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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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Autocrine TGF-β and stromal cell-derived factor-1 (SDF-1) signaling drives the evolution of tumor-promoting mammary stromal myofibroblasts

TL;DR: Findings indicate that the establishment of the self-sustaining TGF-β and SDF-1 autocrine signaling gives rise to tumor-promoting CAF myofibroblasts during tumor progression, which may prove to be an attractive therapeutic target to block the evolution of tumor- Promoting CAFs.
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Distinct emt programs control normal mammary stem cells and tumour-initiating cells

TL;DR: It is shown that normal gland-reconstituting mammary stem cells residing in the basal layer of the mammary epithelium and breast TICs originating in the luminal layer exploit the paralogous EMT-TFs Slug and Snail, respectively, which induce distinct EMT programs.
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Function of a human cyclin gene as an oncogene.

TL;DR: In cultured cells, a cDNA clone of the cyclin D1 gene can contribute to cell transformation by complementing a defective adenovirus E1A oncogene, suggesting a similar role in tumor progression in vivo.
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Telomerase activity is restored in human cells by ectopic expression of hTERT (hEST2), the catalytic subunit of telomerase

TL;DR: It is concluded that synthesis of the hTERT telomerase subunit represents the rate-limiting determinant of telomer enzyme activity in these cells and that this protein, once expressed, becomes part of the functional telomersase holoenzyme.
Journal Article

Regulation of cyclin E transcription by E2Fs and retinoblastoma protein.

TL;DR: The cloning of the cyclin E promoter is reported and the identification of several putative E2F binding sites within the promoter sequence are reported, which suggest the operation of a positive-feedback loop in late G1 that functions to ensure continued cycle regulation and pRB inactivation.