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Eleanor Y. Chen

Researcher at University of Washington

Publications -  61
Citations -  1438

Eleanor Y. Chen is an academic researcher from University of Washington. The author has contributed to research in topics: Rhabdomyosarcoma & Medicine. The author has an hindex of 19, co-authored 49 publications receiving 1090 citations. Previous affiliations of Eleanor Y. Chen include Brigham and Women's Hospital & Harvard University.

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Secretory cell outgrowth, PAX2 and serous carcinogenesis in the Fallopian tube†

TL;DR: This study reveals, for the first time, an entity (SCOUT) that is associated with serous cancer, expands the topography of altered PAX2 expression in the female genital tract mucosa and highlights another potential pathway disturbance involved in early serous carcinogenesis in the Fallopian tube.
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Glycogen synthase kinase 3 inhibitors induce the canonical WNT/β-catenin pathway to suppress growth and self-renewal in embryonal rhabdomyosarcoma.

TL;DR: An unconventional tumor suppressive role for the canonical WNT/β-catenin pathway in regulating self-renewal of ERMS is identified and therapeutic strategies to target differentiation of TPCs in ERMS are revealed.
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In Vivo Imaging of Tumor-Propagating Cells, Regional Tumor Heterogeneity, and Dynamic Cell Movements in Embryonal Rhabdomyosarcoma

TL;DR: Time-lapse imaging of late-stage ERMS revealed that myf5+ cells populate newly formed tumor only after seeding by highly migratory myogenin+ ERMS cells, suggesting that non-tumor-propagating cells likely have important supportive roles in cancer progression and facilitate metastasis.
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A pathologist's road map to benign, precancerous, and malignant intraepithelial proliferations in the fallopian tube.

TL;DR: This review addresses 4 categories of tubal epithelial change: metaplasias; nonmalignant atypias; potential precursors, including secretory cell outgrowths and p53 signatures; and tubal intraepithelial carcinomas.
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Cellular angiofibroma with atypia or sarcomatous transformation: clinicopathologic analysis of 13 cases.

TL;DR: Clinopathologic features in 13 cases of cellular angiofibroma with morphologic atypia or sarcomatous transformation are characterized, finding overexpression of p16 in the atypical cells and sarcoma NOS suggests a possible underlying molecular mechanism.