Dean G. Tang

This study quantifies cancer stemness in prostate cancer across progression stages, showing its association with therapy resistance, poor survival, and lineage plasticity.

This study identifies STAG2's role in regulating chromatin architecture and gene expression in muscle invasive bladder cancer, revealing its context-specific activation and repression of genes involved in oncogenic signaling.

This study identifies an opioid-mediated signaling axis in pancreatic cancer that drives extracellular matrix remodeling and tumor aggressiveness, suggesting methylnaltrexone as a potential therapeutic.

This study validates BCL-2 as a therapeutic target in CRPC by showing its upregulation under AR inhibition and demonstrating efficacy of BCL-2 inhibitors in preclinical and clinical models.

The paper shows that loss of ATG5 in prostate cancers leads to tumor growth by accumulating p62, suggesting ATG5 acts as a tumor suppressor in this context.

This study shows EphA2 overexpression and loss of its ligands in prostate cancer promote bone metastasis through noncanonical signaling in a ligand-deficient bone microenvironment.

This study evaluates folate-conjugated miR-34a as a potential prostate cancer therapeutic, finding limited efficacy due to low FOLR1 expression in prostate cancer cells.

The paper identifies heterogeneous subpopulations of slow-cycling cells in TNBC and shows AP-1, particularly the JunB subunit, regulates dormancy and drug resistance.

This study compares four ChIP-Seq library preparation protocols for three different protein targets, finding that each protocol performs best for specific enrichment patterns and input DNA levels.

The paper identifies intron retention as a hallmark of aggressive prostate cancer and highlights the spliceosome as a therapeutic target by analyzing splicing dysregulation across prostate cancer progression.

This study identifies FAM35A as a REV7-associated protein that modulates DNA damage responses, showing altered expression in prostate cancer and resistance to PARP inhibitors in BRCA1-defective cells.