Aims Dedifferentiation is a histological phenomenon characterised by abrupt transition of histology to a sarcomatous component with high-grade malignant potential in solitary fibrous tumour (SFT). The authors histologically reviewed SFT cases to reveal the histological background of dedifferentiated SFTs.
Methods Clinicopathological and histopathological findings of 145 SFT cases were reviewed. Immunohistochemical staining and genetic analysis were also performed.
Results The non-dedifferentiated components showed a cellular component in 45 of 145 (31%), high mitotic rate (≥4/10 high-powered field) in 12 of 145 (8.2%) tumours, necrosis in 7 of 145 (4.8%) tumours, multinodular growth pattern in 39 of 132 (29.5%) available tumours and intratumoural fibrous septa in 37 of 131 (28.2%). Immunohistochemically, the non-dedifferentiated components were positive for CD34 in 128 of 141 (90.7%), bcl-2 in 101 of 133 (75.9%), nuclear pattern of β-catenin in 64 of 127 (50.3%) and p16 in 22 of 140 (15.7%). Loss of Rb protein expression was detected in 17 of 110 (15.4%) cases. Statistically, cellular component, multinodular structure, p16 overexpression and Rb protein loss were significantly associated with dedifferentiation. Moreover, cellular component and multinodular structure were significantly associated with p16 overexpression and Rb protein loss. All the non-deddifferentiated components showed wild type of p53 expression. The dedifferentiated components of all 10 dedifferentiated tumours presented positivity for p16 in 9 of 10 (90%) and mutational type of p53 in 5 of 10 (50%). Loss of Rb protein expression was detected in 6 of 10 (60%).
Conclusions The authors propose that cellular or multinodular transformation may be associated with dedifferentiation. They also suggest that cellular and multinodular transformation may be associated with p16 overexpression and Rb downregulation.
- soft tissue neoplasms
Data availability statement
No data are available. Clinical and genetic data of patients are included in the investigation. Lab email address: firstname.lastname@example.org.
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Handling editor Dhirendra Govender.
Contributors YY performed the research and wrote the paper. KK, IK, HY, TIwas, MY, SI, YI, YKum, YKog, MH, YN, DKiy, DKit, FN, YKub and TN contributed to research design and slide review. TIn, MM, YH, GT, KTsu, FF, KTag, KN, ST, YOsh, MF, YN, SS and TIwak contributed to sample collection and research design. YOda designed the research and gave final approval of the manuscript. All authors critically reviewed and approved the manuscript.
Funding This study was supported by a JSPS KAKEN Grant (no. 19H03444, 17K15645).
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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