Bio

Melissa is a bioinformatician specializing in spatial biology and image registration. At the Snyder Lab, she identified tumor biomarkers using multi-omics data and contributed to projects like HuBMAP and HTAN. She holds an MSc in Bioinformatics from Johns Hopkins University and an MPhil in Medicine from the University of Sydney, where she researched IGFBP-3 in triple-negative breast cancer under the tutelage of Robert Baxter. In addiition, she received a BSc majoring in Immunology and Pharmacology under a full scholarship offered by the Malaysian government. Her prior work includes CRISPR-Cas9 models and tumor organoids at the National University of Singapore and National Cancer Centre Singapore. Melissa integrates AI and biology for personalized medicine.

Current Role at Stanford

Bioinformatician

Supervisors

Honors & Awards

  • HAI seed grant, Stanford Human-Centered Artificial Intelligence (HAI) (2024)

Education & Certifications

  • MSc Bioinformatics, Johns Hopkins University (2022)
  • MPhil Medicine, University of Sydney (2015)
  • BSc Immunology and Pharmacology, University of Sydney (2012)

Personal Interests

Genomics, Artificial Intelligence, Spatial Biology, Bioinformatics, Multi-Omics, Single-Cell, Cancer

Contact

Additional Info

All Publications

  • Global loss of promoter-enhancer connectivity and rebalancing of gene expression during early colorectal cancer carcinogenesis. Nature cancer Zhu, Y., Lee, H., White, S., Weimer, A. K., Monte, E., Horning, A., Nevins, S. A., Esplin, E. D., Paul, K., Krieger, G., Shipony, Z., Chiu, R., Laquindanum, R., Karathanos, T. V., Chua, M. W., Mills, M., Ladabaum, U., Longacre, T., Shen, J., Jaimovich, A., Lipson, D., Kundaje, A., Greenleaf, W. J., Curtis, C., Ford, J. M., Snyder, M. P. 2024

    Abstract

    Although three-dimensional (3D) genome architecture is crucial for gene regulation, its role in disease remains elusive. We traced the evolution and malignant transformation of colorectal cancer (CRC) by generating high-resolution chromatin conformation maps of 33 colon samples spanning different stages of early neoplastic growth in persons with familial adenomatous polyposis (FAP). Our analysis revealed a substantial progressive loss of genome-wide cis-regulatory connectivity at early malignancy stages, correlating with nonlinear gene regulation effects. Genes with high promoter-enhancer (P-E) connectivity in unaffected mucosa were not linked to elevated baseline expression but tended to be upregulated in advanced stages. Inhibiting highly connected promoters preferentially represses gene expression in CRC cells compared to normal colonic epithelial cells. Our results suggest a two-phase model whereby neoplastic transformation reduces P-E connectivity from a redundant state to a rate-limiting one for transcriptional levels, highlighting the intricate interplay between 3D genome architecture and gene regulation during early CRC progression.

    View details for DOI 10.1038/s43018-024-00823-z

    View details for PubMedID 39478119

    View details for PubMedCentralID 7541718

https://orcid.org/0009-0004-8050-1207