Cancer arises from breakdown in the normal cellular regulatory system. This malfunction can be a consequence of genetic mutation as well as epigenetic changes. Key epigenetic alterations, including histone modification and DNA methylation, often result in global as well as localized chromatin packaging that influences the transcription of genes important to cancer. Drugs that modify the epigenetic state promise to be effective new cancer therapies. However, the mechanism(s) underlying the epigenetic regulation of cancer cells, as well as the way in which drugs manipulate the epigenetic state and transcription, remain largely unknown. Moreover, as epigenetic regulation is critical for maintaining normal cellular function, the characterization of cancer-specific epigenetic reprogramming is an essential step for increasing specificity of epigenetic therapy. Noncoding RNA, particularly long non-coding RNA (lncRNA), has recently become a new area of focus in cancer biology, with evidence suggesting that they are essential to epigenetic reprogramming during cancer development and progression.
Our laboratory applies a variety of genomic, epigenomic experimental and computational approaches to elucidate the functional role of epigenetic regulation in cancer development, progression, drug response and resistance, with a special focus on the interplay between epigenetic regulator and noncoding RNA under stress conditions such as hypoxia. Our research focuses on three major directions.
Understand epigenetic regulation in cancer development, progression, drug response, and resistance.
Identify epigenetic biomarkers in tumor and liquid biopsies.
Target cancer specific epigenetic regulation for cancer therapy.
Dr. Hansen He and team at Princess Margaret Cancer Centre traced the full path of one tiny genetic change in a seemingly unimportant region of DNA to see how it had such a large effect on prostate cancer outcomes.