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Won-Shik Choi

Researcher at University of Alberta

Publications -  8
Citations -  175

Won-Shik Choi is an academic researcher from University of Alberta. The author has contributed to research in topics: Cancer cell & Mitotic catastrophe. The author has an hindex of 4, co-authored 7 publications receiving 83 citations. Previous affiliations of Won-Shik Choi include Cross Cancer Institute.

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Prolonged mitotic arrest induced by Wee1 inhibition sensitizes breast cancer cells to paclitaxel.

TL;DR: This study shows premature mitotic cells that arise from MK-1775 treatment exhibited centromere fragmentation, a morphological feature of mitotic catastrophe that is characterized by centromeres and kinetochore proteins that co-cluster away from the condensed chromosomes and finds that paclitaxel enhances MK- 1775 mediated cell killing in breast cancer cells.
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Upregulation of Myt1 Promotes Acquired Resistance of Cancer Cells to Wee1 Inhibition.

TL;DR: It is demonstrated that upregulating Myt1 is a mechanism by which cancer cells acquire resistance to Adavosertib, and downregulating myt1 enhanced ectopic Cdk1 activity and restored sensitivity to Advosert ib.
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NFIB promotes cell survival by directly suppressing p21 transcription in TP53‐mutated triple‐negative breast cancer

TL;DR: The results indicate that NFIB is an important TNBC factor that drives tumour cell growth and drug resistance, leading to poor clinical outcomes, and targeting NFIB in TP53‐mutated TNBC may reverse oncogenic properties associated with mutant p53 by restoring p21 activity.
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Trastuzumab Mechanism of Action; 20 Years of Research to Unravel a Dilemma

TL;DR: A review of the various mechanisms of action of trastuzumab for HER2-targeted breast cancer patients can be found in this article, where the authors aimed to provide a detailed insight into the various mechanism of action.
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The FABP12/PPARγ pathway promotes metastatic transformation by inducing epithelial-to-mesenchymal transition and lipid-derived energy production in prostate cancer cells.

TL;DR: A novel role is pointed to for a FABP‐PPAR pathway in promoting PCa metastasis through induction of EMT and lipid bioenergetics and increased reliance on fatty acids for energy production.