ReviewJournal of translational medicine2026
Molecular mechanisms underlying liposarcoma subtype transition and proteasome-associated targeted interventions.
Review in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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6 authors.
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Abstract
backgroundLiposarcoma (LPS) is one of the most common soft tissue sarcomas and is characterized by marked heterogeneity and a strong tendency toward recurrence. Conventional histopathologic classification mainly includes well-differentiated and dedifferentiated liposarcoma, myxoid and round cell liposarcoma, and pleomorphic liposarcoma. In recent years, molecular hallmarks, such as amplification of MDM2 and CDK4 and fusion genes including FUS::DDIT3 and CPSF6-related fusions, have become essential for accurate diagnosis and subtype assignment. MAIN BODY: LPS development and subtype transition are driven by integrated molecular events, including 12q13-15 amplification with MDM2/CDK4 overexpression, PPARγ dysregulation, PI3K-AKT-mTOR activation, epigenetic alterations, and tumor microenvironment interactions. Together, these changes promote malignant transformation, dedifferentiation, and therapeutic heterogeneity across subtypes. Within this broader framework, the proteasome has emerged as a therapeutically relevant regulatory layer, particularly in selected contexts such as MDM2-amplified WDLS/DDLS, where protein turnover directly influences the stability of key driver proteins. Clinically, complete surgical resection remains the standard treatment when feasible, while doxorubicin plus ifosfamide is the mainstay for advanced or metastatic disease. Targeted therapies, such as palbociclib for MDM2-amplified WDLS/DDLS, as well as immunotherapy, have shown activity in some patients. Emerging investigational strategies also seek to target MDM2-p53, CDK4/6, epigenetic dysregulation, and proteostasis-related vulnerabilities.
conclusionThis 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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.