Trabectedin MLS — SCE Medical Oncology MCQ
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Correct answer: C — Trabectedin, exploiting the fusion-driven transcriptional vulnerability
Myxoid liposarcoma has unusually high sensitivity to trabectedin: a pretreated advanced-disease series reported a 51% objective response rate, and mechanistic work shows that trabectedin detaches FUS-DDIT3 from target DNA and permits adipocytic differentiation. NICE TA185 provides the UK post-anthracycline soft-tissue-sarcoma position. Eribulin, exploiting adipocytic-lineage sensitivity after anthracycline treatment: eribulin is active in liposarcoma but does not have the same fusion-linked evidence. Gemcitabine-docetaxel, exploiting high-grade pleomorphic-sarcoma sensitivity: this combination is more characteristic of other sarcoma contexts. Pazopanib, exploiting angiogenic dependence after anthracycline treatment: the pivotal pazopanib setting excluded adipocytic sarcoma. Ifosfamide, exploiting fusion-driven transcriptional vulnerability: ifosfamide can be active chemotherapy but does not detach FUS-DDIT3 from its transcriptional targets.
Reference: Trabectedin activity in advanced pretreated myxoid liposarcoma (Published July 2007): https://pubmed.ncbi.nlm.nih.gov/17586092/; FUS-DDIT3 detachment as a mechanism of trabectedin efficacy in myxoid liposarcoma (Published November 2024): https://pmc.ncbi.nlm.nih.gov/articles/PMC11590625/; NICE TA185 trabectedin for advanced soft-tissue sarcoma (Updated February 2021; current NICE TA): https://www.nice.org.uk/guidance/ta185/chapter/1-Recommendations