Liposarcoma

P2, N=33, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Jul 2026 --> Jul 2027 | Trial primary completion date: Jul 2026 --> Jul 2027

In conclusion, our multi-omics analysis identifies HMGA2 fusion as a promising diagnostic and prognostic biomarker for DDLPS with rhabdomyosarcomatous differentiation. The comprehensive molecular and immune landscape of this tumor subtype not only deepens our understanding of its pathophysiology but also provides critical insights for future precision medicine strategies.

B7-H3 is a promising treatment target in sarcomas as it is highly expressed particular in high grade bone and soft tissue sarcomas, such as pleomorphic liposarcomas and osteosarcomas.

Dedifferentiated liposarcoma is a rare mesenchymal malignancy driven by amplification of chromosome 12q13-15, which includes the oncogenes CDK4 and MDM2. These fractionally resistant cells were defined by selective enrichment of cyclin-dependent kinase 2 (CDK2), cyclin B1, and phosphorylated ribosomal protein S6 (pS6), and showed enhanced sensitivity to the CDK2 inhibitor, tagtociclib. Together, these findings reveal nongenetic cell cycle plasticity as a mechanism of escape from CDK4/6 inhibition in dedifferentiated liposarcoma and nominate CDK2 and the PI3K-mTOR pathway as candidate targets for combination therapy.

At 4 years, no recurrence was seen, with no facial nerve palsy or masticatory dysfunction. Combined coronal-intraoral exposure with zygomatic arch osteotomy may facilitate marginal en bloc resection of temporal-infratemporal ALT.

Survivors of hereditary retinoblastoma, caused by germline mutations in the RB1 gene, have a substantially increased risk of developing benign and malignant lipomatous tumors including atypical spindle cell/pleomorphic lipomatous tumor and dysplastic lipoma. This report describes the MRI findings of several such lesions in a survivor of bilateral retinoblastoma including features such as enhancement that might otherwise be concerning for higher-grade malignancy.

P1, N=18, Recruiting, Washington University School of Medicine | Trial primary completion date: Nov 2028 --> May 2031 | Trial completion date: Oct 2033 --> Apr 2036

P1, N=30, Recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: May 2026 --> May 2027 | Trial primary completion date: May 2026 --> May 2027

This review summarizes the classification, subtype-specific characteristics, molecular mechanisms, treatment strategies, and prognosis of LPS, and further discusses how proteasome-associated mechanisms may create therapeutic vulnerabilities in selected subtypes. A better understanding of the molecular basis underlying tumor initiation, progression, and subtype transition may support the development of more precise and mechanism-based therapeutic strategies for LPS.

P2, N=48, Active, not recruiting, Fox Chase Cancer Center | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Nov 2020 --> Dec 2026

This case highlights that DDLPS can trigger CRS, which manifests with clinical features mimicking severe infection and leading to critical cytopenias that complicate surgical management. IL-6 pathway blockade with agents such as tocilizumab may be an effective bridging therapy to stabilize the systemic inflammatory state and create a safe window for surgical intervention.

DDIT3 expression reflects chromosomal co-amplification within the 12q13-15 amplicon and lacks prognostic significance. Combined MDM2 and DDIT3 IHC with careful morphological assessment aids differential diagnosis, particularly when molecular testing is unavailable.