Biomedical Research Education & Training
Faculty Member

Eischen, Christine M., Ph.D.
Associate Professor of Pathology, Microbiology and Immunology
Associate Professor of Cancer Biology

Lab Url: http://CC-2210 MCN

Phone Number: 343-2303

Email Address: christine.eischen@vanderbilt.edu

Eischen, Christine's picture
Academic history
B.S., Creighton University
Ph.D., Mayo Clinic
Postdoc, St. Jude Children

Office Address   Mailing Address

CC-2210 MCN

Department of Pathology; C3321 MCN; 37232-2561


Research Description
My lab investigates the genes that regulate tumor development. We study the influence tumor suppressors and oncogenes have on apoptosis, proliferation, chromosomal stability, and transformation. We have demonstrated that development to a malignancy is accelerated when there are alterations in the tumor suppressors p53 and ARF, which function to protect cells from hyperproliferative signals from oncogenes, such as Myc. Alternatively, a deficiency in the oncogene Mdm2, which normally inhibits apoptosis, results in the suppression of tumor development. Studies are underway to elucidate novel genes, microRNAs ,and pathways that regulate cellular transformation. Mouse models (knockout and transgenic mice), primary, immortal, and tumor cell cultures, retroviral gene transfer, biochemical purification, and gene chip and proteomic technologies are utilized in our investigations. Results from our studies will provide a better understanding of the genes and pathways that regulate tumorigenesis. Ultimately our studies will lead to a better understanding of cancer development, which will be used for improved therapeutic intervention strategies for human malignancies.


Publications
Eischen, CM, Lozano, G. The Mdm Network and its Regulation of p53 Activities: A Rheostat of Cancer Risk. Hum Mutat, 2014

McGirt, LY, Adams, CM, Baerenwald, DA, Zwerner, JP, Zic, JA, Eischen, CM. miR-223 Regulates Cell Growth and Targets Proto-Oncogenes in Mycosis Fungoides/Cutaneous T-Cell Lymphoma. J Invest Dermatol, 2013

Anderson, PD, McKissic, SA, Logan, M, Roh, M, Franco, OE, Wang, J, Doubinskaia, I, van der Meer, R, Hayward, SW, Eischen, CM, Eltoum, IE, Abdulkadir, SA. Nkx3.1 and Myc crossregulate shared target genes in mouse and human prostate tumorigenesis. J Clin Invest, 122(5), 1907-19, 2012

Eischen, CM, Boyd, K. Decreased Mdm2 expression inhibits tumor development and extends survival independent of Arf and dependent on p53. PLoS One, 7(9), e46148, 2012

Gramling, MW, Eischen, CM. Suppression of Ras/Mapk pathway signaling inhibits Myc-induced lymphomagenesis. Cell Death Differ, 19(7), 1220-7, 2012

Melo, AN, Eischen, CM. Protecting the genome from mdm2 and mdmx. Genes Cancer, 3(3-4), 283-90, 2012

Cho, SH, Ahn, AK, Bhargava, P, Lee, CH, Eischen, CM, McGuinness, O, Boothby, M. Glycolytic rate and lymphomagenesis depend on PARP14, an ADP ribosyltransferase of the B aggressive lymphoma (BAL) family. Proc Natl Acad Sci U S A, 108(38), 15972-7, 2011

Lushnikova, T, Bouska, A, Odvody, J, Dupont, WD, Eischen, CM. Aging mice have increased chromosome instability that is exacerbated by elevated Mdm2 expression. Oncogene, 2011

Arrate, MP, Vincent, T, Odvody, J, Kar, R, Jones, SN, Eischen, CM. MicroRNA biogenesis is required for Myc-induced B-cell lymphoma development and survival. Cancer Res, 70(14), 6083-92, 2010

Odvody, J, Vincent, T, Arrate, MP, Grieb, B, Wang, S, Garriga, J, Lozano, G, Iwakuma, T, Haines, DS, Eischen, CM. A deficiency in Mdm2 binding protein inhibits Myc-induced B-cell proliferation and lymphomagenesis. Oncogene, 29(22), 3287-96, 2010

Bouska, A, Eischen, CM. Mdm2 Affects Genome Stability Independent of p53. Cancer Res, 69(5), 1697-701, 2009

Cho, SH, Goenka, S, Henttinen, T, Gudapati, P, Reinikainen, A, Eischen, CM, Lahesmaa, R, Boothby, M. PARP-14, a member of the B aggressive lymphoma (BAL) family, transduces survival signals in primary B cells. Blood, 2009 PMCID:2656269

Eischen, CM, Lozano, G. p53 and MDM2: Antagonists or Partners in Crime. Cancer Cell, 15(3), 161-2, 2009

Bouska, A, Lushnikova, T, Plaza, S, Eischen, CM. Mdm2 promotes genetic instability and transformation independent of p53. Mol Cell Biol, 28(15), 4862-74, 2008 PMCID:2493369

Mudhasani, R, Zhu, Z, Hutvagner, G, Eischen, CM, Lyle, S, Hall, LL, Lawrence, JB, Imbalzano, AN, Jones, SN. Loss of miRNA biogenesis induces p19Arf-p53 signaling and senescence in primary cells. J Cell Biol, 181(7), 1055-63, 2008 PMCID:2442212

Iwakuma, T, Tochigi, Y, Van Pelt, CS, Caldwell, LC, Terzian, T, Parant, JM, Chau, GP, Koch, JG, Eischen, CM, Lozano, G. Mtbp haploinsufficiency in mice increases tumor metastasis. Oncogene, 2007

Wang, P, Lushnikova, T, Odvody, J, Greiner, TC, Jones, SN, Eischen, CM. Elevated Mdm2 expression induces chromosomal instability and confers a survival and growth advantage to B cells. Oncogene, 2007

Tompkins, VS, Hagen, J, Frazier, AA, Lushnikova, T, Fitzgerald, MP, Tommaso, AD, Ladeveze, V, Domann, FE, Eischen, CM, Quelle, DE. A novel nuclear interactor of ARF and Mdm2 (NIAM) that maintains chromosomal stability. J Biol Chem, 2006

Wang, P, Greiner, TC, Lushnikova, T, Eischen, CM. Decreased Mdm2 expression inhibits tumor development induced by loss of ARF. Oncogene, 25(26), 3708-18, 2006

Alt, JR, Bouska, A, Fernandez, MR, Cerny, RL, Xiao, H, Eischen, CM. Mdm2 binds to Nbs1 at sites of DNA damage and regulates double strand break repair. J Biol Chem, 280(19), 18771-81, 2005

Eischen, CM, Alt, JR, Wang, P. Loss of one allele of ARF rescues Mdm2 haploinsufficiency effects on apoptosis and lymphoma development. Oncogene, 23(55), 8931-40, 2004

Alt, JR, Greiner, TC, Cleveland, JL, Eischen, CM. Mdm2 haplo-insufficiency profoundly inhibits Myc-induced lymphomagenesis. EMBO J, 22(6), 1442-50, 2003 PMCID:151074

Eischen, CM, Rehg, JE, Korsmeyer, SJ, Cleveland, JL. Loss of Bax alters tumor spectrum and tumor numbers in ARF-deficient mice. Cancer Res, 62(7), 2184-91, 2002

Eischen, CM, Packham, G, Nip, J, Fee, BE, Hiebert, SW, Zambetti, GP, Cleveland, JL. Bcl-2 is an apoptotic target suppressed by both c-Myc and E2F-1. Oncogene, 20(48), 6983-93, 2001

Eischen, CM, Roussel, MF, Korsmeyer, SJ, Cleveland, JL. Bax loss impairs Myc-induced apoptosis and circumvents the selection of p53 mutations during Myc-mediated lymphomagenesis. Mol Cell Biol, 21(22), 7653-62, 2001 PMCID:99936

Eischen, CM, Woo, D, Roussel, MF, Cleveland, JL. Apoptosis triggered by Myc-induced suppression of Bcl-X(L) or Bcl-2 is bypassed during lymphomagenesis. Mol Cell Biol, 21(15), 5063-70, 2001 PMCID:87232

Nip, J, Strom, DK, Eischen, CM, Cleveland, JL, Zambetti, GP, Hiebert, SW. E2F-1 induces the stabilization of p53 but blocks p53-mediated transactivation. Oncogene, 20(8), 910-20, 2001

Eischen, CM, Weber, JD, Roussel, MF, Sherr, CJ, Cleveland, JL. Disruption of the ARF-Mdm2-p53 tumor suppressor pathway in Myc-induced lymphomagenesis. Genes Dev, 13(20), 2658-69, 1999 PMCID:317106

Zindy, F, Eischen, CM, Randle, DH, Kamijo, T, Cleveland, JL, Sherr, CJ, Roussel, MF. Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization. Genes Dev, 12(15), 2424-33, 1998 PMCID:317045

Eischen, CM, Kottke, TJ, Martins, LM, Basi, GS, Tung, JS, Earnshaw, WC, Leibson, PJ, Kaufmann, SH. Comparison of apoptosis in wild-type and Fas-resistant cells: chemotherapy-induced apoptosis is not dependent on Fas/Fas ligand interactions. Blood, 90(3), 935-43, 1997

Eischen, CM, Williams, BL, Zhang, W, Samelson, LE, Lynch, DH, Abraham, RT, Leibson, PJ. ZAP-70 tyrosine kinase is required for the up-regulation of Fas ligand in activation-induced T cell apoptosis. J Immunol, 159(3), 1135-9, 1997

Eischen, CM, Schilling, JD, Lynch, DH, Krammer, PH, Leibson, PJ. Fc receptor-induced expression of Fas ligand on activated NK cells facilitates cell-mediated cytotoxicity and subsequent autocrine NK cell apoptosis. J Immunol, 156(8), 2693-9, 1996


Postdoctoral Position Available
Yes

Postdoctoral Position Details
There is one immediate opening for a post-doctoral fellow interested in cancer research. Applications are invited for experienced and highly motivated individuals who are interested in genetic, molecular, or biochemical mechanisms of tumor development. Utilizing genetically engineered mouse models, primary cell culture, retroviral gene transfer technologies, and protein purification, this laboratory has elucidated critical functions of members of the p53 tumor suppressor pathway (G&D 1999; MCB 2001, 2008; EMBO 2003; Oncogene 2004, 2005, 2006, 2008; JBC 2005). Multiple projects to characterize novel proteins and microRNAs and their role in tumor development are available for post-doctoral fellows. Applicants should have a strong background in molecular biology, biochemistry, cell biology, and/or mouse models. Interested individuals should send CV and contact information for three references to christine.eischen@vanderbilt.edu.

Updated Date
02/24/2014