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Journal ArticleDOI

EMT: A mechanism for escape from EGFR-targeted therapy in lung cancer.

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TLDR
It is proposed that therapeutic inhibition of EMT-activated mechanisms of cell survival in NSCLC would eliminate pools of persister cells and prevent or delay cancer recurrence when applied in combination with the agents targeting EGFR.
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This article is published in Biochimica et Biophysica Acta.The article was published on 2019-01-01. It has received 127 citations till now. The article focuses on the topics: Epithelial–mesenchymal transition & Targeted therapy.

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Citations
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The epigenetics of epithelial-mesenchymal plasticity in cancer

TL;DR: In this article, a review of the interactions between EMT-inducing transcription factors and epigenetic modulators during cancer progression and the therapeutic implications of exploiting this intricate regulatory process is presented.
Journal ArticleDOI

Communication between EMT and PD-L1 signaling: New insights into tumor immune evasion.

TL;DR: Recent findings on EMT-induced immune suppression and evasion in the tumor microenvironment (TME) and the value of preclinical or clinical trials using EMT targeted therapy combined with PD-L1 inhibitors are investigated.
Journal ArticleDOI

Dynamic EMT: a multi-tool for tumor progression.

TL;DR: The epithelial-mesenchymal transition (EMT) is fundamental for embryonic morphogenesis as discussed by the authors, and it is increasingly understood to orchestrate a large variety of complementary cancer features, such as tumor cell stemness, tumorigenicity, resistance to therapy and adaptation to changes in the microenvironment.
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Acquired resistance to targeted therapies in NSCLC: Updates and evolving insights.

TL;DR: A broad overview of the mechanisms of resistance to targeted therapy that have been demonstrated across molecular subtypes of NSCLC is provided, highlighting the dynamic interplay between driver oncogene, bypass signaling pathways, shifting cellular phenotypes, and surrounding tumor microenvironment.
Journal ArticleDOI

Contribution of Epithelial Plasticity to Therapy Resistance.

TL;DR: The recognition of the presence in tumours of intermediate hybrid epithelial/mesenchymal states as the most likely manifestation of epithelial plasticity and their potential link to stemness and tumour heterogeneity, provide new clues to understanding resistance and could be exploited in the search for anti-resistance strategies.
References
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Journal ArticleDOI

Hallmarks of cancer: the next generation.

TL;DR: Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer.
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A genetic model for colorectal tumorigenesis

TL;DR: A model for the genetic basis of colorectal neoplasia that includes the following salient features is presented, which may be applicable to other common epithelial neoplasms, in which tumors of varying stage are more difficult to study.
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Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib

TL;DR: A subgroup of patients with non-small-cell lung cancer have specific mutations in the EGFR gene which correlate with clinical responsiveness to the tyrosine kinase inhibitor gefitinib, and these mutations lead to increased growth factor signaling and confer susceptibility to the inhibitor.
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Epithelial-Mesenchymal Transitions in Development and Disease

TL;DR: The mesenchymal state is associated with the capacity of cells to migrate to distant organs and maintain stemness, allowing their subsequent differentiation into multiple cell types during development and the initiation of metastasis.
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