R. M. White

This study shows that fatty acid β-oxidation and TLR4 signaling drive melanoma progression by altering histone acetylation and inflammatory gene expression.

This study identifies lipid droplets as a metabolic vulnerability in melanoma by linking the pigmented cell state to increased fatty acid uptake and oxidative metabolism.

This study develops a bioluminescent zebrafish model to screen kinase inhibitors for cancer therapy, finding that NanoLuc luciferase enables sensitive and rapid in vivo drug response evaluation.

The paper shows that anatomic position influences oncogenic specificity in melanoma by identifying position-specific gene programs that interact with oncogenes like CRKL.

This study uses spatial transcriptomics to identify a conserved tumor-microenvironment interface in zebrafish and human melanoma characterized by cilia gene upregulation.

This study shows SATB2 drives melanoma invasion and drug resistance by inducing a neural crest mesenchyme-like transcriptional program in zebrafish and human models.

The paper shows that BRAFV600E transforming ability depends on the cell of origin's transcriptional program, with neural crest and melanoblasts being more susceptible due to higher chromatin modifying enzyme expression and ATAD2-SOX10 complex formation.

The paper identifies a stress-like cancer cell state in melanoma that promotes tumorigenesis and drug resistance, validated across zebrafish and human models.

This study identifies that RTKs EGFR and KDR/VEGFR2, not Brachyury, can induce chordoma in zebrafish by disrupting notochord differentiation through RTK/Ras signaling.

Cancer cells under stress from oncogene or mTOR inhibition dysregulate the error-prone DNA polymerase polκ, which contributes to drug resistance in melanoma cells.

The paper introduces TEAZ, a method to rapidly model cancer in zebrafish by delivering gene constructs to specific cells, enabling faster tumor development and tracking.