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Hung-jiun LiawProfessor
E - Mail
liawh@mail.ncku.edu.tw
Office Phone
+886-6-275-7575 ext. 58127
Laboratory Phone
58104 or 58114轉22
Highest Education
Brief Biography
2023
Professor, Department of Life Sciences, National Cheng Kung University
2016
Associate Professor, Department of Life Sciences, National Cheng Kung University
2010
Assistant Professor, Department of Life Sciences, National Cheng Kung University
2006
Postdoctoral Fellow, National Human Genome Research Institute, NIH, USA
Professor, Department of Life Sciences, National Cheng Kung University
2016
Associate Professor, Department of Life Sciences, National Cheng Kung University
2010
Assistant Professor, Department of Life Sciences, National Cheng Kung University
2006
Postdoctoral Fellow, National Human Genome Research Institute, NIH, USA
Research Areas
Research Directions:
Cancer cells are characterized by genomic instability, including aneuploidy (abnormal chromosome numbers instead of 23 pairs) and gross chromosomal rearrangements. Genomic instability is often caused by dysregulation of DNA replication, repair, and recombination mechanisms. Due to the failure of these processes, cells experience persistent replication stress, which leads to chromosome breakage and rearrangement. Mutations in genes regulating these pathways are frequently observed in cancer cells. For example, mutations in homologous recombination genes such as BRCA1 and BRCA2, as well as genes in the Fanconi anemia repair pathway, are closely associated with genomic instability and tumorigenesis.
Therefore, my research focuses on investigating genes involved in DNA replication, repair, and recombination, and elucidating how their mutations induce replication stress and lead to genomic instability at the molecular level.
My laboratory has developed multiple tools to study replication stress, recombination, and genomic instability, including DNA fiber assay, DNA combing, metaphase spreads, sister chromatid exchange, homologous recombination assay, iPOND, and SIRF. Using these platforms, we can investigate how gene mutations affect DNA replication, including replication speed, fork density, stalled forks, new origin firing, ssDNA replication gaps, chromosome breakage, recombination, and protein binding at replication forks. These platforms are also available for use by researchers in Taiwan and internationally.
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Cancer cells are characterized by genomic instability, including aneuploidy (abnormal chromosome numbers instead of 23 pairs) and gross chromosomal rearrangements. Genomic instability is often caused by dysregulation of DNA replication, repair, and recombination mechanisms. Due to the failure of these processes, cells experience persistent replication stress, which leads to chromosome breakage and rearrangement. Mutations in genes regulating these pathways are frequently observed in cancer cells. For example, mutations in homologous recombination genes such as BRCA1 and BRCA2, as well as genes in the Fanconi anemia repair pathway, are closely associated with genomic instability and tumorigenesis.
Therefore, my research focuses on investigating genes involved in DNA replication, repair, and recombination, and elucidating how their mutations induce replication stress and lead to genomic instability at the molecular level.
My laboratory has developed multiple tools to study replication stress, recombination, and genomic instability, including DNA fiber assay, DNA combing, metaphase spreads, sister chromatid exchange, homologous recombination assay, iPOND, and SIRF. Using these platforms, we can investigate how gene mutations affect DNA replication, including replication speed, fork density, stalled forks, new origin firing, ssDNA replication gaps, chromosome breakage, recombination, and protein binding at replication forks. These platforms are also available for use by researchers in Taiwan and internationally.
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