MYC (V-myc avian myelocytomatosis viral oncogene homolog)

Furthermore, PPIL2 deficiency effectively hindered tumor growth in a xenograft mouse model. Collectively, these findings identify the PPIL2/c-Myc/p21 axis as a critical regulator of HCC proliferation and senescence, positioning PPIL2 as a promising therapeutic target.

Mechanistically, MeRIP-qPCR, RIP-qPCR, dual-luciferase reporter assay, and actinomycin D treatment revealed that IGF2BP1 targeted the 3'UTR of the C-MYC transcript for m6A modification and enhanced its stability. Furthermore, IGF2BP1 induced epithelial-mesenchymal transition (EMT) through the overexpression of C-MYC. In conclusion, these findings suggest that IGF2BP1-mediated m6A modification of C-MYC promotes LSCC progression via the EMT pathway, providing potential biomarkers and therapeutic targets for LSCC.

In pediatric patients with metastatic medulloblastoma, primary tumor resection might be avoidable. A biopsy-based approach followed by timely multimodal therapy can preserve survival outcomes while minimizing surgical risks, as long-term prognosis is likely related to the disease subtype and prompt oncological treatment. The proposed strategy warrants further investigation and might have broader implications for medulloblastoma treatment paradigms.

Concurrently, dysregulated signaling, such as the Wnt/β-catenin pathway, inhibits dendritic cell maturation and recruits Myeloid-Derived Suppressor Cells (MDSCs) and regulatory T cells (Tregs) into the tumor microenvironment, thereby blunting the anti-tumor T cell response. This review examines the role of key pluripotency regulators in TNBC-mediated immune evasion, highlighting emerging immunotherapeutic strategies targeting these networks and summarizing current clinical research.

HOXB2 appeared to promote Huh7 cell proliferation and motility through MYC transcriptional activation, whereas miR‑5590‑3p overexpression suppressed tumor growth in vivo. In conclusion, miR‑5590‑3p may inhibit HCC cell proliferation and motility, and induce apoptosis by targeting HOXB2 and suppressing MYC transcription.

Hierarchical analysis of MYC, BCL2, BCL6 rearrangements and 11q aberration is therefore essential. It directly impacts diagnosis, prognostic stratification, and therapeutic management.

Notably, we reveal a non-canonical trans-acting role for IGF1R-AS1 whereby it interacts with chromatin remodeling complexes and architectural proteins to facilitate long-range chromatin looping between distal MYC enhancers and its promoter, leading to MYC overexpression and enhanced tumorigenicity. Collectively, our findings elucidate a mechanism by which a tumor-specific trans-acting lncRNA modulates oncogenic MYC expression through long-range chromatin interactions, suggesting IGF1R-AS1 may play an important role in the pathogenesis of MYC-driven malignancies.

However, PRMT5 inhibitors (e.g., GSK3326595 and JNJ-64619178) demonstrate antitumor effects in preclinical models and methylthioadenosine phosphorylase (MTAP) deletion may serve as a potential biomarker for patient selection. The clinical translation of PRMT5 inhibitors is limited by hematological toxicity, lack of robust predictive biomarkers beyond MTAP and potential resistance from compensatory PRMT family members. It is key to clarify GI cancer-specific PRMT5 mechanisms and potentially develop optimized combination therapies in the future.

This esterase-responsive albumin-binding PROTAC design could overcome pharmacokinetic barriers of conventional BRD4-targeting PROTACs by enhancing tumor-specific delivery and esterase-responsive BRD4 degradation in solid tumors. In summary, esterase-responsive albumin-binding PROTAC is proven as a promising strategy that effectively modulates the pharmacokinetics and therapeutic performance of PROTACs for cancer immunotherapy.

PTEN loss occurred frequently (59% 12/22 mice), and contributed to osteosarcomagenesis, as demonstrated by tumor initiation with in vivo CRISPR/Cas9-mediated deletion experiments (2 mice). Together, these results demonstrate that a preclinical model of osteosarcoma can generate the genomic heterogeneity and complexity of the human disease, thereby facilitating research into mechanisms of tumor initiation and drivers of progression and relapse.

P2/3, N=501, Active, not recruiting, Karyopharm Therapeutics Inc | Recruiting --> Active, not recruiting | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Dec 2025 --> Dec 2026

This signature effectively stratifies MASLDpatients, discriminating molecular risk groups associated with progression to HCC. Integrating transcriptomic, clinical and experimental data suggests the role of miR-26a-5p, along with the MASLD-HCC gene signature (EpCAM, DTNA, and KPNA2), may serve as an early molecular indicator and mechanistic modulator of hepatocarcinogenesis, warranting further functional investigation.