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Kathleen C. Flanders

Researcher at National Institutes of Health

Publications -  150
Citations -  19846

Kathleen C. Flanders is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Transforming growth factor & Transforming growth factor beta. The author has an hindex of 68, co-authored 150 publications receiving 19278 citations. Previous affiliations of Kathleen C. Flanders include Gyeongsang National University & New York State Department of Health.

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Induction of Transforming Growth Factor β1 in Human Breast Cancer in Vivo following Tamoxifen Treatment

TL;DR: In vivo evidence is found that 3 months of tamoxifen treatment causes a consistent induction of extracellular TGF-beta 1 in breast cancer biopsies, compared with matched pretreatment samples from the same patient.
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Transforming growth factor-beta 1: histochemical localization with antibodies to different epitopes.

TL;DR: Results from RIA and ELISAs indicate that anti-LC(1-30) and anti-CC(1 -30) recognize different epitopes of this peptide and of TGF-beta 1 itself, suggesting that T GF-beta synthesis sites may be bound to matrix proteins.
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TRANSFORMING GROWTH FACTOR-βS IN NEURODEGENERATIVE DISEASE

TL;DR: Transforming growth factors-betas (TGF-Betas), a family of multifunctional peptide growth factors, affect cells of the central nervous system (CNS) as discussed by the authors.
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Erythropoietin receptor signalling is required for normal brain development

TL;DR: Evidence is provided that erythropoietin acts to stimulate neural progenitor cells and to prevent apoptosis in the embryonic brain and that induction of erythroid differentiation and its receptor by hypoxia may contribute to selective cell survival in the brain.
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Smad3 is key to TGF-β-mediated epithelial-to-mesenchymal transition, fibrosis, tumor suppression and metastasis

TL;DR: Focusing on models involving epithelial-to-mesenchymal transition (EMT), including injury to the lens and retina of the eye and to the kidney, it is found that loss of Smad3 blocks EMT and attenuates development of fibrotic sequelae.