MEF2C (Myocyte Enhancer Factor 2C)

P=N/A, N=22068, Recruiting, Weill Medical College of Cornell University

Some previously reported MSAd cases displayed subtle variations in their histopathological and immunohistochemical characteristics, underscoring the importance of molecular fusion confirmation. Given its typically indolent behavior, MSAd patients can be managed similarly to those with other low-grade salivary gland carcinomas.

Regulation of SOX18 by miR-24-3p highlights a potential therapeutic vulnerability. These findings underscore the significance of SOX transcription factors as biomarkers and potential targets for novel treatment strategies in NSCLC.

Additionally, the transcription factor myocyte enhancer factor 2 C (MEF2C) was found to bind to the promoters of PDGFA, PDGFB, ANGPT1, and ANGPT2, initiating their transcription. Knockdown of MEF2C inhibited the pro-angiogenic activity of MCAM+ myCAFs both in vitro and in vivo MCAM+ myCAFs promote the transcription of pro-angiogenic factors through MEF2C, thereby enhancing angiogenesis and promoting tumor growth in solid-type ACC.

Our findings suggest that MEF2C is downregulated in cisplatin-resistant ovarian cancer cells, and its overexpression re-sensitizes these cells to cisplatin through the activation of intrinsic apoptotic pathways. Clinically, elucidating the molecular mechanisms of chemoresistance and targeting key regulators such as MEF2C may provide a promising strategy to reprogram resistant tumor cells and enhance the efficacy of standard chemotherapy, offering a potential translational pathway toward improved therapeutic responses in ovarian cancer.

Molecular analysis identified an MEF2C::SS18 gene fusion and an immunohistochemical profile consistent with MSA. This report highlights the histological variation and the potential for late metastatic progression in MSA, emphasizing the need for accurate molecular diagnosis and long-term clinical surveillance, even in tumors that appear histologically low-grade at initial presentation.

Structure-based virtual screening identified a potent small-molecule antagonist targeting MCTP1, which markedly attenuates tumor burden, ALPL activity, and neuroendocrine marker expression in prostate cancer in vitro and in vivo models. Collectively, these findings establish MCTP1 as a novel therapeutically exploitable vulnerability in therapy-induced NEPC, providing critical insights into the calcium-dependent oncogenic signaling networks mediated by the MCTP1/FYN/MEF2C axis in advanced prostate cancer.

show that embryonically derived VSIG4⁺ macrophages suppress CD8⁺ T cell responses across cancers. They identify IL-11 as a key effector and MEF2C as a transcriptional regulator of VSIG4⁺ macrophages, highlighting new therapeutic avenues for targeting immunosuppressive tumor-associated macrophages to improve immunotherapy outcomes.

Protein-protein interaction (PPI) network analysis showed that the effect of MEF2C on OS may be related to genes such as APOE and SOX18. The results of this study suggest that MEF2C is associated with an increased risk of OS and that MEF2C has the potential to be a prognostic biomarker for OS.

No adjuvant therapy was administered, and the patient remained recurrence-free during a 3-year follow-up. This tumor confirms the slow-growing nature of microsecretory adenocarcinoma, emphasizes the importance of molecular testing for diagnosis, and clarifies the diagnostic differences between microsecretory adenocarcinoma and similar-looking salivary gland tumors.

Ultimately, through the utilisation of both Mendelian randomisation analysis and molecular docking, that Perifosine, 7-Hydroxystaurosporine, and Mitoxantrone could represent efficacious treatment options for ccRCC patients by targeting PRAME. The findings provide novel evidence that hypertension influences the progression of ccRCC and offer new insights into the disease's pathophysiology.