Lab Publications
Peer-reviewed research, reviews, and translational studies from the Dhanasekaran Lab at Stanford Medicine.
Highlighted Articles
Spatial analysis reveals targetable macrophage-mediated mechanisms of immune evasion in hepatocellular carcinoma minimal residual disease
HCC frequently recurs from minimal residual disease (MRD) that persists after therapy. We identified a spatial neighborhood in which PD-L1+ M2-like macrophages interact with stem-like tumor cells, correlating with CD8+ T cell exhaustion and poor survival. Combined blockade of Pdl1 and Tgfβ eliminated residual stem-like tumor cells in mouse models.
MYC Overexpression Drives Immune Evasion in Hepatocellular Carcinoma That Is Reversible through Restoration of Proinflammatory Macrophages
MYC genomic amplification increased immune checkpoint expression, predicted non-responsiveness to immune checkpoint blockade, and was associated with reduced CD8 T cell infiltration across 33 human cancers. Combined PDL1 and CTLA4 blockade reversed MYC-driven immune suppression through recruitment of pro-inflammatory macrophages.
Genomic Analysis of Vascular Invasion in HCC Reveals Molecular Drivers and Predictive Biomarkers
Vascular invasion is a critical risk factor for HCC recurrence. We evaluated the molecular landscape of invasive tumors, identifying MYC-driven transcriptional changes. MYC upregulates fibronectin expression promoting HCC invasiveness, and fibronectin is a promising noninvasive proteomic biomarker of vascular invasion.
MYC and Twist1 cooperate to drive metastasis by eliciting crosstalk between cancer and innate immunity
Conditional expression of MYC and Twist1 enables HCC to metastasize in >90% of mice. MYC and Twist1 cooperate to activate innate immunity through a cytokinome that recruits and polarizes tumor-associated macrophages. CCL2 and IL13 predicted poor survival in 33 human cancers.