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Original research
Histological background of dedifferentiated solitary fibrous tumour
  1. Yuichi Yamada1,
  2. Kenichi Kohashi1,
  3. Izumi Kinoshita1,
  4. Hidetaka Yamamoto1,
  5. Takeshi Iwasaki1,
  6. Masato Yoshimoto1,
  7. Shin Ishihara1,
  8. Yu Toda1,
  9. Yoshihiro Ito1,
  10. Yuki Kuma1,
  11. Yui Yamada-Nozaki1,
  12. Yutaka Koga1,
  13. Mikiko Hashisako1,
  14. Daisuke Kiyozawa1,
  15. Daichi Kitahara1,
  16. Fumiya Narutomi1,
  17. Yusuke Kuboyama1,
  18. Takahito Nakamura1,
  19. Takeshi Inoue2,
  20. Munenori Mukai3,
  21. Yumi Honda4,
  22. Gouji Toyokawa1,
  23. Kenji Tsuchihashi5,
  24. Fumiyoshi Fushimi6,
  25. Kenichi Taguchi7,
  26. Kenichi Nishiyama8,
  27. Sadafumi Tamiya9,
  28. Yumi Oshiro10,
  29. Masutaka Furue11,
  30. Yasuharu Nakashima12,
  31. Satoshi Suzuki13,
  32. Toru Iwaki13,
  33. Yoshinao Oda1
  1. 1 Department of Anatomic Pathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
  2. 2 Department of Pathology, Osaka City General Hospital, Osaka, Japan
  3. 3 Department of Pathology, Koseiren Takaoka Hospital, Takaoka, Toyama, Japan
  4. 4 Department of Surgical Pathology, Kumamoto University Hospital, Kumamoto, Japan
  5. 5 Department of Medicine and Biosystemic Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
  6. 6 Department of Pathology, Kyushu Central Hospital of the Mutual Aid Association of Public School Teachers, Fukuoka, Japan
  7. 7 Department of Pathology, National Kyushu Cancer Center, Fukuoka, Japan
  8. 8 Department of Pathology, Fukuoka Red Cross Hospital, Fukuoka, Japan
  9. 9 Department of Pathology, Kitakyushu Municipal Medical Center, Kitakyushu, Fukuoka, Japan
  10. 10 Department of Pathology, Matsuyama Red Cross Hospital, Matsuyama, Ehime, Japan
  11. 11 Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
  12. 12 Department of Orthopaedic Surgery, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
  13. 13 Department of Neuropathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
  1. Correspondence to Professor Yoshinao Oda, Anatomic Pathology, Kyushu University, Fukuoka 812-8582, Japan; oda{at}surgpath.med.kyushu-u.ac.jp

Abstract

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.

  • pathology
  • surgical
  • sarcoma
  • soft tissue neoplasms

Data availability statement

No data are available. Clinical and genetic data of patients are included in the investigation. Lab email address: pathol@surgpath.med.kyushu-u.ac.jp.

https://doi.org/10.1136/jclinpath-2020-207311

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    Data availability statement

    No data are available. Clinical and genetic data of patients are included in the investigation. Lab email address: pathol@surgpath.med.kyushu-u.ac.jp.

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    Footnotes

    • 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.

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.