MEF2D (Myocyte Enhancer Factor 2D)

Our findings demonstrate the clinical utility of integrative transcriptomic profiling in refining B-ALL taxonomy, guiding risk-adapted therapies, and informing future revisions of diagnostic standards. This study supports the incorporation of high-throughput molecular diagnostics into routine leukemia classification and precision treatment planning.

B-ALL with MEF2D fusions frequently demonstrates multilineage involvement, poor response to conventional chemotherapy, and extramedullary infiltration. Incorporating venetoclax and the histone deacetylase inhibitor chidamide into induction, salvage, or preconditioning regimens may probably improve outcomes for MEF2D-positive patients, though certainly required further clinical validation.

The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 33: 2606‑2612, 2015; DOI: 10.3892/or.2015.3861].

Furthermore, patients with TCF3::PBX1 or MEF2D fusion and high EVI1 expression had RFS and OS similar to those without the corresponding fusions, and patients with ZNF384 fusion and low EVI1 expression had RFS and OS comparable to those without ZNF384 fusions (all p > 0.05). Low EVI1 transcript levels at diagnosis are related to poor prognosis in adult Ph-negative B-ALL, and EVI1 expression may improve fusion gene-defined risk stratification.

ChIP-seq data of the Kasumi-7 cell line showed that the MEF2D::HNRNPUL1 fusion protein directly bound to the region next to an intronic enhancer sequence of CIITA, indicating a MEF2D-CIITA-MHC potential pathogenic mechanism. This study offers a comprehensive analysis of MEF2D-fusion cases, detailing the fusion features and functional alterations, thus providing insights for future investigations.

A novel finding is that BET inhibitor induces DNA damage by downregulating DNA repair genes. These findings highlight that anti-leukemic activity of BET inhibitors offers a promising strategy to improve outcomes in this high-risk leukemia subtype.

RNF39 is identified as an oncogenic E3 ubiquitin ligase that is upregulated in colorectal adenocarcinoma and associated with poor prognosis. Mechanistically, RNF39 targets the tumour suppressor RINT1 for K48-linked polyubiquitination and proteasomal degradation. By degrading RINT1, RNF39 suppresses the unfolded protein response (UPR) and limits endoplasmic reticulum (ER) stress-induced apoptosis, thereby promoting tumour progression. The study reveals a novel MEF2D-RNF39-RINT1 axis governing stress adaptation, positioning RNF39 as a potential prognostic biomarker and therapeutic target in colorectal cancer.

Targeting NRP1 signaling disrupts the KC2-to-KC1-like differentiation and reduces niche inflammation, thereby inhibiting liver tumorigenesis in male mice. Thus, preventing aberrant KC subtype conversion in the precancerous microenvironment is a viable strategy for early cancer prevention.

MEF2D blocks T-cell-mediated antitumor immunity by regulating the expression of CD70 and activating the CD70-CD27 signaling axis. Strategies to manipulate this pathway may improve the efficacy of liver cancer immunotherapy.

Recently, 5 myxoid epithelioid smooth muscle tumors with MEF2D::NCOA2 gene fusion were reported in the vulvovaginal region. Given the characteristic histological and molecular findings, this case may represent a new entity in the gastrointestinal tract related to the vulvovaginal tumor, serving as a foundation for future studies.