Yiping He
Principal Investigator
Associate Professor in Pathology
Member of the Duke Cancer Institute
Contact Information

Research Interests

Our laboratory focuses on developing and applying genetic approaches for identifying new cancer genes and studying their functions.

  1. Study mechanisms underlying epigenetic dysregulation-driven tumorigenesis, using brain tumor and prostate cancer models. Specifically, we focus on histone modification pathways recently identified as being common drivers for many types of human cancers. Several genes, including MLL2 (also named KMT2D), MLL3 and UTX, encode proteins with histone methylation modifying activity; however, their tumorigenic roles and the underlying mechanism are unknown. We aim to understand the role of the MLL2/MLL3 pathway with an ultimate goal of applying our findings to the clinical setting. The gigantic sizes of MLL2 and MLL3 pose a challenge for studying them. We have established somatic gene modification-based human cell models, knockout mouse models, and novel genetic assays to overcome this challenge. Using these new tools, we aim to identify downstream cellular signaling pathway and events that mediate the tumorigenic roles of MLL2/MLL3 deficiency, and illuminate the roles of MLL2 in different cellular contexts.
  2. Exploiting genetic alterations for cancer treatments. Specifically, we focus on MTAP deletion in glioblastoma.  We have collaborated with colleagues in the Duke Cancer Institute, primarily by applying Nest Generation Sequencing to exome sequencing, in projects aiming to discover novel cancer genes in glioblastoma, and applying them to glioblastoma classification and therapeutics. In one ongoing projects, we focus on exploiting methylthioadenosine phosphorylase (MTAP) deletion (occurs in ~half of all glioblastoma patients) for glioblastoma treatment. We have established patient-derived primary tumor cultures and sequenced their exomes to identify somatic alterations, including MTAP status. We are studying the metabolic and functional effects of MTAP deletion on glioblastoma biology, and devising novel therapeutic approaches to target glioblastoma with MTAP deletion.


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