Sarcoma

P=N/A, N=7, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Nov 2025 --> Nov 2026 | Trial primary completion date: Nov 2025 --> Nov 2026

P=N/A, N=90, Recruiting, University of Aarhus | Not yet recruiting --> Recruiting

c-Myb - CKB - N-cadherin axis was identified as pathway regulating OSA cell migration and metastasis.

P1/2, N=75, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Nov 2025 --> Nov 2026 | Trial primary completion date: Nov 2025 --> Nov 2026

These results suggest that LANA TR binding establishes an enhancer domain for infected KSHV episomes. The strength of this enhancer, regulated by TR length or transcription memories from prior activation, determines the degree of KSHV lytic replication.

Leveraging the observed sensitivity of muscle cells to atorvastatin in clinical settings and utilizing untargeted metabolomic analysis of atorvastatin-treated RD rhabdomyosarcoma cells, we identified reduced levels of aminoadipic acid, an intermediate in lysine catabolism...However, we demonstrated that it is catabolically cleaved to p-nitroanilide, with this molecule driving the cytotoxic activity observed in our experiments. Although lysine metabolism was not fully suppressed by lysine-p-nitroanilide, these findings provide valuable insights for developing novel therapies for rhabdomyosarcoma.

Besides, patients in the high-risk group exhibited lower IC50 values for vorinostat, elesclomol, OSI-906, pyrimethamine, thapsigargin, and doxorubicin, but a higher IC50 value for cisplatin, compared to those in the low-risk group, indicating differential drug sensitivities. In summary, we established a robust DRGs signature comprising BTN3A1, CEBPA, KCNAB2, TBX21, and MYC, which showed strong prognostic value and predictive potential for immune status and drug sensitivity in OS. Notably, functional experiments confirmed that BTN3A1 acted as a tumor suppressor in OS, highlighting it as a promising therapeutic target.

FET-rearranged MET are epigenetically unrelated to cutaneous and salivary gland MET, and their malignant counterparts are best classified as sarcomas rather than carcinomas.

Considering the rarity and heterogeneity of WT-GISTs, a regulatory detection procedure should be established for WT-GISTs, including NGS for qWT-GISTs, to identify the molecular mechanisms and potential therapeutic targets. Implications: WT-GISTs are heterogenous tumors which should be managed using different treatments and follow-up strategies.

Moreover, these effects were partially reversed by the ferroptosis inhibitor Ferrostatin-1. Collectively, these results indicate that α-Hederin exerts antitumor effects against osteosarcoma by inducing ferroptosis and impairing mitochondrial function, partly through inhibition of the PI3K/AKT signaling pathway, providing a potential therapeutic strategy for osteosarcoma.

Our spatial transcriptomic results from thousands of spots across multiple KS tumors indicated a correlation between high levels of STC1 and decreased expression of macrophage markers. Together, these analyses offer potential mechanisms by which KSHV infection may remodel skin tissue, inhibit immune responses against KSHV infection, and confer resistance to anticancer therapies.

The patient has been on imatinib since July 2023 with controlled disease. To the best of our knowledge, this is the first reported case of CSS with a DIS3L2 variant. Further reports and studies are needed to establish a definitive association between this gene and CSS.