Andrea Strakova-Peterikova, Franco Fedeli, Boris Rychly, Jiri Soukup, Michael Michal, Petr Martinek, Marian Grendar, Elaheh Mosaieby, Nikola Ptakova, Maryna Slisarenko, Michal Michal, Kvetoslava Michalova
{"title":"肝脏钙化嵌套间质上皮肿瘤:两例WT1突变和明显表观遗传特征的报告。","authors":"Andrea Strakova-Peterikova, Franco Fedeli, Boris Rychly, Jiri Soukup, Michael Michal, Petr Martinek, Marian Grendar, Elaheh Mosaieby, Nikola Ptakova, Maryna Slisarenko, Michal Michal, Kvetoslava Michalova","doi":"10.1007/s00428-025-04281-5","DOIUrl":null,"url":null,"abstract":"<p><p>Calcifying nested stromal-epithelial tumor (CNSET) is an extremely rare primary liver tumor of uncertain histogenesis that predominantly occurs in the pediatric age group and young adults. Knowledge regarding the molecular genetic profile of this entity remains limited, with only two molecular studies conducted to date, which identified pathogenic mutations in the CTNNB1 gene and TERT promoter mutations in all analyzable cases. A more aggressive biological potential than previously reported has been only recently unveiled as well. To further advance the understanding of pathogenic mechanisms of CNSET and to investigate the distinctiveness of this rare entity, we analyzed two cases using immunohistochemistry, next-generation sequencing (NGS), and methylation profiling. The latter was employed to compare the epigenetic landscape of CNSET with that of clinicopathologically similar entities, such as hepatoblastoma and solid pseudopapillary neoplasm (SPN) of the pancreas. Both CNSET cases occurred in women (aged 24 and 23 years) and measured 24 cm and 16 cm in diameter, respectively. Both cases showed similar histological features, being composed of organoid nests of bland spindled to epithelioid cells embedded in myofibroblastic stroma. Both cases were immunohistochemically positive for CD56, WT1, and CAM5.2 and negative for hepatocellular and neuroendocrine markers. Case 2 showed aberrant nuclear expression of β-catenin, while in case 1, there was cytoplasmic positivity only. Using Illumina TruSight Oncology 500 NGS panel, case 1 revealed a pathogenic mutation in the WT1 gene and a TERT promoter mutation, and case 2 had a CTNNB1 mutation. DNA methylation analysis showed that CNSET forms a distinct cluster, separate from other reference entities. Follow-up in case 2 revealed a disease-free status 21 months after partial hepatectomy. This study showed that the molecular landscape of CNSET of the liver is characterized by CTNNB1, TERT promoter, and WT1 gene mutations, with the latter representing a novel alteration. Similarly to CTNNB1, the WT1 gene plays a significant role in the Wnt signaling pathway. Given the metastatic potential and chemotherapy resistance of CNSET, understanding its molecular background is important for potential alternative targeted treatment. Methylation profiling confirms CNSET as a distinct entity, separate from hepatoblastoma and SPN of the pancreas.</p>","PeriodicalId":23514,"journal":{"name":"Virchows Archiv","volume":" ","pages":""},"PeriodicalIF":3.1000,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Calcifying nested stromal-epithelial tumor of the liver: Report of two cases revealing novel WT1 mutation and distinct epigenetic features.\",\"authors\":\"Andrea Strakova-Peterikova, Franco Fedeli, Boris Rychly, Jiri Soukup, Michael Michal, Petr Martinek, Marian Grendar, Elaheh Mosaieby, Nikola Ptakova, Maryna Slisarenko, Michal Michal, Kvetoslava Michalova\",\"doi\":\"10.1007/s00428-025-04281-5\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Calcifying nested stromal-epithelial tumor (CNSET) is an extremely rare primary liver tumor of uncertain histogenesis that predominantly occurs in the pediatric age group and young adults. Knowledge regarding the molecular genetic profile of this entity remains limited, with only two molecular studies conducted to date, which identified pathogenic mutations in the CTNNB1 gene and TERT promoter mutations in all analyzable cases. A more aggressive biological potential than previously reported has been only recently unveiled as well. To further advance the understanding of pathogenic mechanisms of CNSET and to investigate the distinctiveness of this rare entity, we analyzed two cases using immunohistochemistry, next-generation sequencing (NGS), and methylation profiling. The latter was employed to compare the epigenetic landscape of CNSET with that of clinicopathologically similar entities, such as hepatoblastoma and solid pseudopapillary neoplasm (SPN) of the pancreas. Both CNSET cases occurred in women (aged 24 and 23 years) and measured 24 cm and 16 cm in diameter, respectively. Both cases showed similar histological features, being composed of organoid nests of bland spindled to epithelioid cells embedded in myofibroblastic stroma. Both cases were immunohistochemically positive for CD56, WT1, and CAM5.2 and negative for hepatocellular and neuroendocrine markers. Case 2 showed aberrant nuclear expression of β-catenin, while in case 1, there was cytoplasmic positivity only. Using Illumina TruSight Oncology 500 NGS panel, case 1 revealed a pathogenic mutation in the WT1 gene and a TERT promoter mutation, and case 2 had a CTNNB1 mutation. DNA methylation analysis showed that CNSET forms a distinct cluster, separate from other reference entities. Follow-up in case 2 revealed a disease-free status 21 months after partial hepatectomy. This study showed that the molecular landscape of CNSET of the liver is characterized by CTNNB1, TERT promoter, and WT1 gene mutations, with the latter representing a novel alteration. Similarly to CTNNB1, the WT1 gene plays a significant role in the Wnt signaling pathway. Given the metastatic potential and chemotherapy resistance of CNSET, understanding its molecular background is important for potential alternative targeted treatment. Methylation profiling confirms CNSET as a distinct entity, separate from hepatoblastoma and SPN of the pancreas.</p>\",\"PeriodicalId\":23514,\"journal\":{\"name\":\"Virchows Archiv\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":3.1000,\"publicationDate\":\"2025-10-08\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Virchows Archiv\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s00428-025-04281-5\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"PATHOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Virchows Archiv","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s00428-025-04281-5","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"PATHOLOGY","Score":null,"Total":0}
Calcifying nested stromal-epithelial tumor of the liver: Report of two cases revealing novel WT1 mutation and distinct epigenetic features.
Calcifying nested stromal-epithelial tumor (CNSET) is an extremely rare primary liver tumor of uncertain histogenesis that predominantly occurs in the pediatric age group and young adults. Knowledge regarding the molecular genetic profile of this entity remains limited, with only two molecular studies conducted to date, which identified pathogenic mutations in the CTNNB1 gene and TERT promoter mutations in all analyzable cases. A more aggressive biological potential than previously reported has been only recently unveiled as well. To further advance the understanding of pathogenic mechanisms of CNSET and to investigate the distinctiveness of this rare entity, we analyzed two cases using immunohistochemistry, next-generation sequencing (NGS), and methylation profiling. The latter was employed to compare the epigenetic landscape of CNSET with that of clinicopathologically similar entities, such as hepatoblastoma and solid pseudopapillary neoplasm (SPN) of the pancreas. Both CNSET cases occurred in women (aged 24 and 23 years) and measured 24 cm and 16 cm in diameter, respectively. Both cases showed similar histological features, being composed of organoid nests of bland spindled to epithelioid cells embedded in myofibroblastic stroma. Both cases were immunohistochemically positive for CD56, WT1, and CAM5.2 and negative for hepatocellular and neuroendocrine markers. Case 2 showed aberrant nuclear expression of β-catenin, while in case 1, there was cytoplasmic positivity only. Using Illumina TruSight Oncology 500 NGS panel, case 1 revealed a pathogenic mutation in the WT1 gene and a TERT promoter mutation, and case 2 had a CTNNB1 mutation. DNA methylation analysis showed that CNSET forms a distinct cluster, separate from other reference entities. Follow-up in case 2 revealed a disease-free status 21 months after partial hepatectomy. This study showed that the molecular landscape of CNSET of the liver is characterized by CTNNB1, TERT promoter, and WT1 gene mutations, with the latter representing a novel alteration. Similarly to CTNNB1, the WT1 gene plays a significant role in the Wnt signaling pathway. Given the metastatic potential and chemotherapy resistance of CNSET, understanding its molecular background is important for potential alternative targeted treatment. Methylation profiling confirms CNSET as a distinct entity, separate from hepatoblastoma and SPN of the pancreas.
期刊介绍:
Manuscripts of original studies reinforcing the evidence base of modern diagnostic pathology, using immunocytochemical, molecular and ultrastructural techniques, will be welcomed. In addition, papers on critical evaluation of diagnostic criteria but also broadsheets and guidelines with a solid evidence base will be considered. Consideration will also be given to reports of work in other fields relevant to the understanding of human pathology as well as manuscripts on the application of new methods and techniques in pathology. Submission of purely experimental articles is discouraged but manuscripts on experimental work applicable to diagnostic pathology are welcomed. Biomarker studies are welcomed but need to abide by strict rules (e.g. REMARK) of adequate sample size and relevant marker choice. Single marker studies on limited patient series without validated application will as a rule not be considered. Case reports will only be considered when they provide substantial new information with an impact on understanding disease or diagnostic practice.