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Elinor Ng Eaton

Researcher at Massachusetts Institute of Technology

Publications -  22
Citations -  18846

Elinor Ng Eaton is an academic researcher from Massachusetts Institute of Technology. The author has contributed to research in topics: Stem cell & Epithelial–mesenchymal transition. The author has an hindex of 17, co-authored 21 publications receiving 17475 citations.

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The Epithelial-Mesenchymal Transition Generates Cells with Properties of Stem Cells

TL;DR: It is reported that the induction of an EMT in immortalized human mammary epithelial cells (HMLEs) results in the acquisition of mesenchymal traits and in the expression of stem-cell markers, and it is shown that those cells have an increased ability to form mammospheres, a property associated with mammARY epithelial stem cells.
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hSIR2SIRT1 Functions as an NAD-Dependent p53 Deacetylase

TL;DR: It is proposed that hSir2, the human homolog of the S. cerevisiae Sir2 protein known to be involved in cell aging and in the response to DNA damage, binds and deacetylates the p53 protein with a specificity for its C-terminal Lys382 residue.
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hEST2, the Putative Human Telomerase Catalytic Subunit Gene, Is Up-Regulated in Tumor Cells and during Immortalization

TL;DR: The cloning of a human gene, hEST2, that shares significant sequence similarity with the telomerase catalytic subunit genes of lower eukaryotes is reported, suggesting that the induction of hEST 2 mRNA expression is required for the telomersase activation that occurs during cellular immortalization and tumor progression.
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Inhibition of telomerase limits the growth of human cancer cells

TL;DR: It is shown here that expression of a mutant catalytic subunit of human telomerase results in complete inhibition of telomer enzyme activity, reduction in telomere length and death of tumor cells, validating human telomersase reverse transcriptase as an important target for the development of anti-neoplastic therapies.
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Paracrine and autocrine signals induce and maintain mesenchymal and stem cell states in the breast.

TL;DR: In this article, the authors describe three signaling pathways, involving transforming growth factor (TGF)-β and canonical and noncanonical Wnt signaling, that collaborate to induce activation of the EMT program and thereafter function in an autocrine fashion to maintain the resulting mesenchymal state.