Sarcoma

P=N/A, N=300, Recruiting, Washington University School of Medicine | Not yet recruiting --> Recruiting

Identification of PLAG1 rearrangement is crucial for confirming the diagnosis. With the growing number of molecularly defined soft-tissue tumours of diagnostic and prognostic significance, incorporating molecular analysis is essential in the evaluation of soft-tissue lesions.

Herein, we report the first documented case of phenotypic conversion to SCLC in a patient with advanced pulmonary sarcomatoid carcinoma (PSC) who received pemetrexed, carboplatin, and camrelizumab only, with no targeted agents administered. TP53 and RET mutations may be implicated in this phenotypic transition. This case provides new insights into the biological mechanism underlying the evolution of PSC to SCLC.

These findings reveal that geniposide inhibits osteosarcoma through dual mechanisms: Ndufs8-mediated oxidative phosphorylation activation and PD-L1/PD-L1 axis suppression, offering a novel therapeutic strategy. These findings suggest that geniposide is a promising therapeutic agent for osteosarcoma and may enhance the efficacy of immunotherapy combined with PD-L1 blockade.

We systematically deconstructed the molecular subtypes of primary GISTs by integrated genomic and transcriptomic analysis. A specific GIST subtype characterized by poor treatment responses and prognosis, marked by the activation of aerobic metabolism and HRD features, may be a potential candidate for PARP inhibitors.

Cells with fibroblast characteristics derived from PDXs were permissive for de novo KSHV infection, and one lineage produced CXCL12, which was also elevated in the sera of patients with KSHV-associated diseases compared with those of patients who had KS alone. Together, the reproducible expansion of KSHV-infected endothelial cells in PDXs from multiple donors and the similar recapitulation of molecular and pathologic features of KS support KS PDXs as a preclinical model for the discovery of pathogenic mechanisms and candidate therapeutics.

These findings will not only aid in understanding the mechanisms by which EV71 infection impacts the host immune system but also provide a scientific basis for identifying early diagnostic biomarkers and developing new therapeutic strategies.

Mechanistically, the viral non-structural protein NSP2 disrupts super-enhancer activity by recruiting the CUL2-RBX1-ELOC complex, which triggers K63-linked ubiquitination and degradation of RPB1. Together, these findings uncover a previously unrecognized mechanism underlying M1 activity in osteosarcoma, support further preclinical evaluation of M1 in this setting, and identify RPB1 as a candidate biomarker for virotherapy response.

Spatial transcriptomics identified immunosuppressive niches in a treatment-resistant lesion and immune checkpoint blockade synergized with GCAR1 in a xenograft model. Altogether, our data provide a proof of concept for treating GPNMB-expressing solid tumors with GCAR1 and more broadly targeting surface antigens driven by oncogenic gene fusions with CAR T cell therapies.

P1, N=24, Active, not recruiting, Michael Wagner, MD | Trial primary completion date: Jun 2026 --> Jan 2027

P1, N=27, Not yet recruiting, Baylor College of Medicine | Initiation date: May 2026 --> Aug 2026