Richard Mark White

The paper shows that keratinocyte EMT-like transformation in melanoma reduces tumor invasion and improves survival through altered cell-cell interactions.

The paper shows that 3'UTR-3'UTR interactions drive Wnt gene activation by enabling co-translational protein complex assembly, independent of protein abundance.

TRANCERs convert enhancers into autonomous tissue-specific promoters, enabling precise and programmable gene expression for research and therapy.

This study uses a zebrafish model to identify genetic dependencies in melanocyte and melanoma development, revealing that gene loss can paradoxically promote aggressive phenotypes.

The paper shows that desmosome mutations in keratinocytes of the tumor microenvironment promote melanoma proliferation through reduced desmosome gene expression and increased melanoma cell growth.

This study shows that dual FGFR/VEGFR inhibition causes regression of acral melanoma by targeting the tumor microenvironment rather than directly killing cancer cells.

The paper identifies DHRS3 as a lipid droplet protein that regulates melanoma cell state by modulating retinoid signaling.

This study uses real-time imaging in zebrafish to show that macrophage protrusive motility, regulated by Rac2, influences melanoma invasion.

This study analyzes acral melanoma genomes and transcriptomes from Mexican patients, finding ancestry-related mutation patterns and survival differences.

This study shows mechanical confinement drives phenotype switching in melanoma via chromatin remodeling mediated by HMGB2.

This study shows that the transcription factor MITF interacts with the MRN complex to modulate the DNA damage response in melanoma, contributing to cancer predisposition.

BayesTME is a Bayesian method for spatial transcriptomics that unifies analysis goals, outperforms existing methods, and identifies spatial transcriptional programs in human and zebrafish melanoma tissues.