Stuart Gallagher

EZH2 Cooperates with DNA Methylation to Downregulate Key Tumor Suppressors and IFN Gene Signatures in Melanoma

Targeting DNA Methylation and EZH2 Activity to Overcome Melanoma Resistance to Immunotherapy

SIRT6 haploinsufficiency induces BRAFV600E melanoma cell resistance to MAPK inhibitors via IGF signalling

Marked Global DNA Hypomethylation Is Associated with Constitutive PD-L1 Expression in Melanoma

Epigenetic modulation in cancer immunotherapy

Anti-PD-1-induced high-grade hepatitis associated with corticosteroid-resistant T cells: a case report

HDAC inhibitors restore BRAF‐inhibitor sensitivity by altering PI3K and survival signalling in a subset of melanoma

Somatic Copy Number Amplification and Hyperactivating Somatic Mutations of EZH2 Correlate With DNA Methylation and Drive Epigenetic Silencing of Genes Involved in Tumor Suppression and Immune Responses in Melanoma

Inducible but Not Constitutive Expression of PD-L1 in Human Melanoma Cells Is Dependent on Activation of NF-κB

Combining BET and HDAC inhibitors synergistically induces apoptosis of melanoma and suppresses AKT and YAP signaling

Targeting activating mutations of EZH2 leads to potent cell growth inhibition in human melanoma by derepression of tumor suppressor genes

Control of <scp>NF</scp>‐<scp>kB</scp> activity in human melanoma by bromodomain and extra‐terminal protein inhibitor <scp>I</scp>‐<scp>BET</scp>151

The Epigenetic Regulator I-BET151 Induces BIM-Dependent Apoptosis and Cell Cycle Arrest of Human Melanoma Cells

<scp>EZH</scp>2: an emerging role in melanoma biology and strategies for targeted therapy

Intralesional immunotherapy for melanoma

The BH3-mimetic ABT-737 sensitizes human melanoma cells to apoptosis induced by selective BRAF inhibitors but does not reverse acquired resistance

Histone Deacetylases (HDACs) as Mediators of Resistance to Apoptosis in Melanoma and as Targets for Combination Therapy with Selective BRAF Inhibitors