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<p>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 (<i>AFP</i>, <i>GPC3</i>, <i>GATA3</i>, 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).</p>

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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

  • 期刊论文

  • 发表日期：

    2025年8月18日

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  • Costantino Ricci,
  • Luisa Di Sciascio,
  • Francesca Ambrosi,
  • Marco Grillini,
  • Veronica Mollica,
  • Francesco Massari,
  • Michelangelo Fiorentino,
  • Antonio De Leo,
  • Muhammad T. Idrees,
  • Thomas M. Ulbright,
  • Andres Martin Acosta

摘要

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).