ETV1 (ETS Variant Transcription Factor 1)

P4, N=400, Completed, Henan Provincial People's Hospital; Henan Provincial People's Hospital

This dual IHC and dual RNA-ISH approach represents a novel and reliable platform for multiplex detection of key prostate cancer biomarkers on a single slide. The method offers significant advantages for molecular classification, tissue-based biomarker validation, and comprehensive evaluation of tumor heterogeneity in translational and diagnostic research.

Unlike the other NPs, the GRP1 and GRP2 NPs upregulated expression of genes for proteins involved in immune function. The present work will serve as an important resource for investigators interested in further defining the transit amplifying progenitors of the mammalian SVZ.

This study supplements the current knowledge of the underlying mechanism behind acquired chemoresistance in OVCA. Four differentially methylated genes identified in this study may have the potential to serve as promising epigenetic clinical biomarkers for HGSC chemotherapy resistance.

AKT-mediated degradation of FOXO1 and subsequent loss of the ERG/PRC2 interaction provides a mechanism for ERG synergy with PTEN deletion in prostate cancer. Implications: These findings indicate that ETS transcription factors that drive prostate cancer and Ewing sarcoma utilize similar mechanisms and thus could be targeted by similar therapeutic approaches.

While several oncogenic features were consistently present across strains, others were unexpectedly variable such as ETV1 expression, Y chromosome loss, a reliance on WNT and glucocorticoid receptor activity, and distinct AR alterations maintaining AR pathway activation. These results document the inherent molecular heterogeneity and ongoing genomic instability that drive diverse prostate cancer phenotypes and provide a foundation for the accurate interpretation and reproduction of research findings.

show that ETS variant transcription factor 1 (Etv1) SUMOylation not only maintains cancer stem cells (CSCs) but also enables their communications with non-CSC cancer cells to induce tumorigenesis of non-CSCs. The finding reveals a new function of CSCs in driving aggressive tumorigenesis that is SUMOylation dependent.

We performed bionformatic analyses to provide insights into the transcription factor interactions that are likely regulating their development as well as the functional consequences of these diffferences in gene expression. The present work will serve as an important resource for investigators interested in further defining the transit amplifying progenitors of the mammalian SVZ.

P2, N=14, Completed, Memorial Sloan Kettering Cancer Center | Recruiting --> Completed | N=24 --> 14 | Trial completion date: Mar 2026 --> Aug 2025 | Trial primary completion date: Mar 2026 --> Aug 2025

Accordingly, combined inhibition of EGFR and STAT3 using Erlotinib and TTI-101, respectively, led to a significant reduction in 2D and 3D cell growth of early and advanced PCa cells overexpressing ETV1. Collectively, our findings highlight EGFR-STAT3 activation as a novel ETV1-regulated oncogenic pathway, providing a rationale for repurposing EGFR inhibitors in combination with STAT3 inhibitors as a therapeutic strategy for the 8-10% of prostate carcinomas characterized by ETV1 rearrangements/overexpression.

Indeed, the deletion of pro-survival BCL2A1 re-sensitized COP1 mutant cells to vemurafenib treatment. These observations indicate that the post-translational regulation of ETV5 by CRL4COP1/DET1 modulates transcriptional outputs in ERK-dependent cancers, and its inactivation contributes to therapeutic resistance.