Steven P. Balk

The paper examines immune infiltration in prostate cancer, finding higher T-cell density correlates with reduced CD8 effector cells and increased TIGIT, suggesting immune suppression.

This paper identifies FOXJ1 as a mediator of taxane resistance in prostate cancer by regulating microtubule dynamics, with clinical implications for patient stratification.

This study shows that AR inhibition does not enhance PARP inhibitor efficacy in HR-proficient prostate cancer and instead impairs response in castration-sensitive cells.

This study shows that in prostate cancer with TMPRSS2:ERG fusion, androgen deprivation increases AKT activation, which may reduce the effectiveness of AR-targeted therapy, suggesting combination therapy could be beneficial.

This paper introduces BSJ-5-63, a PROTAC that degrades CDK12, CDK7, and CDK9, inducing BRCAness and blocking AR signaling to enhance PARP inhibitor sensitivity in prostate cancer.

This study shows that ARv7 drives AR activity in castration-resistant prostate cancer through increased chromatin accessibility mediated by NFI factors.

The paper identifies S-phase RNAs that anchor ORC1 to H2A.Z, enabling DNA replication initiation and revealing an RNA-mediated mechanism for replication origin formation.

This study identifies transcriptional states in mCRPC that mediate treatment resistance, including AR splicing heterogeneity, TGF-β signaling, and immune infiltration patterns.

The paper shows that ctDNA is undetectable in localized prostate cancer but present in metastatic cases, suggesting lower dissemination and detectability in early stages.