NR4A3 (Nuclear receptor subfamily 4 group A member 3)

FISH detection of NR4A3 gene rearrangements provides a crucial value for the diagnosis. It needs to be differentiated from myoepithelial tumors, chordomas and myxoid liposarcomas.

Surgical treatment is the only option for a cure for EMC, while non-surgical treatments are typically considered for recurrent or distant disease. This case report discusses an interesting case of a patient with EMC and further elaborates on the history, examination, imaging, pathological findings, and management of EMC.

We have also identified gene silencing, reduced gene expression of key transcription factors that regulate mitochondrial biogenesis, as well as increased long non-coding RNA as potential drivers of this unique metabolic phenotype. These results highlight the potential benefit of targeting metabolism in sepsis to promote immune homeostasis and recovery.

Overall, our findings confirm that GREB1-rearranged uterine tumours are part of the UTROSCT spectrum, though they frequently exhibit a more diffuse growth pattern and a higher degree of genomic instability.

Moreover, this phenomenon may be associated with the orphan nuclear receptor NOR1//Nr4a3 activation by CD9. These findings indicated that macrophages in the TME exhibited distinct expression patterns during RCC progression and that CD9+ macrophages promoted RCC development, suggesting that CD9 may be a potential therapeutic target for inhibiting RCC progression.

SGMS2 could polarize macrophages toward the M1 phenotype. SGMS2+ macrophages secrete CXCL2 to recruit CD56dimCD16highNR4A3high NK cells, thereby enhancing tumor apoptosis. High infiltration of SGMS2+ macrophages and CD56dimCD16highNR4A3high NK cells correlates with superior PD-1 therapy responsiveness and extended survival.

Transcriptome cluster comparative analysis placed its expression profile close to pancreas neuroendocrine tumors. This case suggests NR4A2 as a functionally substitute for NR4A3 in tumorigenesis and a neuroendocrine lineage differentiation for a subset of EMC.

Furthermore, survival analysis revealed that miR-93-5p (HR = 0.72, p = 0.0246), HCC stage (HR = 2.43, p = 0.0000113), TCF4 (HR = 0.66, p = 0.0106), DNAJB4 (HR = 1.29, p = 0.0214), MCC (HR = 1.35, p = 0.0268), and CYB5A (HR = 0.77, p = 0.0423) affect overall survival (OS). Finally, a combined prognostic model for the miRNA cluster and its target genes via the random forest approach revealed that the miR-106b/25 cluster and its interactome are significantly associated with OS (p < 0.0001), thereby providing a comprehensive understanding of the cluster and its targets in the development and progression of HCC and its use as a potential marker for HCC.

Furthermore, through structural optimization of LZ22 guided by molecular docking, we identified a derivative (LZ22-4) with enhanced anti-tumor proliferative activity. These findings not only identify PABPC1 as a valuable therapeutic target for TNBC but also provide new opportunities and novel insights for advancing anti-TNBC drug development with LZ22 as a potential drug leading compound.

Furthermore, combination treatment significantly downregulated gene expression associated with immune-related pathways, increased levels of immunodysregulatory acute phase proteins and decreased levels of necroptosis mediator RIPK3. Overall, xevinapant plus CRT has an immunosuppressive effect on the tumour-immune microenvironment which may explain its lack of clinical benefit.

Overexpressing FOS alongside NR4A3 knockdown robustly boosted the antitumor responses of CAR T cells by skewing their phenotypes and transcriptional profiles away from exhaustion and toward increased effector function. These findings offer a promising strategy for the clinical modification of CAR T cell therapy.

EMC is most commonly a deep lesion of the extremities demonstrating hyperintense T2-weighted signal, internal septations, and variable patterns of enhancement on MRI. Nodal disease is relatively frequent, and prolonged surveillance is recommended as metastases may develop years after diagnosis. Although analysis is limited by small case numbers, a "solid" (> 80%) pattern of enhancement was significantly associated with metastatic disease.