YAP-Dependent AXL Overexpression Mediates Resistance to EGFR Inhibitors in NSCLC
Elena Ghiso,Cristina Migliore,Vito Ciciriello,Elena Morando,Annalisa Petrelli,Simona Corso,Emmanuele De Luca,Gaia Gatti,Marco Volante,Silvia Giordano +9 more
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TLDR
The reported data demonstrate that YAP and its downstream target AXL play a crucial role in resistance to EGFR TKIs and suggest that a combined inhibition of EGFR and the YAP/AXL axis could be a good therapeutic option in selected NSCLC patients.About:
This article is published in Neoplasia.The article was published on 2017-12-01 and is currently open access. It has received 67 citations till now. The article focuses on the topics: AXL receptor tyrosine kinase & Tyrosine kinase.read more
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Targeting the Hippo pathway in cancer, fibrosis, wound healing and regenerative medicine
TL;DR: The Hippo pathway is an evolutionarily conserved signalling pathway with key roles in organ development, epithelial homeostasis, tissue regeneration, wound healing and immune modulation, and is an attractive target for therapeutic intervention.
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Hippo Pathway in Cancer: Aberrant Regulation and Therapeutic Opportunities
TL;DR: The Hippo pathway remains a central focus in both basic and translational research and is a key modulator of developmental biology and there are multiple efforts to target key components of the pathway for disease intervention.
Journal ArticleDOI
YAP/TAZ Signaling and Resistance to Cancer Therapy.
Chan D.K. Nguyen,Chunling Yi +1 more
TL;DR: Drug resistance is a major challenge in cancer treatment and emerging evidence indicates that deregulation of YAP/TAZ signaling may be a major mechanism of intrinsic and acquired resistance to various targeted and chemotherapies.
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A combat with the YAP/TAZ-TEAD oncoproteins for cancer therapy.
Ajaybabu V. Pobbati,Wanjin Hong +1 more
TL;DR: In this article, the authors classified YAP/TAZ-inhibiting drugs into three groups: group I drugs act on the upstream regulators that are stimulators of YAP and TAZ activities; group II drugs focus on targeting one of the oncogenic downstream YAP-TAZ transcriptional target genes.
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YAP/TAZ Activation as a Target for Treating Metastatic Cancer.
TL;DR: Evidence strongly suggests that inappropriate YAP or TAZ activity plays a causal role in cancer, and that targeting aberrant YAP/TAZ activation is a promising strategy for the treatment of metastatic disease.
References
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MET Amplification Leads to Gefitinib Resistance in Lung Cancer by Activating ERBB3 Signaling
Jeffrey A. Engelman,Kreshnik Zejnullahu,Tetsuya Mitsudomi,Youngchul Song,Courtney Hyland,Joon Oh Park,Neal I. Lindeman,Christopher-Michael Gale,Xiaojun Zhao,James J. Christensen,Takayuki Kosaka,Alison J. Holmes,Andrew M. Rogers,Federico Cappuzzo,Tony Mok,Charles Lee,Bruce E. Johnson,Lewis C. Cantley,Pasi A. Jänne +18 more
TL;DR: It is proposed that MET amplification may promote drug resistance in other ERBB-driven cancers as well after it was found that amplification of MET causes gefitinib resistance by driving ERBB3 (HER3)–dependent activation of PI3K, a pathway thought to be specific to EGFR/ERBB family receptors.
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Cancer drug resistance: an evolving paradigm
TL;DR: There are now unprecedented opportunities to understand and overcome drug resistance through the clinical assessment of rational therapeutic drug combinations and the use of predictive biomarkers to enable patient stratification.
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Acquired Resistance of Lung Adenocarcinomas to Gefitinib or Erlotinib Is Associated with a Second Mutation in the EGFR Kinase Domain
William Pao,Vincent A. Miller,Katerina Politi,Gregory J. Riely,Romel Somwar,Maureen F. Zakowski,Mark G. Kris,Harold E. Varmus +7 more
TL;DR: Biochemical analyses of transfected cells and growth inhibition studies with lung cancer cell lines demonstrate that the T790M mutation confers resistance to EGFR mutants usually sensitive to either gefitinib or erlotinib, which should help guide the search for more effective therapy against a specific subset of lung cancers.
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Elucidation of a universal size-control mechanism in Drosophila and mammals.
Jixin Dong,Georg Feldmann,Jianbin Huang,Shian Wu,Nailing Zhang,Sarah A. Comerford,Mariana F. Gayyed,Robert A. Anders,Anirban Maitra,Duojia Pan +9 more
TL;DR: It is demonstrated that a single phosphorylation site in Yki mediates the growth-suppressive output of the Hippo pathway, and that its dysregulation leads to tumorigenesis, uncovering a universal size-control mechanism in metazoan.
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TEAD mediates YAP-dependent gene induction and growth control
Bin Zhao,Xin Ye,Jindan Yu,Li Li,Li Li,Weiquan Li,Siming Li,Jianjun Yu,Jiandie D. Lin,Cun-Yu Wang,Arul M. Chinnaiyan,Zhi Chun Lai,Kun-Liang Guan +12 more
TL;DR: TEAD is revealed as a new component in the Hippo pathway playing essential roles in mediating biological functions of YAP, and is required for YAP-induced cell growth, oncogenic transformation, and epithelial-mesenchymal transition.