Immunoexpression of ultraviolet photoproducts and p53 mutation analysis in atypical fibroxanthoma and superficial malignant fibrous histiocytoma

Akio Sakamoto, Yoshinao Oda, Eijun Itakura, Yumi Oshiro, Osamu Nikaido, Yukihide Iwamoto, Masazumi Tsuneyoshi

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Abstract

p53 mutation is one of the major results of ultraviolet (UV) radiation. UV photoproducts of cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyrimidone (6-4) photoproducts (64PPs) also play an important role in skin cancer development. Atypical fibroxanthoma (AFX), which mimics malignant fibrous histiocytoma (MFH) histologically, occurs in the sun-exposed skin of the elderly, and therefore, an association with UV has long been suspected. Eighteen fibrohistiocytic skin lesions comprising AFX (n = 7), storiform-pleomorphic type MFH centered in the subcutis (superficial MFH; S-MFH; n = 4) and benign fibrous histiocytoma (BFH; n = 7) were used for immunohistochemical and molecular analysis. Eight cases of deep MFH (D-MFH) were also analyzed for UV photoproduct expression for the purposes of comparison. Immunohistochemically, the CPD scores of AFX (3.6 ± 0.4) were significantly higher than those of S-MFH (1.3 ± 0.8), D-MFH (0.8 ± 0.5), or BHF (1.4 ± 0.7); however, the 64PP scores were extremely low in all these tumors (AFX, 0.1 ± 0.1; S-MFH, 0.0 ± 0.0; D-MFH, 0.0 ± 0.0; and BHF, 0.0 ± 0.0). AFX, S-MFH, and BFH showed immunoexpression for p53 (2/7, 2/4, and 0/7), respectively. p53 mutations were detected in AFX (4/6; 67%) and S-MFH (1/4; 25%), but not in BFH (0/5; 0%) using polymerase chain reaction-single-strand conformation polymorphism, and all of the mutations in AFX were either C-T transitions or at dipyrimidine sites. In conclusion, AFX and S-MFH are both similar fibrohistocytic lesions; however, AFX has high immunoreactivity for CPDs compared with S-MFH, D-MFH, or BFH. These data suggest that CPDs may play an important role in the pathogenesis of AFX.

Original languageEnglish
Pages (from-to)581-588
Number of pages8
JournalModern Pathology
Volume14
Issue number6
DOIs
Publication statusPublished - Jul 3 2001
Externally publishedYes

Fingerprint

Malignant Fibrous Histiocytoma
Mutation
Pyrimidine Dimers
Pyrimidinones
Benign Fibrous Histiocytoma
Skin
Skin Neoplasms
Solar System

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine

Cite this

Immunoexpression of ultraviolet photoproducts and p53 mutation analysis in atypical fibroxanthoma and superficial malignant fibrous histiocytoma. / Sakamoto, Akio; Oda, Yoshinao; Itakura, Eijun; Oshiro, Yumi; Nikaido, Osamu; Iwamoto, Yukihide; Tsuneyoshi, Masazumi.

In: Modern Pathology, Vol. 14, No. 6, 03.07.2001, p. 581-588.

Research output: Contribution to journalArticle

Sakamoto, Akio ; Oda, Yoshinao ; Itakura, Eijun ; Oshiro, Yumi ; Nikaido, Osamu ; Iwamoto, Yukihide ; Tsuneyoshi, Masazumi. / Immunoexpression of ultraviolet photoproducts and p53 mutation analysis in atypical fibroxanthoma and superficial malignant fibrous histiocytoma. In: Modern Pathology. 2001 ; Vol. 14, No. 6. pp. 581-588.
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abstract = "p53 mutation is one of the major results of ultraviolet (UV) radiation. UV photoproducts of cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyrimidone (6-4) photoproducts (64PPs) also play an important role in skin cancer development. Atypical fibroxanthoma (AFX), which mimics malignant fibrous histiocytoma (MFH) histologically, occurs in the sun-exposed skin of the elderly, and therefore, an association with UV has long been suspected. Eighteen fibrohistiocytic skin lesions comprising AFX (n = 7), storiform-pleomorphic type MFH centered in the subcutis (superficial MFH; S-MFH; n = 4) and benign fibrous histiocytoma (BFH; n = 7) were used for immunohistochemical and molecular analysis. Eight cases of deep MFH (D-MFH) were also analyzed for UV photoproduct expression for the purposes of comparison. Immunohistochemically, the CPD scores of AFX (3.6 ± 0.4) were significantly higher than those of S-MFH (1.3 ± 0.8), D-MFH (0.8 ± 0.5), or BHF (1.4 ± 0.7); however, the 64PP scores were extremely low in all these tumors (AFX, 0.1 ± 0.1; S-MFH, 0.0 ± 0.0; D-MFH, 0.0 ± 0.0; and BHF, 0.0 ± 0.0). AFX, S-MFH, and BFH showed immunoexpression for p53 (2/7, 2/4, and 0/7), respectively. p53 mutations were detected in AFX (4/6; 67{\%}) and S-MFH (1/4; 25{\%}), but not in BFH (0/5; 0{\%}) using polymerase chain reaction-single-strand conformation polymorphism, and all of the mutations in AFX were either C-T transitions or at dipyrimidine sites. In conclusion, AFX and S-MFH are both similar fibrohistocytic lesions; however, AFX has high immunoreactivity for CPDs compared with S-MFH, D-MFH, or BFH. These data suggest that CPDs may play an important role in the pathogenesis of AFX.",
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AU - Sakamoto, Akio

AU - Oda, Yoshinao

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AU - Oshiro, Yumi

AU - Nikaido, Osamu

AU - Iwamoto, Yukihide

AU - Tsuneyoshi, Masazumi

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N2 - p53 mutation is one of the major results of ultraviolet (UV) radiation. UV photoproducts of cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyrimidone (6-4) photoproducts (64PPs) also play an important role in skin cancer development. Atypical fibroxanthoma (AFX), which mimics malignant fibrous histiocytoma (MFH) histologically, occurs in the sun-exposed skin of the elderly, and therefore, an association with UV has long been suspected. Eighteen fibrohistiocytic skin lesions comprising AFX (n = 7), storiform-pleomorphic type MFH centered in the subcutis (superficial MFH; S-MFH; n = 4) and benign fibrous histiocytoma (BFH; n = 7) were used for immunohistochemical and molecular analysis. Eight cases of deep MFH (D-MFH) were also analyzed for UV photoproduct expression for the purposes of comparison. Immunohistochemically, the CPD scores of AFX (3.6 ± 0.4) were significantly higher than those of S-MFH (1.3 ± 0.8), D-MFH (0.8 ± 0.5), or BHF (1.4 ± 0.7); however, the 64PP scores were extremely low in all these tumors (AFX, 0.1 ± 0.1; S-MFH, 0.0 ± 0.0; D-MFH, 0.0 ± 0.0; and BHF, 0.0 ± 0.0). AFX, S-MFH, and BFH showed immunoexpression for p53 (2/7, 2/4, and 0/7), respectively. p53 mutations were detected in AFX (4/6; 67%) and S-MFH (1/4; 25%), but not in BFH (0/5; 0%) using polymerase chain reaction-single-strand conformation polymorphism, and all of the mutations in AFX were either C-T transitions or at dipyrimidine sites. In conclusion, AFX and S-MFH are both similar fibrohistocytic lesions; however, AFX has high immunoreactivity for CPDs compared with S-MFH, D-MFH, or BFH. These data suggest that CPDs may play an important role in the pathogenesis of AFX.

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