C
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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Journal ArticleDOI
Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization
Frederique Zindy,Christine M. Eischen,David H. Randle,Takehiko Kamijo,John L. Cleveland,Charles J. Sherr,Martine F. Roussel +6 more
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.
Journal ArticleDOI
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
Christine M. Eischen,Timothy Kottke,Timothy Kottke,Luis M. Martins,Luis M. Martins,Guriqbal S. Basi,Guriqbal S. Basi,Jay S. Tung,Jay S. Tung,William C. Earnshaw,William C. Earnshaw,Paul J. Leibson,Paul J. Leibson,Scott H. Kaufmann,Scott H. Kaufmann +14 more
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.
Christine M. Eischen,David D. L. Woo,Martine F. Roussel,Martine F. Roussel,John L. Cleveland +4 more
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
Laura Y. McGirt,Peilin Jia,Devin A. Baerenwald,Robert Duszynski,Kimberly B. Dahlman,John A. Zic,Jeffrey P. Zwerner,Donald Hucks,Utpal P. Davé,Zhongming Zhao,Christine M. Eischen +10 more
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.