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Juan Chen

Researcher at University of Iowa

Publications -  26
Citations -  689

Juan Chen is an academic researcher from University of Iowa. The author has contributed to research in topics: Medicine & Interstitial lung disease. The author has an hindex of 11, co-authored 19 publications receiving 569 citations. Previous affiliations of Juan Chen include Jilin University.

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Cloned ferrets produced by somatic cell nuclear transfer.

TL;DR: The successful production of live cloned, reproductively competent, ferrets using species-specific SCNT methodologies is reported, making it feasible to begin generating genetically defined ferrets for studying transmissible and inherited human lung diseases.
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Adeno-associated virus–targeted disruption of the CFTR gene in cloned ferrets

TL;DR: This study describes the production of a CFTR gene-deficient model in the domestic ferret using recombinant adeno-associated virus-mediated gene targeting in fibroblasts, followed by nuclear transfer cloning.
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Wnt signaling as potential therapeutic target in lung cancer

TL;DR: The results from clinical studies suggest that inhibitors targeting the Wnt pathway show promise against lung cancer, and the regulatory roles of microRNAs in Wnt signaling are expounded, as well as the potential of the WNT pathway to provide biomarkers and therapeutic targets in lung cancer.
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Nrf2-Mediated Metabolic Reprogramming in Cancer

TL;DR: This minireview aims for the development of noninvasive biomarkers and novel therapeutic approaches for cancer based on Nrf2-directed cancer metabolic reprogramming in the near future and to highlight the role of NRF2 in the regulation of malignant transformation, cancer proliferation, and theDevelopment of treatment resistance via metabolic adaptations.
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Increased expression of miR-641 contributes to erlotinib resistance in non-small-cell lung cancer cells by targeting NF1.

TL;DR: It is suggested that increased expression of miR‐641 significantly contributes to erlotinib resistance development in NSCLC cells through activating ERK signaling by targeting NF1 and that inhibition of mi R‐641 may reverse acquired resistance of NS CLC cells to erotinib treatment.