Jong-In Park, PhD
Dr. Park earned a PhD in Biochemistry and Molecular Genetics from the University of New South Wales, Sydney, Australia in 2000 for studies in Ras pathway-mediated stress responses.& His postdoctoral training in Cancer Biology was completed at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University in 2005. Previously, he earned Bachelor’s and Master’s degrees in Biochemistry from Yonsei University, Seoul, Korea, and worked for the pharmaceutical branch of SAMSUNG, Inc. He joined the faculty of the Biochemistry Department at the Medical College of Wisconsin in 2006.
Dr. Park’s current basic cancer research programs are supported by the NIH-National Cancer Institute and the American Cancer Society (ACS). He also participates in clinical cancer research by serving the NCI-MATCH Precision Medicine Cancer Trial as the Translational Chair of the Dabrafenib & Trametinib combination therapy arm, which targets BRAF-driven cancer. He is currently an ACS Research Scholar and a member of the ACS MEN2 Thyroid Cancer Consortium.
(414) 955-4098 | (414) 955-6510 (fax) | email@example.com
Proliferative programs of normal mammalian cells are interfaced with a variety of, so called, “innate tumor-suppressive mechanisms” that can trigger growth arrest or cell death in response to aberrant cell proliferation signals such as oncogenic mutations. Therefore, for carcinogenesis to occur, these mechanisms must be inactivated (A model is depicted at right). This inactivation usually requires reprogramming of signaling and metabolic pathways. Very intriguingly, certain oncogene-associated tumor suppressive mechanisms can be reactivated in cancer, providing a rationale for the design of a strategy to trigger “synthetic lethality” in cancer. The primary goal of our research is to understand the molecular mechanisms underlying these events and to translate the knowledge into an advanced therapeutic strategy.
Our current research focuses include:
- Investigating the role of mortalin/GRP75/HSPA9 in Ras/Raf-transformed cancer. The Ras and Raf families of oncogenes have been known for decades as transforming genes, and activation of the Raf/MEK/ERK pathway is a central signature of many epithelial cancers. However, paradoxically, aberrant activation of Ras or Raf elicits growth inhibitory effects, mainly characterized by cell cycle arrest and senescence, in a variety of cell types and in vivo. These responses are appreciated as innate tumor defense mechanisms against Ras- and Raf-mediated tumorigenesis. We recently demonstrated that mortalin, a mitochondrial molecular chaperone often upregulated in cancers, can determine cell fate in the face of oncogenic Ras/Raf mutations. Importantly, mortalin depletion or inhibition reactivated the tumor suppressive mechanisms associated with Raf/MEK/ERK in cancer cells. Current studies, supported by the NIH/NCI, focus on further elucidating the molecular and biochemical mechanisms underlying mortalin-regulated signaling and metabolic pathways. Moreover, we evaluate therapeutic potential of small molecule inhibitors relevant in this context.
- Investigating oncogenic signaling pathways and mitochondrial metabolism in thyroid cancer. Somatic as well as inherited mutations in the RET receptor tyrosine kinase are a key etiological factor for thyroid cancer. Further, inherited RET mutations are an important prognostic marker for the multiple endocrine neoplasia type 2 (MEN2) syndrome, wherein medullary thyroid cancer is a key pathological presentation. As a member of the American Cancer Society MEN2 consortium, we study the underlying molecular and biochemical mechanisms altered in thyroid cancer. We recently demonstrated that metabolic reprogramming in mitochondria is critical for medullary thyroid cancer cell survival and RET expression, thus proposing mitochondria as a potential therapeutic target for this tumor. Our current research further evaluates therapeutic potential of targeting mitochondrial metabolism in thyroid cancer.
- Participation in the NCI-MATCH Precision Medicine Cancer Trial. This clinical trial is a “genotype to phenotype” phase II study. An important goal of this study is to identify the features of various tumor types with the same mutation that cause them to either respond to or resist treatment with a targeted therapy. More information is available at the NCI-Molecular Analysis for Therapy Choice (NCI-MATCH) Trial Website.