TRIM33 (Tripartite Motif Containing 33)

NRAS-mutant melanomas harbor a coordinated transcriptional program within 1p13.2, driven by CNV gains. This locus contains genes with potential druggability, offering new avenues for combinatorial targeting alongside mitogen-activated protein kinase pathway inhibition.

We detected highly frequent genetic alterations in autoantibody-related genes, supporting their role in the CAD pathogenic mechanisms. Moreover, our findings suggest that distinct TCR repertoire and immune signatures between tumoural and nontumoural tissues may underlie divergent cancer and dermatomyositis outcomes.

Distinct cytokine signatures in the JDM subgroups underscore their role in disease heterogeneity and clinical presentation. These findings support cytokine profiling as a potential tool for patient classification and personalized treatment.

In vivo, Sal B synergized with anti-PD-1 therapy, significantly reducing tumor burden versus monotherapy. These findings establish ZFPL1 as a key regulator of CRC progression through ASS1-dependent urea cycle activation and immunomodulation, nominating the ZFPL1-ASS1 axis as a therapeutic target, with Sal B demonstrating combinatorial potential with immunotherapy.

Cycloheximide (CHX) chase experiments revealed that LINC00667 overexpression accelerated POTEE degradation, while treatment with the proteasome inhibitor MG132 stabilized POTEE levels...Collectively, our findings demonstrate that LINC00667 inhibits breast cancer progression by promoting TRIM33-mediated ubiquitination and subsequent degradation of POTEE, thereby regulating mitochondrial OXPHOS activity. These results highlight the critical role of LINC00667 in the posttranslational regulation of protein stability and mitochondrial function in BC, and suggest that targeting the LINC00667-POTEE axis may represent a potential therapeutic strategy for this disease.

This case underscores the importance of early recognition and management of paraneoplastic syndromes such as tumor-associated DM. A multidisciplinary approach combining immunotherapy and surgical intervention for the underlying malignancy can lead to favorable outcomes. This case also highlights the significance of long-term monitoring for both cancer recurrence and autoimmune complications in such patients.

The analysis of mutations in the Zn ion binding sites of the ZBPs revealed that mutations affect the proteins' structure, function, and binding affinity, potentially leading to cancer. Investigating mutations in the Zn binding sites of these proteins will pave the way for cancer treatments by enhancing our understanding of their role in cancer spread and invasion.

Despite diagnostic advancements, some entities, like OANOS, remain provisional, pending widespread access to transcriptomic tools. Recognising the molecular heterogeneity and clinicopathologic nuances of oncocytic carcinomas is essential for improving diagnostic precision, prognostication, and guiding targeted therapy.

This review identifies TRIM proteins that are involved in urological cancers. Some of these proteins have the potential to be the therapeutic target.

We observed that TRIM33 and AR share overall chromatin interaction profiles, in which TRIM33 is involved in downstream responsive transcriptomic output. In contrast to prior reports, we show that TRIM33 does not impact AR protein stability, but instead propose a model in which TRIM33 facilitates maximal AR activity by interfering with H2BK120 ubiquitination levels.

Nivolumab was discontinued, and intravenous and oral steroids, intravenous immunoglobulin and rituximab were initiated for the treatment of dermatomyositis. Both paraneoplastic dermatomyositis in patients with metastatic melanoma and dermatomyositis presenting as an immune-related adverse event in patients receiving immune checkpoint inhibitors (ICI) are rare. In this case, we highlight features that are consistent with both paraneoplastic dermatomyositis and ICI-induced dermatomyositis.

Furthermore, the proteasome inhibitor MG132 (10 µM) and TRIM33, an E3 ubiquitin ligase involved in proteasome-mediated protein degradation, knockdown via shRNA both abrogated the DMC-GF-mediated decrease in SLC25A1 protein levels (p < 0.05). These findings underscore the potential of DMC-GF as an efficacious targeted therapeutic against GSCs, offering enhanced brain specificity and stability, and elucidating its mechanism involving mitochondrial dysfunction and SLC25A1 degradation.