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Shen Mynn Tan

Researcher at Harvard University

Publications -  6
Citations -  1848

Shen Mynn Tan is an academic researcher from Harvard University. The author has contributed to research in topics: PTEN & microRNA. The author has an hindex of 6, co-authored 6 publications receiving 1702 citations. Previous affiliations of Shen Mynn Tan include Boston Children's Hospital.

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Coding-Independent Regulation of the Tumor Suppressor PTEN by Competing Endogenous mRNAs

TL;DR: This study identified and validated endogenous protein-coding transcripts that regulate PTEN, antagonize PI3K/AKT signaling, and possess growth- and tumor-suppressive properties and presents a road map for the prediction and validation of ceRNA activity and networks and thus imparts a trans-regulatory function to protein- coding mRNAs.
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A Genome-wide siRNA Screen Identifies Proteasome Addiction as a Vulnerability of Basal-like Triple-Negative Breast Cancer Cells

TL;DR: A genome-wide siRNA lethality screen compared two human breast epithelial cell lines transformed with the same genes to identify basal-like TNBC dependencies, and expression of the screen's 154 BPLER dependency genes correlated with poor prognosis in breast, but not lung or colon, cancer.
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Sequencing of Captive Target Transcripts Identifies the Network of Regulated Genes and Functions of Primate-Specific miR-522

TL;DR: An unbiased sequencing-based systems approach is applied to characterize miR-522, a member of the oncogenic primate-specific chromosome 19 miRNA cluster, highly expressed in poorly differentiated cancers and suggested that it regulates cell proliferation, detachment, migration, and epithelial-mesenchymal transition.
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Characterization of dual PTEN and p53-targeting microRNAs identifies microRNA-638/Dnm2 as a two-hit oncogenic locus.

TL;DR: It is found that miR-638 overexpression promotes tumorigenesis and cooperativity between miR -638 and its host gene Dnm2 is demonstrated, suggesting that the Dnm1 locus encodes two distinct oncogenic components that play important roles in tumorsigenesis.