Jui Lan

TL;DR: Findings highlight ASS1 as a novel tumor suppressor in myxofibrosarcomas, with loss of expression linked to promoter methylation, clinical aggressiveness, and sensitivity to ADI-PEG20.

TL;DR: Conclusively, STAT6 nuclear expression was distinctive in the vast majority of SFTs, including all fusion-positive tumors, and exploitable as a robust diagnostics of CD34-negative cases, despite the associations of NAB2–STAT6 fusion variants with several clincopathological factors.

TL;DR: TOP2A expression is upregulated in a subset of NPCs and its increased immunoexpression significantly correlated with advanced stages and tumor aggressiveness, justifying the potentiality of TOP2A as a prognostic biomarker and a novel therapeutic target of NPC.

TL;DR: The majority of intrathoracic SFTs exhibited STAT6 nuclear staining, and NAB2ex4‐STAT6ex2/3 was the predominant fusion type, but clinical aggressiveness is associated with atypical/malignant histology primarily contributed by increased mitosis but was unrelated to fusion variants.

TL;DR: In summary, ASS1 protein deficiency was seen in approximately a half of NPCs and associated with advanced T classification, DNA methylation, and clinical aggressiveness, consistent with its tumor suppressor role.