TY - JOUR
T1 - Histological background of dedifferentiated solitary fibrous tumour
AU - Yamada, Yuichi
AU - Kohashi, Kenichi
AU - Kinoshita, Izumi
AU - Yamamoto, Hidetaka
AU - Iwasaki, Takeshi
AU - Yoshimoto, Masato
AU - Ishihara, Shin
AU - Toda, Yu
AU - Ito, Yoshihiro
AU - Kuma, Yuki
AU - Yamada-Nozaki, Yui
AU - Koga, Yutaka
AU - Hashisako, Mikiko
AU - Kiyozawa, Daisuke
AU - Kitahara, Daichi
AU - Narutomi, Fumiya
AU - Kuboyama, Yusuke
AU - Nakamura, Takahito
AU - Inoue, Takeshi
AU - Mukai, Munenori
AU - Honda, Yumi
AU - Toyokawa, Gouji
AU - Tsuchihashi, Kenji
AU - Fushimi, Fumiyoshi
AU - Taguchi, Kenichi
AU - Nishiyama, Kenichi
AU - Tamiya, Sadafumi
AU - Oshiro, Yumi
AU - Furue, Masutaka
AU - Nakashima, Yasuharu
AU - Suzuki, Satoshi
AU - Iwaki, Toru
AU - Oda, Yoshinao
N1 - Publisher Copyright:
©
PY - 2022/6/1
Y1 - 2022/6/1
N2 - 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.
AB - 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.
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U2 - 10.1136/jclinpath-2020-207311
DO - 10.1136/jclinpath-2020-207311
M3 - Article
C2 - 33975913
AN - SCOPUS:85106001253
SN - 0021-9746
VL - 75
SP - 397
EP - 403
JO - Journal of Clinical Pathology
JF - Journal of Clinical Pathology
IS - 6
ER -