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Post Doctoral - Cancer Biology University of California San Diego (UCSD) / Salk Institute - 2013
Ph.D. - Cancer Biology / Metabolism Johns Hopkins University, School of Medicine - 2006
D.V.M. - Veterinary Medicine KonKuk University, College of Veterinary Medicine, Korea - 2000
Jay Kim lab is focused on understanding the heterogeneous metabolic signatures and targetable vulnerabilities in human cancers utilizing genetically engineered mouse models (GEMMs) and patient-derived xenograft (PDX) systems. Another major focus of our research is to understand the significance of hypoxic signaling and metabolic reprogramming of fibroblasts in cancer progression and fibrotic diseases.
Heme Sequestration Effectively Suppresses the Development and Progression of Both Lung Adenocarcinoma and Squamous Cell Carcinoma 2022 - Journal Article
Oxidative Stress and the Intersection of Oncogenic Signaling and Metabolism in Squamous Cell Carcinomas 2021 - Journal Article
Heme Sequestration Effectively Suppresses the Development and Progression of Both Lung Adenocarcinoma and Squamous Cell Carcinoma 2021 - Journal Article
Convergence of cancer metabolism and immunity: An overview 2018 - Journal Article
Pathology Young Investigator Award - Johns Hopkins School of Medicine 
Pre-doctoral Fellowship - Howard Hughes Medical Institute (HHMI) 
Associate Professor University of Oklahoma Health Science Center [2023–Present]
Adjunct Professor University of Texas at Dallas [2020–Present]
Research Director VIP Animal Medical Center [2021–2022]
Senior Principal Scientist Barer Institute Inc. [2020–2021]
Assistant Professor University of Texas at Dallas [2013–2020]
Postdoctoral Fellow University of California San Diego / Salk Institute [2008–2013]
Research Fellow University of Pennsylvania [2000–2002]
Glucose reliance and metabolic vulnerabilities in human squamous cell carcinomas
Despite intensive efforts, targeting augmented glucose metabolism has resulted in varied, unsatisfactory outcomes to be considered as a viable therapeutic option for further development. Among multiple factors preventing effective therapeutic responses, a poorly understood tumor-intrinsic metabolic heterogeneity across different cancers, arising potentially from diverse microenvironmental or lineage-specific factors, may preclude effective therapeutic strategies to target cancer metabolism. In our recently published study, we uncovered the molecular mechanism in which, a squamous lineage-specific program p63 and SOX2 promotes GLUT1 expression through the intronic enhancer transactivation of the SLC2A1 (that encodes GLUT1) in human squamous cell carcinomas (SCC). This previously unrecognized metabolic feature embedded in squamous cancers argue that remarkably heightened GLUT1 expression and glucose influx is not a uniform metabolic hallmark of all cancers, but a potent and unique characteristic of squamous lineage cancers. We are studying epigenetic and molecular events underlying this control mechanism by characterizing how various transcription factors are binding and transcriptional activities within and across the locus and its boundaries enable SLC2A1 overexpression in SCC. The overarching goal of this project is to develop novel ways to silence the SLC2A1 gene selectively in SCC.
Metabolic reprogramming and plasticity in the tumor microenvironment and fibrotic diseases
Metabolic dysregulation in stromal cells is associated with various human diseases including cancer and fibrosis. We previously reported that fibroblastic hypoxic signaling plays critical roles in tumor growth, tumor vascular remodeling, and therapeutic responses. In addition, our group has demonstrated that genetic as well as pharmacological inhibition of hypoxia-inducible factor-1 (HIF-1)-mediated metabolic reprogramming significantly attenuate the progression of interstitial pulmonary fibrosis. Our studies suggest a critical biological and clinical consideration for evaluating metabolic alterations in myofibroblast activation and fibrotic progression in the tumor microenvironment and fibrotic progression. We employ various transgenic animal model systems for an integrated understanding of cellular and molecular mechanistic link between metabolic alterations and plasticity and accelerated myofibroblastic activation and differentiation in highly desmoplastic cancers (e.g. pancreatic cancer) as well as pulmonary fibrosis.
Dietary intervention for cancer therapeutics
A growing body of evidence has demonstrated that dietary modulation could improve the response to cancer therapy. Given that cancers display diverse metabolic requirements influenced by numerous factors such as intrinsic oncogenic alterations, microenvironmental components, and therapeutic intervention, individualized strategies are essential for effective targeting metabolic vulnerabilities of specific cancer via dietary intervention. We have shown that ketogenic diet specifically inhibited the development of lung squamous cancers in KrasG12D;LKB1-null (KL) of human non-small cell lung cancer (NSCLC) model as well as esophagus, head and neck squamous cancer xenograft tumor models. We further demonstrated that the anti-SCC effects of ketogenic diet is due to systemic glucose restriction and an associated suppression of insulin/PI3K/AKT signaling in SCC cells. We are exploring combinatorial regimens to improve therapeutic efficacy of ketogenic diet and other dietary modulations. In addition, we are studying the impact of systemic responses by dietary intervention on stromal components such as immune cells in the tumor microenvironment.
More than $4.5 million in new funding from state and federal agencies will support cancer-related research over the next five years at The University of Texas at Dallas.
Two projects related to brain cancer, each totaling $200,000 over two years, recently received High-Impact/High-Risk Research Awards from the Cancer Prevention & Research Institute of Texas (CPRIT). A third CPRIT grant, of nearly $3.6 million over five years, will be used to establish a new core imaging facility for preclinical research. That award will be combined with $400,000 in matching funds from the University.
The Department of Defense (DOD) also recently awarded the University more than $527,000 for lung cancer research.
A biologist at The University of Texas at Dallas and his colleagues have discovered that two enzymes previously linked independently with keeping cancer cells alive actually work in tandem to spur tumor growth. “There has been no reason to suspect these two proteins interact, but now we know they do. This finding was totally unexpected,” said Dr. Jung-Whan (Jay) Kim, assistant professor of biological sciences and co-lead author of the study published online Dec. 14 in the journal Nature Communications.
New findings about the biological links between obesity and insulin resistance and Type 2 diabetes may also shed light on the connection between obesity and cancer, says a scientist at The University of Texas at Dallas. In a study published in the journal Cell, UT Dallas’ Dr. Jung-whan Kim and colleagues at the University of California, San Diego found that a protein called HIF-1 alpha plays a key role in the development of insulin resistance and Type 2 diabetes in obese mice.
Two summers and many late nights devoted to research in a UT Dallas laboratory have earned one high school student a trip to Washington, D.C., to compete for honors among the nation’s elite young scientists.
Joshua Choe, a senior at St. Mark’s School of Texas in Dallas, is one of 40 high school students chosen as finalists in the prestigious Intel Science Talent Search, the nation’s oldest pre-college science and math competition. Choe is the only finalist from Texas for the competition, which will be March 10-16 and present more than $1 million in awards.