M. D. Long

Epigenetic disruption of the RARγ complex impairs its function to bookmark AR enhancer interactions required for enzalutamide sensitivity in prostate cancer

This study identifies RARγ's role in bookmarking AR enhancer interactions in prostate cancer, showing its impact on enzalutamide sensitivity and lineage plasticity.

The MYC axis in advanced prostate cancer is impacted through concurrent targeting of ERβ and AR using a novel ERβ-selective ligand alongside Enzalutamide

This study shows that combining a novel ERβ ligand with Enzalutamide reduces MYC signaling and growth in advanced prostate cancer.

Leukemic mutation FLT3-ITD is retained in dendritic cells and disrupts their homeostasis leading to expanded Th17 frequency

This study shows FLT3-ITD mutations in AML retain in dendritic cells, altering their phenotype and increasing Th17 T cell frequency.

IgG sialylation occurs via the FcRn-mediated recycling pathway in endothelial cells

The paper shows that endothelial cells regulate IgG sialylation through the FcRn-mediated recycling pathway, impacting inflammatory responses.

Vitamin D receptor cistrome-transcriptome analyses establishes quantitatively distinct receptor genomic interactions in African American prostate cancer regulated by BAZ1A

The paper analyzes VDR genomic interactions in African American prostate cancer cells and identifies BAZ1A as a regulator of VDR-dependent transcriptional responses.

Reduced NCOR2 expression accelerates androgen deprivation therapy failure in prostate cancer

This study shows reduced NCOR2 expression accelerates androgen deprivation therapy failure in prostate cancer by promoting DNA hypermethylation and neuroendocrine gene expression.

Genome-wide analyses of transcription factors and co-regulators across seven cohorts identified reduced PPARGC1A expression as a driver of prostate cancer progression

The miR-96 and RAR&gamma signaling axis governs androgen signaling and prostate cancer progression

This study identifies miR-96 as a regulator of RARγ expression, which in turn controls androgen signaling and prostate cancer progression through gene network alterations.