NCOA1 (Nuclear Receptor Coactivator 1)

These genetic alterations were conspicuously absent in primary tumors, suggesting their potential role in metastatic progression. Our findings represent the first demonstration of CNV-driven oncogenic evolution in UTROSCTs, particularly implicating SWI/SNF complex dysregulation in metastatic competence.

In conclusion, ZFTA::NCOA1/2-rearranged epithelioid mesenchymal tumors represent a novel, morphologically distinct entity, genetically and epigenetically overlapping with chondroid lipoma. Expanded cohorts and long-term follow-up are necessary to clarify their precise classification and biologic behavior.

This integrative analysis prioritizes high-impact ESR2 variants that likely impair ERβ1 structure and shows context-dependent clinical effects. Despite their generally low frequency (except for rs4986938), prospective validation linking variant class to ERβ expression and survival outcomes is needed to support biomarker development and therapeutic applications.

The changes identified indicate a complex reprogramming of transcriptional activity affecting cell cycle processes, DNA repair, metabolism, and the epithelial-mesenchymal transition. The findings expand our understanding of the molecular mechanisms of trastuzumab resistance and open prospects for the development of novel therapeutic strategies to overcome drug resistance in HER2-positive breast cancer.

We conclude that SCRMS with ZFP64::NCOA2/3 fusions represent a distinct, clinically aggressive sarcoma, characterized by fascicular and sometimes round cell morphology, occasional chondro-osseous differentiation and variable skeletal muscle marker expression. Recognition of this emerging subtype of SCRMS may have prognostic and therapeutic implications.

All but 1 tumor harbored a PRRX1::NCOA1 fusion, while 1 case harbored a novel PRRX1::EP300 fusion. We herein provide additional data on these exceptionally uncommon tumors, expand their molecular spectrum, and compare them to their close morphologic mimics to aid in accurate diagnosis and avoid confusion with potentially more aggressive neoplasms.

However, we report the first pediatric case in an 11-year-old patient presenting with 5.5 cm mass in the head and neck region. Our case is also the second reported case of a PRRX1 (exon 1)::NCOA1 (exon 15) fusion transcript to date.

This study elucidates the possibility that miR-137 subtly modulates metabolic genes in prostate cancer, suggesting its latent therapeutic potential as a biomarker for disease progression.

Our systematic review of UTROSCTs summarized the clinical and pathological features and revealed several novel markers, including ESR1-NCOA2-3, GREB1-NCOA1-3, GREB1-CTNNB1, and GREB1-NR4A3. UTROSCTs are rare mesenchymal tumors with unclear histogenesis and uncertain malignant potential. Although our understanding of UTROSCTs remains incomplete, the promising findings and increasing availability of clinical data will contribute to the further understanding and development of this rare neoplasm.

The framework further reveals distinct patterns in energy metabolism, oxidative stress, and pH regulation between cancer-prone and non-cancer-prone inflammatory diseases. These insights enhance our understanding of inflammation-associated tumorigenesis and contribute to the identification of potential biomarkers and therapeutic targets.

The integral components of BYXD are identified to selectively engage with a range of critical targets, modulating the associated signaling pathways that are pivotal in the pathophysiology of CHD. Such targeted modulation provides a substantive scientific basis for the clinical application of BYXD.