Sarcoma

P1, N=40, Active, not recruiting, Iovance Biotherapeutics, Inc. | Recruiting --> Active, not recruiting

P1/2, N=107, Recruiting, STORM Therapeutics LTD | N=188 --> 107 | Trial completion date: Jun 2027 --> Jun 2028 | Trial primary completion date: Dec 2026 --> Dec 2027

P2, N=20, Suspended, M.D. Anderson Cancer Center | Not yet recruiting --> Suspended

P2, N=20, Active, not recruiting, SpringWorks Therapeutics, Inc. | Recruiting --> Active, not recruiting | Trial completion date: Dec 2030 --> Oct 2029 | Trial primary completion date: May 2028 --> Mar 2027

P=N/A, N=42, Recruiting, University Hospital Heidelberg | Trial completion date: Jul 2026 --> Jul 2029 | Trial primary completion date: Jul 2026 --> Jul 2028

P1/2, N=40, Recruiting, Mayo Clinic | Trial completion date: Jul 2027 --> Jun 2028 | Trial primary completion date: Jul 2027 --> Jun 2028

MCS is a rare, high-grade sarcoma with limited treatment options. Targeted therapies against HEY1::NCOA2-associated pathways are promising and are currently under investigation.

Lymphangiosarcoma has not been previously reported in non-human primates, to our knowledge. Our case highlights the importance of integrating histopathology, immunohistochemistry, and ultrastructural analysis to accurately diagnose rare vascular tumors, such as lymphangiosarcoma.

Surgical margins were negative, and one-year follow-up showed that the patient remained disease-free. This case highlights the importance of immunohistochemistry and molecular testing for accurate diagnosis and appropriate management.

Resistance to drugs in sarcoma is multifactorial and changeable. Nevertheless, fusing mechanistic knowledge with biomarker - guided combination/sequential therapies offers a clear way to improve patient situations.

GA markedly inhibits proliferation, migration, and induces apoptosis in OS cells primarily by regulating the glycolytic pathway, i.e., reduction in lactate levels, subsequent targeting of KAT2A, downregulation of H3K18 lactylation, and ultimate transcriptional regulation of apoptosis. It is hereby recognized that GA mediates metabolic inhibition by selective epigenetic reprogramming of the KAT2A-H3K18 lactylation axis. The current findings establish histone lactylation as a key mechanism in OS inhibition and highlight metabolicepigenetic cross-talk as a promising therapeutic regimen for aggressive bone malignancies.

We present the primary M-GNET in the pancreas, confirmed by molecular fluorescence in situ hybridization (FISH) detection of EWSR1-ATF1 gene fusion. This article will summarize the clinicopathological features and differential diagnosis and review the relevant literature.