Dan (Rosaline) Sun

• Own scientific strategy for multiple discovery-stage programs, defining mechanism of action, model selection, and translational relevance • Design and execute in vitro mechanistic and in vivo efficacy studies using PDX, CDX, orthotopic, and allograft models • Drive go/no-go decisions by delivering clear, data-driven interpretations to scientific and executive leadership. • Collaborate with academic and industry partners to integrate emerging discoveries and strengthen translational impact across therapeutic areas • Mentor junior scientists, promoting analytical rigor, reproducibility, and publication-quality science • Lead the cancer biology team in Drug Discovery Division

-Conducted mechanistic studies on epigenetic regulation of tumor dormancy and metastatic reactivation -Managed advanced confocal microscopy workflows and supported interdisciplinary oncology projects

I have been leading a collaborative project and our work uncovered the regulatory roles of a unique histone protein variant (macroH2A) in a Mitogen-Activated-Protein-Kinase (MAPK)-mediated pathway in the molecular network of cancer cell dormancy. During my postdoc training, I have discovered epigenetic mechanisms enforcing metastatic dormancy, leading to first-author publication in Science Advances. And Integrated RNA-seq, ChIP-seq, and functional assays to uncover transcriptional and signaling programs. Collaborated with computational biologists, pathologists, and clinicians to translate findings into cancer-relevant models.

I spearheaded the development of a novel imaging and analytical framework to investigate the mechanisms behind cellular proliferation and quiescence (non-cycling states). By collaborating across disciplines with computer science and bioinformatics experts, we built an automated cell-cycle profiling platform capable of high-throughput tracking and state identification. Key Achievements & Insights: -Technical Innovation: Developed an end-to-end automated platform for cell identification, tracking, and cell-cycle analysis. -Scientific Discovery: Identified that spontaneous quiescence is highly heterogeneous, often driven by asynchronous "decisions" in daughter cells following mitosis. -Clinical Relevance: Uncovered how cancer dormancy signals influence these cellular decisions, providing critical insights into how tumor cells develop resistance to therapy.

My research focuses on the regulation of cycling and non-cycling cell cycle status transition in developmental and cancerous tissues. We are investigating how cells decide to proliferate or to enter non-cycling state (called quiescence) at proper times and places via real-time, live imaging. I established prostate cell lines with stable expressing cell-cycle fluorescent sensors via lenti-virus transduction. Another project I once executed explored a novel role of a well-known tumor suppressor, Protein Phosphatase 2A (PP2A), in promoting entry into quiescence in differentiating tissues in Drosophila model system. With the implementation of genetic and biochemical methods, I discovered the molecular mechanism of PP2A modulating the proliferation-quiescence decision. Together with other lab members, we developed flow cytometry protocols to analyze cells from live tissues in fruit flies.

As a teaching assistant in the course of cell biology, I motivated senior undergrads in scientific literature study and also evaluated their presentations. In addition, I also designed and executed problem-solving activities which helped students understand the lecture materials in depth. I also helped in quiz question design to check students' understandings and in exam paper grading.