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Elizabeth E. Hoskins

Researcher at Cincinnati Children's Hospital Medical Center

Publications -  18
Citations -  2121

Elizabeth E. Hoskins is an academic researcher from Cincinnati Children's Hospital Medical Center. The author has contributed to research in topics: Fanconi anemia & Cancer. The author has an hindex of 13, co-authored 14 publications receiving 1779 citations.

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Directed differentiation of human pluripotent stem cells into intestinal tissue in vitro

TL;DR: A robust and efficient process is established to direct the differentiation of human PSCs into intestinal tissue in vitro using a temporal series of growth factor manipulations to mimic embryonic intestinal development and indicates that human intestinal stem cells form de novo during development.
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Human Papillomavirus 16 E7 Oncoprotein Attenuates DNA Damage Checkpoint Control by Increasing the Proteolytic Turnover of Claspin

TL;DR: It is suggested that the HPV-16 E7 oncoprotein alleviates DNA damage checkpoint responses and promotes mitotic entry by accelerating claspin degradation through a mechanism that involves deregulation of components of the SCF(beta-TrCP)-based claspin degraded machinery.
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DEK proto-oncogene expression interferes with the normal epithelial differentiation program.

TL;DR: Up-regulated DEK protein levels in both human papilloma virus-positive hyperplastic murine skin and a subset of human squamous cell carcinomas are reported here to suggest that DEK up-regulation may contribute to carcinoma development at least in part through increased proliferation and retardation of differentiation.
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Fanconi anemia deficiency stimulates HPV-associated hyperplastic growth in organotypic epithelial raft culture

TL;DR: These findings support a new role for FA pathways in the maintenance of differentiation-dependent cell cycle exit, with the implication that FA deficiencies may contribute to the high risk of FA patients for developing HPV-associated SCC.
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Coordinate regulation of Fanconi anemia gene expression occurs through the Rb/E2F pathway

TL;DR: The data demonstrate FA gene co-regulation in synchrony with the cell cycle and suggest that deregulated expression of individual FA genes—in addition to FA gene mutation—may promote FA-related human cancer.