G
Gary D. Shipley
Researcher at Oregon Health & Science University
Publications - 41
Citations - 5513
Gary D. Shipley is an academic researcher from Oregon Health & Science University. The author has contributed to research in topics: Growth factor & Epidermal growth factor. The author has an hindex of 27, co-authored 41 publications receiving 5486 citations. Previous affiliations of Gary D. Shipley include Mayo Clinic.
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Journal Article
Growth Factors and Cancer
TL;DR: The excitement and attention focused on cellular oncogenes in recent years is now turning toward growth factors, not only as they concern the control of normal cell growth but also the involvement of growth factor-initiated pathways in the etiology of cancer.
Journal Article
Reversible inhibition of normal human prokeratinocyte proliferation by type beta transforming growth factor-growth inhibitor in serum-free medium.
TL;DR: Normal prokeratinocytes are demonstrated to secrete TGF beta/GI-like molecules into the culture medium and to have specific cell surface receptors for this molecule, and a human squamous cell carcinoma, SCC-25, does not arrest growth when exposed to TGFbeta/GI.
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Induction of c-sis mRNA and activity similar to platelet-derived growth factor by transforming growth factor β: A proposed model for indirect mitogenesis involving autocrine activity
Edward B. Leof,Jacqueline A. Proper,Anton Scott Goustin,Gary D. Shipley,Paul E. DiCorleto,Harold L. Moses +5 more
TL;DR: A model is proposed in which the monolayer mitogenicity of transforming growth factor beta is mediated by the induction of c-sis and PDGF and the subsequent autocrine stimulation ofc-fos, c-myc, and other PDGF-inducible genes.
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Integrated control of growth and differentiation of normal human prokeratinocytes cultured in serum-free medium: Clonal analyses, growth kinetics, and cell cycle studies
TL;DR: The data show that proliferative keratinocytes can be growth arrested in medium that does not induce differentiation and that such a procedure significantly limits the cell's subsequent proliferative potential, suggesting that proliferation and differentiation are regulated in an integrated manner.
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Suramin inhibition of growth factor receptor binding and mitogenicity in AKR‐2B cells
TL;DR: Suramin's spectrum of action for growth factors and their receptors should be extended to include TGFβ, HBGF‐2, and EGF as well as PDGF, and the data suggest that the spontaneous growth of AKR‐MCA cells in soft agar is dependent on growth factor binding to cell surface receptors.