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Christine M. Eischen

Researcher at Thomas Jefferson University

Publications -  109
Citations -  7519

Christine M. Eischen is an academic researcher from Thomas Jefferson University. The author has contributed to research in topics: Apoptosis & Mdm2. The author has an hindex of 39, co-authored 96 publications receiving 6762 citations. Previous affiliations of Christine M. Eischen include Mayo Clinic & Vanderbilt University.

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Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization

TL;DR: MEFs that survive myc overexpression sustain p53 mutation or ARF loss during the process of establishment and become immortal, and ARF regulates a p53-dependent checkpoint that safeguards cells against hyperproliferative, oncogenic signals.
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Disruption of the ARF–Mdm2–p53 tumor suppressor pathway in Myc-induced lymphomagenesis

TL;DR: It is reported that p53 and ARF also potentiate Myc-induced apoptosis in primary pre-B-cell cultures, and that spontaneous inactivation of the ARF-Mdm2-p53 pathway occurs frequently in tumors arising in Emu-myc transgenic mice.
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Comparison of Apoptosis in Wild-Type and Fas-Resistant Cells: Chemotherapy-Induced Apoptosis Is Not Dependent on Fas/Fas Ligand Interactions

TL;DR: The results indicate that antineoplastic treatments induce apoptosis through a Fas-independent pathway even though Fas- and chemotherapy-induced pathways converge on common downstream apoptotic effector molecules.
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Apoptosis triggered by Myc-induced suppression of Bcl-X(L) or Bcl-2 is bypassed during lymphomagenesis.

TL;DR: It is reported that the synergy between Bcl-2 and Myc in transforming hematopoietic cells in fact reflects a Myc-induced pathway that selectively suppresses the expression of the B cl-XL or BCl-2 antiapoptotic protein.
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Whole genome sequencing reveals oncogenic mutations in mycosis fungoides

TL;DR: Genetic alterations in specific pathways in MF were identified that may be viable, effective new targets for treatment and identified 2 other potential contributing factors to MF, ultraviolet light, and a polymorphism in the tumor suppressor p53.