Acquired MET expression confers resistance to EGFR inhibition in a mouse model of glioblastoma multiforme.
about
The dynamic nature of the kinomeTargeted molecular therapies against epidermal growth factor receptor: past experiences and challengesContemporary murine models in preclinical astrocytoma drug developmentCooperativity between MAPK and PI3K signaling activation is required for glioblastoma pathogenesis.Combined PDK1 and CHK1 inhibition is required to kill glioblastoma stem-like cells in vitro and in vivoDNA double-strand breaks cooperate with loss of Ink4 and Arf tumor suppressors to generate glioblastomas with frequent Met amplification.Phase II study of cetuximab in combination with cisplatin and radiation in unresectable, locally advanced head and neck squamous cell carcinoma: Eastern cooperative oncology group trial E3303.Combination strategy targeting VEGF and HGF/c-met in human renal cell carcinoma modelsNT113, a pan-ERBB inhibitor with high brain penetrance, inhibits the growth of glioblastoma xenografts with EGFR amplification.Growth-factor-driven rescue to receptor tyrosine kinase (RTK) inhibitors through Akt and Erk phosphorylation in pediatric low grade astrocytoma and ependymomaTargeting aPKC disables oncogenic signaling by both the EGFR and the proinflammatory cytokine TNFα in glioblastomaExogenous HGF Bypasses the Effects of ErbB Inhibition on Tumor Cell Viability in Medulloblastoma Cell LinesActivation of MET pathway predicts poor outcome to cetuximab in patients with recurrent or metastatic head and neck cancerTyrosine kinase inhibitor SU11274 increased tumorigenicity and enriched for melanoma-initiating cells by bioenergetic modulation.Targeting EGFR for treatment of glioblastoma: molecular basis to overcome resistance.The retinoic acid derivative, ABPN, inhibits pancreatic cancer through induction of Nrdp1Inhibition of DYRK1A destabilizes EGFR and reduces EGFR-dependent glioblastoma growth.Tumor metabolism of malignant gliomas.EGFR-dependent mechanisms in glioblastoma: towards a better therapeutic strategy.Immune Checkpoint Blockade Biology in Mouse Models of Glioblastoma.Gene expression profile identifies tyrosine kinase c-Met as a targetable mediator of antiangiogenic therapy resistance.Role and Therapeutic Targeting of the HGF/MET Pathway in Glioblastoma.Therapeutic targeting of chemoresistant and recurrent glioblastoma stem cells with a proapoptotic variant of oncolytic herpes simplex virus.BCL6 promotes glioma and serves as a therapeutic target.Inhibition of EGFR induces a c-MET-driven stem cell population in glioblastoma.Immunotherapies for malignant glioma.BET inhibition overcomes receptor tyrosine kinase-mediated cetuximab resistance in HNSCC.Small-molecule PROTACs: An emerging and promising approach for the development of targeted therapy drugsA PDGFRα-driven mouse model of glioblastoma reveals a stathmin1-mediated mechanism of sensitivity to vinblastine
P2860
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P2860
Acquired MET expression confers resistance to EGFR inhibition in a mouse model of glioblastoma multiforme.
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
Acquired MET expression confer ...... el of glioblastoma multiforme.
@en
type
label
Acquired MET expression confer ...... el of glioblastoma multiforme.
@en
prefLabel
Acquired MET expression confer ...... el of glioblastoma multiforme.
@en
P2093
P2860
P356
P1433
P1476
Acquired MET expression confer ...... del of glioblastoma multiforme
@en
P2093
A Boskovitz
C A Whittaker
D E Housman
J Acquaviva
P2860
P2888
P304
P356
10.1038/ONC.2011.474
P407
P577
2011-10-24T00:00:00Z
P5875
P6179
1046554846