ArticleJournal of bone oncology2026
Ultrastructural pathological features and clinical significance of recurrent chordoma.
Article in Journal of bone oncology, 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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5 authors.
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Abstract
Chordoma is a low-grade malignant osseous neoplasm characterized by an exceedingly high postoperative recurrence rate. Conventional histopathological assessment cannot identify early subcellular alterations that drive tumor recurrence, and the ultrastructural mechanisms mediating chordoma recurrence and malignant progression remain poorly delineated. This study was designed to characterise the distinct subcellular pathological features of recurrent chordoma and evaluate their clinical value in prognostic assessment and risk stratification. 50 surgically resected recurrent chordoma specimens were included as the recurrent cohort, with 50 contemporaneously collected primary chordoma specimens serving as the primary control cohort. Among these, 16 pairs consisted of matched TEM specimens from the same patient's primary and recurrent chordomas, while the remaining 34 pairs comprised non-matched primary and recurrent chordomas from different patients.; Transmission electron microscopy (TEM) was employed to systematically compare ultrastructural differences across cytoplasmic vacuolar patterns, organellar architecture, intercellular junctional complexes, nuclear morphology, and stromal microvascular ultrastructure, and the prevalence of each ultrastructural abnormality was analysed statistically. Compared with primary chordoma, recurrent lesions displayed extensive and progressive subcellular pathological remodelling, including atypical cytoplasmic vacuolation with giant cystic fusion, diffuse mitochondrial injury and rough endoplasmic reticulum degranulation, widespread disintegration of mitochondria-associated endoplasmic reticulum membrane (MAM) complexes, marked nuclear atypia, loss of intercellular desmosomal junctions, activation of invasive invadopodia, and stromal microvascular dysplasia. The prevalence of all these ultrastructural aberrations was significantly higher in the recurrent cohort than in the primary control cohort (all
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