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Meijun Du

Meijun Du

Research Scientist II

Biography

I am a cancer genomics and epigenetics researcher with over 10 years of experience investigating the molecular mechanisms underlying cancer initiation, progression, and therapeutic response using next-generation sequencing (NGS) technologies and integrative bioinformatics analyses. My work combines high-throughput genomic profiling, chromatin biology, and liquid biopsy approaches to identify clinically relevant biomarkers and therapeutic targets.

During my postdoctoral training at the Medical College of Wisconsin (MCW), I developed Chromosome Conformation Capture Multi-Target Sequencing (3C-MTS), a high-throughput platform that maps chromatin interactions between prostate cancer risk loci and their target genes in a single experiment. This technology enabled systematic analysis of hundreds of cis-regulatory DNA interactions and provided new insights into genetic variants associated with prostate cancer susceptibility and aggressiveness.

As a research scientist, I contributed to the development of blood-based cell-free DNA (cfDNA) and exosomal RNA sequencing assays for biomarker discovery. Our studies demonstrated that cfDNA and exosomal RNA are highly sensitive and specific biomarkers for cancer diagnosis, prognosis, and monitoring of treatment response, particularly in metastatic prostate cancer and small cell lung cancer (SCLC). I have also established genome-wide epigenomic and three-dimensional (3D) genome profiling platforms, including CUT&RUN, CUT&Tag, and Micro-C, to map histone modifications, transcription factor binding, and chromatin architecture at high resolution. Currently, my research focuses on defining epigenetic regulatory mechanisms that drive SCLC heterogeneity and therapeutic resistance. I am conducting genome-wide characterization of histone post-translational modifications and transcription factors (especially E2F7) binding across the four major SCLC molecular subtypes (ASCL1, NEUROD1, POU2F3, and YAP1). In parallel, I investigate how KMT2D-mediated enhancer priming regulates lineage maintenance and subtype plasticity. Through these studies, I aim to identify key regulatory elements and gene networks that can be leveraged for biomarker development and precision therapeutic strategies in SCLC.