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Liu-Yilun

Yilun Liu, Ph.D.

  • Associate Professor and Associate Chair, Department of Cancer Genetics and Epigenetics

Yilun Liu, Ph.D.

Research Focus :
  • Cancer Genetics and Epigenetics
  • 1992-1993 - Research Assistant, Laboratory of Prof. Richard J. Wurtman, MIT Clinical Research Center and Department of Brain and Cognitive Science, Cambridge, MA
  • 1994-1995 - Research Assistant, Laboratory of Prof. Phillips W. Robbins, MIT Center for Cancer Research, Cambridge, MA
  • 1995-2000 Graduate Research Fellow, Laboratory of Prof. Nancy Maizels, Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT
  • 1998 - Teaching Assistant, Department of Molecular Biophysics and Biochemistry graduate course Molecular Genetics of Eukaryotes, Yale University, New Haven, CT
  • 1997-1998 - Teaching Assistant, Department of Molecular Biophysics and Biochemistry graduate course Molecular Genetics of Prokaryotes, Yale University, New Haven, CT
  • 2006 - 2011 - Assistant Professor, Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, CT
  • 2011- present - Associate Professor, Department of Cancer Genetics and Epigenetics, Beckman Research Institute, City of Hope, Duarte, CA
  • 2011- present - Associate Chair, Department of Cancer Genetics and Epigenetics, Beckman Research Institute, City of Hope, Duarte, CA
  • Cancer Genetics and Epigenetics

Degrees

  • Ph.D.
  • 1995 - 2000, Yale University, New Haven, CT, Department of Molecular Biophysics and Biochemistry, Ph.D.
  • 1991 - 1995, MIT, Cambridge, MA, Department of Biology, B.S.

Fellowship

  • 2001-2006 - Postdoctoral Fellow in Biochemistry, Laboratory of Dr. Stephen C. West, Cancer Research UK, Hertfordshire, United Kingdom

Dr. Liu’s laboratory aims to understand how defects in DNA synthesis and repair contribute to cancer pathogenesis and aging. Specifically, her team focuses on a set of proteins belonging to the RECQ family of DNA helicases are among the cancer suppressors linked to DNA repair, replication and genome maintenance. During the course of evolution, RECQ genes appear to have been amplified and diverged from a single copy of the RecQ gene in bacteria and yeast to five RECQ homologs in humans. The human RECQ proteins share many similar biochemical properties in vitro, yet these proteins are not redundant, as mutations in different RECQ proteins lead to different clinical syndromes including premature aging. In addition, a defect in one RECQ protein is sufficient to cause cell transformation and tumorigenesis, and this defect cannot be compensated by other RECQ proteins. Dr. Liu’s long-term agenda in dissecting the functions of individual RECQ proteins in human cells and comparing the similarities and differences among the RECQ proteins is to understand what aspects of genome maintenance and DNA metabolism are required for normal development and cancer prevention.

The integrity of our chromosomal material is dependent upon the efficient repair of DNA lesions that are caused by exogenous agents, such as UV and ionizing radiation. Without comprehensive DNA repair and surveillance systems, broken chromosomes and mutations accumulate in cells leading to apoptosis, which could have devastating consequences in growth and development of an organism. Lost of genome integrity can also lead to cell transformation, a precursor of cancer development. Many cancer suppressor genes are linked to DNA repair. Therefore, understanding the roles of these cancer suppressor proteins will not only allow us to understand mechanisms of different repair pathways but also how they are regulated and coordinated with each other as caretakers of the genome.

A set of proteins belonging to the RECQ family are among the cancer suppressors linked to DNA repair. During the course of evolution, RECQ genes appear to have been amplified and diverged from a single copy of the RecQ gene in bacteria and yeast to five RECQ homologs in humans. The human RECQ proteins share many similar biochemical properties in vitro and are implicated in many common processes, suggesting they have overlapping functions in vivo. Yet these proteins are not redundant, as mutations in different RECQ proteins lead to different clinical syndromes. So far, BLM, WRN and RECQ4 have been associated with distinct clinical diseases: Bloom syndrome (BS), Werner syndrome (WS) and Rothmund-Thomson syndrome (RTS), respectively. Individuals with BS or RTS exhibit various physical and mental developmental abnormalities, while WS patients’ most striking phenotype is premature aging. Most importantly, all these patients, in particular BS patients, have a high risk of cancer predisposition. As a consequence, cancer is the primary cause of death for BS patients before the age of 30.

The various clinical features shown by individuals with RECQ-related diseases indicate that the human RECQ homologs have evolved to function in distinct pathways to protect the integrity of our genome and ensure proper development. A defect in one RECQ protein is sufficient to cause cell transformation and tumorigenesis, and this defect cannot be compensated by other RECQ proteins. Our long-term agenda is to dissect the functions of individual RECQ proteins in human cells, and these studies will allow us to compare the similarities and differences among the RECQ proteins. Through these comparisons we can then understand what aspects of genome maintenance and DNA metabolism are required for normal development and cancer prevention.

Xiaohua Yu, Ph.D.
Staff Scientist
 
Staff Scientist
Information listed here is obtained from Pubmed, a public database; City of Hope is not responsible for its accuracy.

 

  • 2009 - 2011 - Member, Yale Comprehensive Cancer Center
  • 2009 - 2011 - Member, Radiation Research Society
  • 2011- present - Member, City of Hope Comprehensive Cancer Center
  • 2012 - 2016 - Member, NIH Molecular Genetic Study Section A (MGA)
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