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Vanderbilt-Ingram Cancer CenterVanderbilt-Ingram Cancer Center

 
Christine Marie  Eischen

Christine Marie Eischen, Ph.D.

Associate Professor of Cancer Biology
Associate Professor of Pathology, Microbiology, and Immunology
VICC Member
Researcher

Contact Information:

Vanderbilt University Medical Center
CC-2210MCN
Nashville , TN 37232-2561
615-343-2303
Fax: 615-343-7023

Research Description

The primary focus of the Eischen lab is on tumor initiation. We want to know how does a normal cell become a cancer cell. Specifically, we want to know what are the genes and pathways that contribute to or inhibit cellular transformation. We study the pathways, proteins, and recently, the miRNA that contribute to or inhibit tumor development. Lymphoma is the cancer that we have almost 2 decades of experience studying, and multiple projects utilize this expertise and several mouse models of lymphoma. However, lung, breast, and ovarian carcinomas are also studied in the lab.

Currently, there are three major areas of research focus that overlap in the Eischen lab.

The first area of research focus is on the oncogene Myc. We study Myc and its roles in proliferation, transformation, tumor development, and tumor cell maintenance. A large part of studying Myc is centered on the apoptosis that it causes when overexpressed in normal, untransformed cells, and the transcription it induces to drive proliferation. Myc induces the p53 pathway and suppression of the expression of anti-apoptotic Bcl-2 family members to induce apoptosis in normal cells. Cells acquire alterations that inactivate the ability of Myc to induce apoptosis. Moreover, Myc-induced transcription is still incompletely understood. We discovered a novel regulator of Myc called MTBP. There are four projects that focus on various aspects of Myc-induced tumor development.

The second area of research in the Eischen lab focuses on Mdm2 and Mdmx, two oncogenes best known for their negative regulation of the p53 tumor suppressor, and their roles in tumorigenesis. We discovered that both Mdm2 and Mdmx have p53-independent functions that contribute to tumorigenesis. We determined that Mdm2 and Mdmx regulate double-strand DNA break repair through interaction with Nbs1, a component of the Mre11/Rad50//Nbs1 DNA repair complex. We observed that increased expression of Mdm2 or Mdmx induces genome instability and increases transformation through a mechanism that is independent of p53. We are further characterizing this function with novel mouse models and investigating how this function can be capitalized on for the treatment of malignancies, half of which have inactivated p53. There are two projects that focus on Mdm2 and Mdmx in tumorigenesis.

The third area of research in the Eischen lab centers on the contribution miRNA have in tumor development. miRNA are small non-coding RNA that inhibit protein translation. We are utilizing lymphoma and lung cancer models to study miRNA in cancer. Our investigations focus on oncogene regulation of miRNA and whether they inhibit or contribute to tumor development. We have identified miRNA that are induced by Myc that lead apoptosis to protect cells from transformation. Another project focuses on a miRNA that appears to be a novel driver of lung tumor development. A third project is on miRNA that are altered in cutaneous T cell lymphoma and may serve as novel diagnostic markers for this malignancy.

There are open graduate student and postdoctoral fellowship positions. There are also opportunities for clinical fellows.

Publications