Angela H Ting Ph.D.

Associate Staff

  • Genomic Medicine Institute
  • Lerner Research Institute
  • 9500 Euclid Avenue
  • Cleveland, Ohio 44195
  • Phone: (216) 444-0682
  • Fax: (216) 636-0009

Epigenetic gene regulation is important for both normal development and disease states. In cancers, aberrant promoter CpG island hypermethylation correlates highly with gene inactivation and can account for lack of gene expression where mutations do not exist. We are interested in dissecting the mechanisms of epigenetic gene silencing and understanding the functional relevance of DNA methylation in diseases. We have 3 major focus areas in the lab:

Pioneering technical and computational tools for genome-wide DNA methylation assay. We developed MBD -isolated Genome Sequencing (MiGS), which is a cost-effective technique to survey whole genome DNA methylation patterns. We also develop computational tools that facilitate sequencing data analyses and interpretation

Defining novel and clinically relevant functions for DNA methylation. Utilizing MiGS and other genomic tools, we have defined abnormal DNA methylation patterns throughout the genome for colon and prostate cancers. Knowing where these disruptions occur enables us to generate and test hypotheses regarding the function of these changes. We investigate both gene promoters and non-promoter regions with the goal to define context-specific functions of DNA methylation.

Delineating the mechanics of DNA methylation in cancer. Wide-spread disruptions to DNA methylation patterns are well-recognized to contribute to tumorigenesis and progression, but the regulatory mechanisms that establish, maintain, and modify these patterns are still being worked out. We are exploring the roles for epigenetic enzymes, small non-coding RNAs, and DICER 1 in the initiation and maintenance of abnormal DNA methylation patterns in cancer.

In other words ...

Epigenetics are modifications on top of the DNA sequences and regulate expression of the DNA within each cell of the body as required for normal development and functioning.  However, these modifications become abnormal during the initiation, development, and progression of human cancers.  We know that some of these cancer-specific epigenetic changes work like molecular switches that turn off specific caretaker genes, whose function is to safeguard the genome and prevent inappropriate proliferation, to facilitate cancer cell formation and growth. With the recent advances in technologies, we are now able to map the epigenetic differences between normal and cancer cells at a genomic scale with high efficiency. These comprehensive epigenomic profiles enable us to understand the cause, function, and consequence of cancer-specific epigenetic changes.  Such knowledge is crucial to developing prevention, screening, and treatment strategies for various types of cancers.

  • Lihua Jin Ph.D.
  • Postdoctoral Fellow
  • Location:NE5-250
  • Phone:(216) 445-3385
  • Vijay Nagampalli Ph.D.
  • Postdoctoral Fellow
  • Location:NE5-250
  • Phone:(216) 445-3385

Select publications (full list of publications can be accessed

  1. Serre D, Lee BH, Ting AH. (2010). MBD-isolated Genome Sequencing provides a high-throughput and comprehensive survey of DNA methylation in the human genome. Nucleic Acids Res., 38(2), 391-399.
  2. Yan H, et al. (2011). Identification and functional analysis of epigenetically silenced microRNAs in colorectal cancer cells. PLoS One, 6(6), e20628.
  3. Xu Y, et al. (2012). Unique DNA methylome profiles in CpG island methylator phenotype colon cancers. Genome Res., 22(2), 283-291.
  4. Lee BH, et al. (2013). Dysregulation of cholesterol homeostasis in human prostate cancer through loss of ABCA1. Cancer Res., 73(3), 1211-1218. *Recommended by the Faculty of 1000*
  5. Bhasin JM, et al. (2015). Methylome-wide sequencing detects DNA hypermethylation distinguishing indolent from aggressive prostate cancer. Cell Rep., 13(10), 2135-2146.
  6. Bhasin JM, Hu B, Ting AH. (2016). MethylAction: detecting differentially methylated regions that distinguish biological subtypes. Nucleic Acids Res., 44(1):106-116.