Wilbert T. Zwart

The paper identifies a subgroup of mCRPC characterized by LINE1 repeat DNA elements flanking the AR gene, which drive AR overexpression and confer resistance to androgen signaling inhibitors.

The paper shows TRIM33 enhances AR activity by reducing H2BK120 ubiquitination, without affecting AR protein stability.

This paper identifies IRE1 activity as a regulator of prostate cancer cell lineage states and shows its role in predicting prognosis and treatment response across localized and metastatic disease.

The paper links genes in cancer-susceptibility loci to known somatic driver genes through tissue-specific co-expression networks derived from non-cancer samples.

This paper introduces PARM, a deep learning model trained on MPRA data to predict human promoter activity and identify TF binding preferences, revealing positional and functional differences in regulatory grammar.

This study identifies 67 epigenetic drugs that modulate CRISPR-Cas9 editing efficiency and repair outcomes based on chromatin context in human cells.

The paper identifies breast cancer risk SNPs that overlap with estrogen receptor binding sites, showing their role in altering estrogen signaling through chromatin interactions.

This study investigates molecular glues targeting the ER/14-3-3 PPI to overcome endocrine resistance in breast cancer, showing suppression of ER activity and cell proliferation.

This study uses an agent-based model to simulate prostate cancer growth and ADT effects, revealing CRPC development and immunomodulatory interactions in the tumor microenvironment.

The paper shows that disrupting nuclear lamina association promotes ABCB1 gene derepression and taxol resistance in RPE cells.

This study develops an agent-based model of prostate cancer progression, showing that stochastic interactions and systematic factors influence tumor development and clinical outcomes.

This study identifies PAXIP1 and STAG2 as co-regulators of the Glucocorticoid Receptor (GR) that maintain 3D genome architecture and enable stress hormone-dependent transcription.

The paper introduces CWAS, a method linking genetic variation to chromatin states, identifying novel prostate cancer risk loci and regulatory mechanisms not detectable by eQTLs.

This study reports that lentiviral-based CRISPR-Cas9 vectors can integrate into the target genomic location, unexpectedly activating the target gene.

This study identifies mechanisms by which androgen and glucocorticoid receptors achieve functional diversification through distinct DNA binding and downstream regulatory events.