Angela H Ting, PhD
Lerner Research Institute,
9500 Euclid Avenue, Cleveland, Ohio 44195
Phone: (216) 444-0682
- Postdoctoral Fellow Positions Available! We are recruiting motivated and talented individuals (PhD or MD/PhD) with expertise in transcription regulation, genome architecture, RNA metabolism, biochemistry, and/or genomics. Please submit a cover letter stating your research experience and goals and CV directly to Angela Ting.
- Computational Data Scientist Positions Available! We are recruiting highly motivated individuals (Bachelor's degree with experiences and higher) with expertise in computer science, biology, or related fields to work on genomic/epigenomic/single cell sequencing data. Please submit a cover letter stating your research experience and goals and CV to Angela Ting.
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. Dr. Ting is interested in dissecting the mechanisms of epigenetic gene silencing and understanding the functional relevance of DNA methylation in diseases. Dr. Ting’s lab has three major focus areas:
Pioneering technical and computational tools for genome-wide DNA methylation assay. Dr. Ting developed MBD-isolated Genome Sequencing (MiGS), which is a cost-effective technique to survey whole genome DNA methylation patterns. The Ting lab also develops computational tools that facilitate sequencing data analyses and interpretation.
Defining novel and clinically relevant functions for DNA methylation. We have defined genome-wide abnormal DNA methylation patternsin colon, bladder, and prostate cancers. Knowing where these disruptions occur enabled us to generate and test hypotheses regarding the function of these changes. We investigate both gene promoters and non-promoter regions with the goal of defining context-specific functions of DNA methylation.
Delineating the mechanics of DNA methylation in cancer. Wide-spread disruptions to DNA methylation patterns are contribute to tumorigenesis and progression, but the regulatory mechanisms that establish, maintain, and modify these patterns are still being worked out. Researchers in Dr. Ting’s lab explore the roles for epigenetic enzymes, small non-coding RNAs, and environmental exposures in the initiation and maintenance of abnormal DNA methylation patterns in cancer.
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. Some of these cancer-specific epigenetic changes work like molecular switches that turn off specific caretaker genes, which function to safeguard the genome and prevent inappropriate proliferation, to facilitate cancer cell formation and growth. With the recent advances in technologies, researchers 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 the understanding of 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.
Select publications (full list of publications can be accessed http://www.ncbi.nlm.nih.gov/sites/myncbi/angela.ting.2/bibliography/43867867/public/?sort=date&direction=ascending)
- Serre D, Lee BH, Ting AH. MBD-isolated genome sequencing provides a high-throughput and comprehensive survey of DNA methylation in the human genome. Nucleic Acids Res. 2010;38(2):391-399.
- Yan H, et al. Identification and functional analysis of epigenetically silenced microRNAs in colorectal cancer cells. PLoS One. 2011;6(6):e20628.
- Xu Y, et al. Unique DNA methylome profiles in CpG island methylator phenotype colon cancers. Genome Res. 2012;22(2):283-291.
- Lee BH, et al. Dysregulation of cholesterol homeostasis in human prostate cancer through loss of ABCA1. Cancer Res. 2013;73(3):1211-1218. *Recommended by the Faculty of 1000*
- Bhasin JM, et al. Methylome-wide sequencing detects DNA hypermethylation distinguishing indolent from aggressive prostate cancer. Cell Rep. 2015;13(10):2135-2146.
- Bhasin JM, Hu B, Ting AH. MethylAction: detecting differentially methylated regions that distinguish biological subtypes. Nucleic Acids Res. 2016;44(1):106-116.
- Nanavaty V, et al. DNA methylation regulates alternative polyadenylation via CTCF and the cohesin complex. Molecular Cell. 2020;78(4):752-764.
Emily Fink, PhD, a postdoctoral fellow in the laboratory of Angela Ting, PhD, Genomic Medicine, recently received the National Cancer Institute Ruth L. Kirschstein Postdoctoral Individual National Research Service Award to support her research into the cause of abnormal DNA methylation in colorectal cancer (CRC) development.
A multidisciplinary team of researchers from Lerner Research Institute and Fred Hutchinson Cancer Research Center have been awarded a three-year, $1 million grant from the W.M. Keck Foundation, one of the nation’s largest philanthropic organizations, to study if and how certain bacteria directly alter the human genome, and perhaps even lead to cancer.
Cleveland Clinic researchers have uncovered for the first time a link between two processes that, when dysregulated, are known to promote cancer development.
Emily Fink, PhD, a postdoctoral fellow in the laboratory of Angela Ting, PhD, Genomic Medicine, was recently awarded funding through a Cancer Biology Training Grant from the National Cancer Institute, through the Case Comprehensive Cancer Center at Case Western Reserve University, to support her research into the impact of abnormal methylation on tumorigenesis.