yoonAssociate Professor

Areas of Interest
Molecular and cellular mechanisms of cancer metastasis, patient-derived xenograft models, pancreatic cancer, cholangiocarcinoma, pediatric solid tumors, adhesion molecules



Dr. Karina Yoon is a tenured Associate Professor of Pharmacology and Toxicology at the University of Alabama at Birmingham. After receiving a Doctor of Philosophy (Ph.D) degree from Florida A&M University in 2001, Dr. Yoon joined St. Jude Children’s Research Hospital as a postdoctoral fellow and staff scientist with Drs. Mary K. Danks, Philip M. Potter and Richard E. Lee. In 2009, she joined the faculty at University of Alabama at Birmingham. Dr. Yoon’s publications reflect her expertise in medicinal chemistry, cancer pharmacology and cancer biology.

  • Research Interests

    Research Focus:

    • Mechanism-based novel combination approaches to cancer therapy
    • Molecular and cellular mechanisms of cancer metastasis
    • Molecular and cellular mechanisms of chemo-resistance
    • The role of cell adhesion molecules in tumor progression and metastasis
    • Novel therapeutic interventions to prevent metastatic progression
    • Pancreatic cancer, ovarian cancer, cholangiocarcinoma, neuroblastoma
    • Patient-derived xenograft (PDX) models of solid tumors

    Our primary research goals are to understand molecular mechanisms of tumor progression and metastasis of solid tumors, to identify molecular interactions or pathways that regulate these processes, and to develop novel, effective mechanism-based therapeutic strategies that target these interactions and pathways. Our long-term goal is to use observations made in the laboratory with preclinical models as a basis for developing therapies for solid tumors.

    My research interests include three major areas: to develop novel therapies for the treatment of cancer, to identify molecular interactions as targets to suppress metastatic progression, and to develop targeted therapies guided by genetic analysis and patient-derived xenograft models.

    Developing novel therapies for the treatment of cancer: using preclinical models that reflect human cancers for therapeutic application: Our laboratory has established a series of patient-derived xenograft (PDX) models of pancreatic ductal adenocarcinoma (PDAC) and cholangiocarcinoma (CCA). We propose that these models represent a useful tool for identifying characteristics common to PDAC and CCA tumors, underlying mechanisms and for evaluating potential therapies such as novel BET bromodomain inhibitors.

    Identifying molecular interactions as targets to suppress metastatic progression: Progressive metastatic disease is a major cause of mortality for patients diagnosed with multiple types of solid tumors. One of the long-term goals of our laboratory is to identify molecular interactions that regulate metastasis, as a basis for developing agents that inhibit this process. Cell adhesion molecules participate in diverse function in normal and tumor cells. We determined that expression of intercellular adhesion molecule-2 (ICAM-2) confers a non-metastatic phenotype in NB cells, and data generated with primary tumor cells are consistent with observations made using model systems. We envision that identification of proteins that comprise key regulators of the metastatic process will facilitate identification of protein interactions that support or suppress a metastatic phenotype in human cancer cells, and will serve as the basis for structural studies and targeted drug development in the future.

    Developing targeted therapies guided by genetic analysis and patient-derived xenograft (PDX) models: To overcome the challenge of eradicating tumors with subpopulations of cells having unique genetic and molecular profiles, we propose to develop personalized treatments based on the genetic, phenotypic, and molecular characteristics of a given tumor. Genetic analyses will focus on detecting mutations that would predict constitutive activation of pathways or gain of function activities that support tumor cell growth and proliferation. Where possible, approaches to treatment will be based on circumventing the dysfunctional pathways, and the efficacy of each treatment will be examined using patient-derived xenograft models.

  • Selected Publications

    Miller AL, Garcia PL, Pressey JG, Beierle EA, Kelly DR, Crossman DK, Council LN, Daniel R, Watts RG, Cramer SL, Yoon KJ (2017) Whole exome sequencing identified novel coding mutations in four neuroblastoma tumors. Scientific Reports (accepted).

    Garcia PL*, Miller AL*, Gamblin TL, Council LN, Christein JD, Arnoletti JP, Heslin MJ, Reddy S, Richardson JH, Cui X, van Waardenburg RCAM, Bradner JE, Yang ES, Yoon KJ (2017) JQ1 induces DNA damage and apoptosis, and inhibits tumor growth in a patient-derived xenograft model of cholangiocarcinoma. Molecular Cancer Therapeutics [Epub ahead of print] PMID: 29142067. *co-first authors

    Garcia PL, Miller AL, Kreitzburg KM, Gamblin TL, Christein JD, Heslin MJ, Arnoletti JP, Richardson JH, Chen D, Hanna CA, Cramer SL, Yang ES, Qi J, Bradner JE, Yoon KJ (2016) The BET bromodomain inhibitor JQ1 suppresses growth of pancreatic ductal adenocarcinoma in patient-derived xenograft models. Oncogene 35(7): 833-845. PMID: 25961927.

    Yoon KJ, Miller AL, Kreitzburg KM (2015) The role of ICAM-2 in neuroblastoma. Oncoscience; 2(11): 915-916. PMID: 26697524.

    Feduska JM, Aller SG, Garcia PL, Cramer SL, van Waardenburg RCAM, Yoon KJ (2015) ICAM-2 confers a non-metastatic phenotype in neuroblastoma cells by interaction with α-actinin. Oncogene 34(12): 1553-1562. PMID: 24704826.

    Garcia PL, Council LN, Christein JD, Arnoletti JP, Heslin MJ, Richardson JH, Gamblin TL, Bjornsti M-A, Yoon KJ (2013) Development and pathophysiological evaluation of tumorgraft models of pancreatic ductal adenocarcinoma. PLoS One, 8(10): e78183. PMID: 24194913.

    Feduska JM, Garcia PL, Brennan SB, Bu S, Council LN, Yoon KJ (2013) N-glycosylation of ICAM-2 is required for ICAM-2-mediated complete suppression of metastatic potential of SK-N-AS neuroblastoma cells. BMC Cancer, 13:261. PMID: 23714211.


Ph.D., Florida A&M University

Postdoctoral Fellowships
Postdoctoral Fellow, St. Jude Children's Research Hospital


Office Location
Volker Hall 241

205-934-6761 (Office)
205-934-6768 (Lab)
205-934-6760 (Tumorgraft Lab )