Hypoxia-induced reactive oxygen species mediate N-cadherin and SERPINE1 expression, EGFR signalling and motility in MDA-MB-468 breast cancer cells.Breast Cancer Cell Line Classification and Its Relevance with Breast Tumor Subtyping.APC loss in breast cancer leads to doxorubicin resistance via STAT3 activation.One-pot three-component synthesis of novel spirooxindoles with potential cytotoxic activity against triple-negative breast cancer MDA-MB-231 cells.Measurement of Epidermal Growth Factor Receptor-Derived Signals Within Plasma Membrane Clathrin Structures.Combined drug therapeutic strategies for the effective treatment of Triple Negative Breast Cancer.Mithramycin A suppresses basal triple-negative breast cancer cell survival partially via down-regulating Krüppel-like factor 5 transcription by Sp1.Cigarette smoke-induced EGFR activation promotes epithelial mesenchymal migration of human retinal pigment epithelial cells through regulation of the FAK-mediated Syk/Src pathway.Significance of EGFR Expression in Circulating Tumor Cells.NOTCH3 inactivation increases triple negative breast cancer sensitivity to gefitinib by promoting EGFR tyrosine dephosphorylation and its intracellular arrest.
P2860
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P2860
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
2011年论文
@zh
2011年论文
@zh-cn
name
Targeting EGFR in Triple Negative Breast Cancer.
@en
Targeting EGFR in Triple Negative Breast Cancer.
@nl
type
label
Targeting EGFR in Triple Negative Breast Cancer.
@en
Targeting EGFR in Triple Negative Breast Cancer.
@nl
prefLabel
Targeting EGFR in Triple Negative Breast Cancer.
@en
Targeting EGFR in Triple Negative Breast Cancer.
@nl
P2860
P356
P1433
P1476
Targeting EGFR in Triple Negative Breast Cancer.
@en
P2093
Dongwei Zhang
Naoto T Ueno
P2860
P304
P356
10.7150/JCA.2.324
P577
2011-05-28T00:00:00Z