W. Zwart

This study shows HOXB13 promotes prostate cancer proliferation by altering chromatin accessibility through interactions with the SWI/SNF complex, particularly in AR-negative castration-resistant prostate cancer.

The paper identifies enhancer plasticity and 3D-genome alterations in endometrial cancer that boost ESR1 expression through non-coding mutations and risk variants.

This study uses a CRISPR screen to identify genes critical for macrophage-mediated killing of prostate cancer cells, revealing AR as an immunomodulator that promotes resistance to macrophage attack.

This study shows that combining dexamethasone with spironolactone enhances myeloma cell killing through GR-MR crosstalk, with potential for dose reduction.

This study shows that loss of ZFP36 promotes NF-κB activation and phenotypic plasticity in prostate cancer, leading to aggressive disease and castration resistance, which can be reversed by NF-κB inhibition.

The authors withdrew their manuscript due to inconsistencies in data and questionable experimental results regarding DNA end-resection and chromatin accessibility.

This study shows MYC overexpression in TNBC reduces immune cell infiltration and interferon signaling, contributing to immune evasion and poor response to immunotherapy.

The paper functionally maps AR enhancer activity using STARRseq, finding most AR binding sites are inactive or constitutively active, with inducible enhancers forming regulatory hubs that drive gene transcription.

This study shows that SPOP and ERG mutations in prostate cancer have opposing effects on androgen receptor signaling and therapy response.

The paper identifies three macrophage subtypes in human prostate cancer using single-cell transcriptomics and develops a gene signature linked to patient survival.

This study uses whole-genome sequencing to identify four distinct genotypes in metastatic castration-resistant prostate cancers, with potential clinical implications for patient stratification.

This study identifies the mechanism by which glucocorticoid receptor activation induces cancer cell dormancy through CDKN1C and FOXO1/IRS2 signaling, with implications for cancer therapy.