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Personalized Genomic Medicine Research Center

Personalized Genomic Medicine Research Center
Objectives
Analysis on genome and epigenome and development of original technology for customized treatment of rare disease based on genome-wide screening
  • Development of customized medicine technology for cancer using genome-wide gene expression control technology
  • Research on cellular differentiation using profiling technology and development of cellular differentiation control technology
Researcher
researchers and research statement
Name Research Fields
Kyung Chan Park
(Associate Director)
  • Large-scale screening and identification of cancer related genes
  • Studies on regulation of metabolic reprograming in cancer and inflammatory diseases
Mi Sun Won
  • Identification and functional verification of genes to develop carcinostatic substances
  • Identification of mechanism of new carcinostatic substances and analysis and verification of genes to overcome resistance to therapeutics
Dong Cho Han
  • Study of cancer cells¡¯ stress responses, migration, metastasis, stemness, and drug resistance using chemical biology
Mi Rang Kim
  • Epigenomic study of stem cell differentiation and cancer development
  • Genome-wide study of DNA methylation and microRNA
Bo Kyung Kim
  • Finding out the feasibility of cancer related gene expression control and treatment targets
  • Analysis and verification of genes to overcome resistance to therapeutics
Jung-Ae Kim
  • Studies on histone modifications involved in gene expression and genome stability
  • Studies on the crosstalks between metabolic regulation and chromatin regulators
Seon-Kyu Kim
  • Finding prognostic signatures based on cancer genomics/epigenomics and development of bioinformatic analysis platforms
research areas
  • Development of customized medicine technology using genome-wide expression control technology
    • Identification of cancer treatment target gene and treatment technology based on genome-wide shRNA
      • Identification of gene that induces resistance to target treatment of lung/liver cancer (Gefitinib/Sorafenib) and development of treatment
      • Identification and verification of treatment target for incurable molecular type of liver cancer
    • Identification of cancer treatment target gene based on Genome-wide CRISPR system and development of treatment
      • Identification of cancer treatment target gene based on CRISPR expression acceleration system and development of treatment
      • Identification of functional gene related to tumor microenvironment including Hypoxia and development of treatment
  • Research on cellular differentiation using whole epigenome analysis technology and development of cellular differentiation control technology
    • Methylation of single cell DNA, analysis on chromatin and technology to analyze various histone variations
    • Establishment of various epigenome information analysis pipeline and development of software
    • Development of cellular differentiation control technology based on the analysis of epigenome
    • Research on the network among epigenomes by analyzing the changes of DNA methylome, Histone modification, transcriptome in the process of stem cell differentiation
    • Development of biomarker to monitor differentiation of stem cell
    • Integrated analysis of Transcriptome, DNA methylome, Histone modification for cancer cells which obtained resistance to target treatment using NGS
    • Identification of epimutation, which is the indicator of resistance to anti-cancer agents
  • Establishment of bio information analysis system for genome-wide functional screening (shRNA, CRISPR-Cas9)
    • Development of analysis process and software for barcode-seq data that combines Genome-wide shRNA with NGS or CRISPR-Cas9 with NGS
    • Establishment of functional screening data base through collection, analysis and integration of various gemone-wide screening data and utilization system
Achievements
  • Finding new cancer gene that controls lactic acid signal
    • Finding out that lactic acid, which used to be known as fatigue material works as an important signal material that controls cell growth and creation of blood vessel
    • Presenting the possibility of developing efficient cancer treatment and treatment for inflammatory disease targeting both metabolic process and signal delivery system of cancer cells by controlling newly found lactic acid signal control gene NDRG3
  • Development of new anti-cancer agents
    • Low molecular compound was made targeting RhoB which is known to deter the growth of cancer cell and applied to the mouse suffered from liver and prostate cancer. It is found that the growth of cancer cell is deterred significantly and the side-effect of losing weight upon injecting existing anti-cancer agent is improved
    • Compared to normal cells, cancer cell is exposed to very severe proteotoxic stress and cancer cell excessively express molecular chaperones through HSF1 activities for their survival and growth (non-oncogene addiction). The low molecular compound targeting¡®HSF1¡¯ (KRIBB11, cantharidin, fisetin) were synthesized and separated and injected to mouse suffered from colon cancer. It is found that the growth of cancer cell deterred significantly and weight loss after injecting toxic anti-cancer agent is not found.
    • The anti-cancer effect was demonstrated by animal test and anti-cancer effect is excellent and safe from the perspective of toxicity. Accordingly, intranational competitiveness in new anti-cancer agents development is secured.
  • Identification of target protein and finding mechanism of LW6, a new anti-cancer agent
    • LW6 chemical probe, which has HIF-1 deterring activity was synthesized and molecular target/fluorescent substance/chemical probe compound was made through photoaffinity labeling and click reaction and separated by electrophoresis. Then MDH2 was confirmed to be LW6 molecular target through proteome analysis
    • It is found that if the LW6, a HIF-1 deterrent is combined with Malate Dehydrogenase 2 (MDH2), the respiratory ability of mitochondria and oxygen partial pressure in cell increases promoting the decomposition of HIF-1