Suwon Kim, PhD

Assistant Professor, Department of Basic Medical Sciences - The University of Arizona College of Medicine—Phoenix in partnership with Arizona State University

Investigator, Cancer and Cell Biology Division - Translational Genomics Institute (TGen)

UA Office Phone: (602) 827-2122
ASU Office Phone: (602) 343-8762
Office: Building 3, Room 3361
Email: suwon@email.arizona.edu

Education:

Post-Doc, Cancer Biology; University of California, San Francisco; 1998-2004

PhD; Yale University School of Medicine; 1998

BA; University of California, Berkeley; 1988

Research Interests:

Cancer Biology and tumor suppressors Cancer emerges from a multi-step process in which a normal cell gains a proliferative advantage by evading growth control mechanisms. My research focuses on the understanding of tumor suppressors that function as intrinsic “checkpoint” molecules against a tumorigenic event.

Loss of contact growth inhibition is a hallmark of cancer cells and is thought to be an early event in tumorigenesis. Using a novel screen, I have identified several genes that can suppress loss of contact inhibition in tissue culture. One of these genes, ING4, is frequently deleted in breast tumors, suggesting its role as a tumor suppressor in breast cancer.

Breast cancer is the single most common cancer in women. Although early detection followed by resection of tumors and tamoxifen treatment for estrogen receptor positive tumor patients have improved the cure frequency, the survival rate sharply declines for patients who have recurring tumors within 5 years of initial treatment. By deciphering oncogenes and tumor suppressors involved in the genesis and progression of breast cancer, better therapies can be developed that target specific molecular lesions associated with individual tumors.

To better characterize the tumor suppressor function of ING4 in breast cancer, we utilize mice as a model organism. In addition to the traditional transgenic approaches, we use a mammary transplant system that enables one to express a gene(s) of choice in the mammary glands. Using this system, we showed that ING4 can effectively suppress the MYC oncogene-induced mammary hyperplasia that resembles an early lesion in human breast cancer (see pictures). This indicates that ING4 can block early steps in breast cancer and further supports the function of ING4 as a tumor suppressor.

Currently, we are investigating the molecular mechanisms of ING4 using state-of-the-art technology including gene expression array profiling, proteomics, 2-hybrid screen, and chromatin IP array study (ChIP on chip). We are also collaborating with the colleagues at the Translational Genomics Institute to identify genetic mutations that cooperate with the ING4 deletions using high-throughput genome survey.

These studies of ING4 set a framework for characterizing other candidate tumor suppressor genes identified by my initial screen. Our long term goals are to elucidate the molecular mechanisms of these tumor suppressors and to seek out collaborations to develop better therapies against cancer, targeting specific pathways. The mouse models generated in our studies can be directly used to test potential therapeutics.

PubMed Link:

Search PubMed for a complete listing of Dr. Kim's publications

Selected Publications:

  1. Kim, S., Chin, K., Gray, J.W., and Bishop, J.M. (2004) A screen for genes that suppress loss of contact inhibition: identification of ING4 as a candidate tumor suppressor gene in human cancer. Proc Natl Acad Sci U S A 101(46):16251-6.
  2. Kim, S. (2005). HuntING4 New Tumor Suppressors. Cell Cycle 4(4):516-7.
  3. Welm, A.L., Kim, S., Welm, B.E., and Bishop, J.M. (2005). MET and MYC cooperate in mammary tumorigenesis. Proc Natl Acad Sci U S A 102(12):4324-9.