Angiofibroma of Soft Tissue on MRI and FDG PET/CT Image

Liu, Xiao; Liu, Yang; Wang, Yueqi; Li, Lin

doi:10.1097/rlu.0000000000004007

Cited by 1 publication

(1 citation statement)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To date, fewer than 100 cases of AFST have been reported in the English literature, 1,3,4,[6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] and the clinicopathological, immunohistochemical, and genetic features of AFST still remain not fully understood. In studies including more than 10 cases of AFST, this is the first report that identified driver fusion genes in all cases.…”

Section: Introductionmentioning

confidence: 99%

Clinicopathologic and genetic characterization of angiofibroma of soft tissue: a study of 12 cases including two cases with AHRR::NCOA3 gene fusion

et al. 2023

View full text Add to dashboard Cite

Aims: Angiofibroma of soft tissue (AFST) is a benign tumour characterised by prominent arborizing blood vessels throughout the lesion. Approximately twothirds of AFST cases were reported to have AHRR:: NCOA2 fusion, and only two cases have been reported to have other gene fusions: GTF2I::NCOA2 or GAB1::ABL1. Although AFST is included in fibroblastic and myofibroblastic tumours in the World Health Organization's 2020 classification, histiocytic markers, especially CD163, have been reported to be positive in almost all examined cases, and it still remains the possibility of a fibrohistiocytic nature of the tumour. Therefore, we aimed to clarify the genetic and pathological spectrum of AFST and identify whether histiocytic marker-positive cells were true neoplastic cells. Methods and results: We evaluated 12 AFST cases, which included 10 cases with AHRR::NCOA2 and two with AHRR::NCOA3 fusions. Pathologically, nuclear palisading, which has not been reported in AFST, was detected in two cases. Furthermore, one tumour resected by additional wide resection revealed severe infiltrative growth. Immunohistochemical analysis indicated varying levels of desmin-positive cells in nine cases, whereas CD163-and CD68positive cells were diffusely distributed in all 12 cases. We also performed double immunofluorescence staining and immunofluorescence in situ hybridisation in four resected cases with >10% desmin-positive tumour cells. The results suggested that the CD163positive cells differed from desmin-positive cells with AHRR::NCOA2 fusion in all four cases. Conclusion: Our findings suggested that AHRR:: NCOA3 could be the second most frequent fusion gene, and histiocytic marker-positive cells are not genuine neoplastic cells in AFST.

show abstract