MYC (V-myc avian myelocytomatosis viral oncogene homolog)

BP1 demonstrates potent anticancer activity against hepatocellular carcinoma cells by destabilizing c-Myc, inhibiting proliferation and motility, inducing apoptosis, and interfering with c-Myc-regulated metabolic pathways. In addition to its favorable pharmacokinetic properties, BP1 represents a promising lead compound for further preclinical development in hepatocellular carcinoma.

In vivo, oral administration of XYD113 (5 mg/kg, daily for 21 days) significantly inhibited 22Rv1 xenograft growth (TGI = 46%) and showed a favorable safety profile in BALB/c-nude mice. Together, these findings highlight XYD113 as a promising therapeutic degrader worthy of further development for the treatment of MYC-driven cancers.

Milademetan-mediated c-Myc depletion is accompanied by the induction of apoptosis and suppression of cell proliferation and prevents tumor growth, independently of p53 status. These findings reveal an unexpected mechanism by which MDM2 coordinates two of the most frequently altered pathways in cancer and provide a rationale for targeting c-Myc-driven tumors, including those lacking functional p53, through MDM2 modulators.

Positive C-MYC and EBV expression results point to a possible aetiology for B-cell lymphoma. We were unable to find any variations in the expression of EBV or C-MYC between the GCB and ABC groups. A large-scale, prospective investigation involving multiple institutions is necessary.

Rescue experiments and xenograft studies further verified this regulatory axis. KDM4D enhances ESCC radiosensitivity through the SRBD1/RPL11/c-Myc/WIP1/CHK1 pathway, highlighting its potential as both a diagnostic biomarker and a therapeutic target.

Intriguingly, GS Rg1 upregulated the expression of NEMO, STAT3, and NHE1, suggesting compensatory mechanisms or alternative signaling modulation. Our findings demonstrate that GS Rg1 exerts multi-faceted anti-tumor effects in glioblastoma cells by targeting the NF-κB signaling pathway.

scGOF-seq further identified cooperating transcription factor modules that complemented cMyc-driven programs and improved T cell responses in solid tumors. These findings establish systematic GOF perturbation as a framework for uncovering latent and temporally constrained regulatory activities in CD8⁺ T cells and guiding immune-state engineering.

In conclusion, we identified molecular subtypes of NPC, constructed preliminary diagnostic and prognostic marker panels, and observed the therapeutic potential of Panobinostat, as a monotherapy and in combination with radiotherapy. These findings provide a solid foundation for precision diagnosis, prognostic stratification, and personalized treatment strategies for NPC.

We validated PCK2 as a driver of proliferation, migration, invasion, glycolysis, and M2 macrophage polarization in MYC-amplified MB cells through short hairpin RNA knockdown experiments. Together, our findings establish metabolic-TIME crosstalk as a prognostic determinant and proffer PCK2 as a therapeutic target for aggressive MB subtypes, offering insights into metabolic subtyping and precision therapy strategies to improve clinical outcomes.

Across orthotopic bladder cancer, subcutaneous xenograft, and orthotopic breast cancer models, POR-BG@Alb-mediated SDT suppresses primary tumors, elicits abscopal antimetastatic effects, establishes immune memory, and extends median survival in subcutaneous xenografts from 17 to 44 days. Collectively, this research unmasks a previously unappreciated role of SDT in inducing immune resistance and shows that POR-BG@Alb integrates potent sonodynamic activity with self-oxygen regulation and self-immunoregulation to enable durable systemic antitumor immunity, providing a promising nanotherapeutic strategy for SDT clinical translation.

This case highlights a critical diagnostic pitfall: primary EAS can diffusely express cytokeratins. More importantly, our findings challenge the traditional view that MYC amplification is exclusive to secondary, radiation-associated angiosarcomas. We propose that MYC amplification can act as a driver in primary EAS and may serve as a biomarker for aggressive clinical behavior.

Although LXQ-87 exerted potent bioactivity at the cellular and molecular level, it only showed limited therapeutic effects in a HeLa xenograft tumor model, which reflects obvious obstacles for subsequent clinical transformation. Collectively, our results establish allosteric PTP1B inhibition as a multi-mechanistic anticancer approach with distinct signaling consequences.