ArticleVirchows Archiv : an international journal of pathology2026
The absence of FOXA2 and HNF1β expression in vasculogenic mesenchymal lesions of germ cell origin suggests an evolutionary pathway similar to that of sarcomatoid yolk sac tumor.
Article in Virchows Archiv : an international journal of pathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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Abstract
Vasculogenic mesenchymal lesions (VMLs) are uncommon phenotypes of germ cell tumor (GCT) origin that are mostly found after chemotherapy of mediastinal yolk sac tumor (YST). These lesions typically lack expression of classical YST markers [α-fetoprotein (AFP) and glypican-3 (GPC3)]. FOXA2 and HNF1β are key inducers of the YST phenotype and co-operate to promote transcription of genes involved in YST development (AFP, GPC3, GATA3, among others). Immunohistochemical studies have shown that FOXA2 and HNF1β are more sensitive than AFP, GPC3, and GATA3 for conventional phenotypes of YST, whereas they are typically negative in sarcomatoid YST. In this study, assessment of VMLs showed that they do not express FOXA2 and HNF1β to a significant degree. These results suggest that the combined downregulation of FOXA2 and HNF1β may underlie the transformation of YST to "mesenchymal" phenotypes, with additional (still undefined) processes determining the final phenotype (sarcomatoid YST or VMLs).
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