Damian Yap

Research Associate
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Dr. Yap received his PhD in Clinical Medicine Research from Imperial College London in 2001 and joined the Aparicio Lab in 2002 when it was based in the University of Cambridge. When the lab moved to BC Cancer in 2005, Dr. Yap followed making him officially the first Vancouver Aparicio Lab member, a title he continues to hold today.

Papers

Pharmacological systems analysis defines EIF4A3 functions in cell-cycle and RNA stress granule formation.

Engineered in-vitro cell line mixtures and robust evaluation of computational methods for clonal decomposition and longitudinal dynamics in cancer.

Atrophin controls developmental signaling pathways via interactions with Trithorax-like.

CLK-dependent exon recognition and conjoined gene formation revealed with a novel small molecule inhibitor.

CX-5461 is a DNA G-quadruplex stabilizer with selective lethality in BRCA1/2 deficient tumours.

Clonal genotype and population structure inference from single-cell tumor sequencing.

Divergent modes of clonal spread and intraperitoneal mixing in high-grade serous ovarian cancer.

A co-culture genome-wide RNAi screen with mammary epithelial cells reveals transmembrane signals required for growth and differentiation.

Dynamics of genomic clones in breast cancer patient xenografts at single-cell resolution.

TITAN: inference of copy number architectures in clonal cell populations from tumor whole-genome sequence data.

Impact of MLL5 expression on decitabine efficacy and DNA methylation in acute myeloid leukemia.

A transgenic mouse model demonstrating the oncogenic role of mutations in the polycomb-group gene EZH2 in lymphomagenesis.

PyClone: statistical inference of clonal population structure in cancer.

Solution NMR structure and histone binding of the PHD domain of human MLL5.

The clonal and mutational evolution spectrum of primary triple-negative breast cancers.

Mll5 is required for normal spermatogenesis.

Retinoblastoma-binding proteins 4 and 9 are important for human pluripotent stem cell maintenance.

The testosterone-dependent and independent transcriptional networks in the hypothalamus of Gpr54 and Kiss1 knockout male mice are not fully equivalent.

Somatic mutations at EZH2 Y641 act dominantly through a mechanism of selectively altered PRC2 catalytic activity, to increase H3K27 trimethylation.

Somatic mutations altering EZH2 (Tyr641) in follicular and diffuse large B-cell lymphomas of germinal-center origin.

Loss of MLL5 results in pleiotropic hematopoietic defects, reduced neutrophil immune function, and extreme sensitivity to DNA demethylation.