Genes, chromosomes & cancer · 2026
Nodular Necrotizing Fibroblastic Sarcoma and Myxoinflammatory Fibroblastic Sarcoma: A Comparative Clinicopathological, Molecular, and Epigenetic Study.
СтатьяСравнительное исследованиеНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Zhu Peipei, Han Dongyan, Sun Yuefang, Bai Qianming, Zhou Xiaoyan, Wang Jian
Аннотация
BACKGROUND: There is morphological overlap between nodular necrotizing fibroblastic sarcoma (NNFS) and myxoinflammatory fibroblastic sarcoma (MIFS). Whether they represent neoplasms within the same tumor spectrum remains unclear. We performed a comparative clinicopathological, molecular, and epigenetic study of these two tumors.
METHODS: We analyzed the clinicopathological features, immunophenotypes, and molecular profiles of three cases each of NNFS and MIFS. DNA methylation profiling was also performed.
RESULTS: All three NNFS cases were located in the trunk, presenting as well-circumscribed subcutaneous nodules with central necrosis, whereas the three MIFS cases all arose in acral sites with an infiltrative or ill-defined growth pattern. Morphologically, both NNFS and MIFS were characterized by large polygonal to epithelioid cells with virocyte-like, ganglion cell-like, or Reed-Sternberg-like appearance. Unlike MIFS, NNFS did not exhibit prominent myxoid stroma or vacuolated pseudolipoblasts. On immunohistochemistry, NNFS cases uniformly showed focal positivity for pancytokeratin (AE1/AE3), whereas MIFS cases exhibited variable CD34 expression. Molecular analysis identified YAP1::MAML2 fusions in all three NNFS cases, while a BRAF rearrangement was detected in one of the three MIFS cases. DNA methylation profiling demonstrated that NNFS and MIFS cases clustered together forming a distinct group.
CONCLUSIONS: Although NNFS and MIFS each harbor unique genetic alterations, our DNA methylation profiling demonstrates a potential relationship between these two morphologically similar entities.
METHODS: We analyzed the clinicopathological features, immunophenotypes, and molecular profiles of three cases each of NNFS and MIFS. DNA methylation profiling was also performed.
RESULTS: All three NNFS cases were located in the trunk, presenting as well-circumscribed subcutaneous nodules with central necrosis, whereas the three MIFS cases all arose in acral sites with an infiltrative or ill-defined growth pattern. Morphologically, both NNFS and MIFS were characterized by large polygonal to epithelioid cells with virocyte-like, ganglion cell-like, or Reed-Sternberg-like appearance. Unlike MIFS, NNFS did not exhibit prominent myxoid stroma or vacuolated pseudolipoblasts. On immunohistochemistry, NNFS cases uniformly showed focal positivity for pancytokeratin (AE1/AE3), whereas MIFS cases exhibited variable CD34 expression. Molecular analysis identified YAP1::MAML2 fusions in all three NNFS cases, while a BRAF rearrangement was detected in one of the three MIFS cases. DNA methylation profiling demonstrated that NNFS and MIFS cases clustered together forming a distinct group.
CONCLUSIONS: Although NNFS and MIFS each harbor unique genetic alterations, our DNA methylation profiling demonstrates a potential relationship between these two morphologically similar entities.