Genome-wide sequencing technologies have allowed an unprecedented discovery of somatic mutations in “epigenetic modifiers” in human cancers. We have applied multidisciplinary and integrative approaches to understand how mutated epi-genes’ function towards disrupting epigenetic landscapes that, in turn, lead to cancer progression in varies cancers. Specifically:
(a) Identifying a chromatin “reader” that influenced prostate cancer progression. (Nature Genetics, 2015)
(b) Identifying DNA methylation dynamics during B cell maturation in chronic lymphocytic leukemia (CLL). (Nature Genetics, 2016)
(c) Identifying recurrent mutations in a cohesion complex component STAG2 or STAG3 involved in resistance to BRAF inhibition in melanoma and the impact to 3D cancer genome upon STAG2 deactivation. (Nature Medicine, 2016; Nature Communications, 2022)
(d) Deciphering a lethal CpG Island Mediated Phenotype (CIMP) in Ependymomas of Infancy. (Nature, 2014)
These findings are expected to reveal novel epigenetic mechanisms underlie cancers and pave new avenues towards cancer therapeutics to help patients afflicted by these devastating cancers.