β-Catenin accumulation and gene mutation in exon 3 in dedifferentiated liposarcoma and malignant fibrous histiocytoma

Akio Sakamoto, Yoshinao Oda, Toshisada Adachi, Tsuyoshi Saito, Sadafumi Tamiya, Yukihide Iwamoto, Masazumi Tsuneyoshi

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Abstract

Context.- β-Catenin is an adhesion molecule that also plays a role in the Wnt signaling pathway. Objective.- To analyze β-catenin mutation and accumulation in a series of liposarcomas and malignant fibrous histiocytomas. Design.- β-Catenin mutation in exon 3 was studied using polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) and direct sequencing analysis in 30 formalin-fixed, paraffin-embedded liposarcomas. The tumors included 12 dedifferentiated liposarcomas, characterized by both high-grade anaplastic components and well-differentiated liposarcoma components, plus 18 well-differentiated liposarcomas (10 lipoma-like and 8 sclerosing-type cases). The 2 components of dedifferentiated liposarcomas were analyzed independently. β-Catenin accumulation in the nuclei or cytoplasm and Ki-67 expression (cell-proliferation marker, MIB-1 labeling index) were examined immunohistochemically. Nine storiform-pleomorphic-type malignant fibrous histiocytomas were also studied. Results.- Dedifferentiated liposarcomas showed mutation in 2 cases (17%) and accumulation in 5 cases (42%). One of the 2 cases that showed mutations had a mutation in the well-differentiated component; this mutation was silent. The other case had mutations that differed between the 2 components. In well-differentiated liposarcomas, mutation was not seen in any of the cases (0/18; 0%); however, accumulation was seen frequently in the sclerosing-type cases (5/8; 63%), but not in the lipoma-like cases (0/10; 0%). Malignant fibrous histiocytomas showed mutation and accumulation in 5 (56%) and 4 (44%) cases, respectively, without any exact correlation between the cases. Cases with accumulation had a higher MIB-1 labeling index than those without, among both the sclerosing-type well-differentiated liposarcomas (P < .05) and the malignant fibrous histiocytomas. Conclusions.- Our results suggest the possible involvement of β-catenin activation caused by β-catenin mutation in liposarcoma and malignant fibrous histiocytoma, but the contribution would seem to be different, depending on the tumor type. β-Catenin accumulation is also thought to be related to cell proliferation in some of the cases.

Original languageEnglish
Pages (from-to)1071-1078
Number of pages8
JournalArchives of Pathology and Laboratory Medicine
Volume126
Issue number9
Publication statusPublished - Sep 1 2002

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Catenins
Malignant Fibrous Histiocytoma
Liposarcoma
Exons
Genes
Mutation
Lipoma
Cell Proliferation
Mutation Accumulation
Wnt Signaling Pathway
Paraffin
Formaldehyde
Neoplasms
Cytoplasm

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine
  • Medical Laboratory Technology

Cite this

β-Catenin accumulation and gene mutation in exon 3 in dedifferentiated liposarcoma and malignant fibrous histiocytoma. / Sakamoto, Akio; Oda, Yoshinao; Adachi, Toshisada; Saito, Tsuyoshi; Tamiya, Sadafumi; Iwamoto, Yukihide; Tsuneyoshi, Masazumi.

In: Archives of Pathology and Laboratory Medicine, Vol. 126, No. 9, 01.09.2002, p. 1071-1078.

Research output: Contribution to journalArticle

Sakamoto, A, Oda, Y, Adachi, T, Saito, T, Tamiya, S, Iwamoto, Y & Tsuneyoshi, M 2002, 'β-Catenin accumulation and gene mutation in exon 3 in dedifferentiated liposarcoma and malignant fibrous histiocytoma', Archives of Pathology and Laboratory Medicine, vol. 126, no. 9, pp. 1071-1078.
Sakamoto, Akio ; Oda, Yoshinao ; Adachi, Toshisada ; Saito, Tsuyoshi ; Tamiya, Sadafumi ; Iwamoto, Yukihide ; Tsuneyoshi, Masazumi. / β-Catenin accumulation and gene mutation in exon 3 in dedifferentiated liposarcoma and malignant fibrous histiocytoma. In: Archives of Pathology and Laboratory Medicine. 2002 ; Vol. 126, No. 9. pp. 1071-1078.
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title = "β-Catenin accumulation and gene mutation in exon 3 in dedifferentiated liposarcoma and malignant fibrous histiocytoma",
abstract = "Context.- β-Catenin is an adhesion molecule that also plays a role in the Wnt signaling pathway. Objective.- To analyze β-catenin mutation and accumulation in a series of liposarcomas and malignant fibrous histiocytomas. Design.- β-Catenin mutation in exon 3 was studied using polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) and direct sequencing analysis in 30 formalin-fixed, paraffin-embedded liposarcomas. The tumors included 12 dedifferentiated liposarcomas, characterized by both high-grade anaplastic components and well-differentiated liposarcoma components, plus 18 well-differentiated liposarcomas (10 lipoma-like and 8 sclerosing-type cases). The 2 components of dedifferentiated liposarcomas were analyzed independently. β-Catenin accumulation in the nuclei or cytoplasm and Ki-67 expression (cell-proliferation marker, MIB-1 labeling index) were examined immunohistochemically. Nine storiform-pleomorphic-type malignant fibrous histiocytomas were also studied. Results.- Dedifferentiated liposarcomas showed mutation in 2 cases (17{\%}) and accumulation in 5 cases (42{\%}). One of the 2 cases that showed mutations had a mutation in the well-differentiated component; this mutation was silent. The other case had mutations that differed between the 2 components. In well-differentiated liposarcomas, mutation was not seen in any of the cases (0/18; 0{\%}); however, accumulation was seen frequently in the sclerosing-type cases (5/8; 63{\%}), but not in the lipoma-like cases (0/10; 0{\%}). Malignant fibrous histiocytomas showed mutation and accumulation in 5 (56{\%}) and 4 (44{\%}) cases, respectively, without any exact correlation between the cases. Cases with accumulation had a higher MIB-1 labeling index than those without, among both the sclerosing-type well-differentiated liposarcomas (P < .05) and the malignant fibrous histiocytomas. Conclusions.- Our results suggest the possible involvement of β-catenin activation caused by β-catenin mutation in liposarcoma and malignant fibrous histiocytoma, but the contribution would seem to be different, depending on the tumor type. β-Catenin accumulation is also thought to be related to cell proliferation in some of the cases.",
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T1 - β-Catenin accumulation and gene mutation in exon 3 in dedifferentiated liposarcoma and malignant fibrous histiocytoma

AU - Sakamoto, Akio

AU - Oda, Yoshinao

AU - Adachi, Toshisada

AU - Saito, Tsuyoshi

AU - Tamiya, Sadafumi

AU - Iwamoto, Yukihide

AU - Tsuneyoshi, Masazumi

PY - 2002/9/1

Y1 - 2002/9/1

N2 - Context.- β-Catenin is an adhesion molecule that also plays a role in the Wnt signaling pathway. Objective.- To analyze β-catenin mutation and accumulation in a series of liposarcomas and malignant fibrous histiocytomas. Design.- β-Catenin mutation in exon 3 was studied using polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) and direct sequencing analysis in 30 formalin-fixed, paraffin-embedded liposarcomas. The tumors included 12 dedifferentiated liposarcomas, characterized by both high-grade anaplastic components and well-differentiated liposarcoma components, plus 18 well-differentiated liposarcomas (10 lipoma-like and 8 sclerosing-type cases). The 2 components of dedifferentiated liposarcomas were analyzed independently. β-Catenin accumulation in the nuclei or cytoplasm and Ki-67 expression (cell-proliferation marker, MIB-1 labeling index) were examined immunohistochemically. Nine storiform-pleomorphic-type malignant fibrous histiocytomas were also studied. Results.- Dedifferentiated liposarcomas showed mutation in 2 cases (17%) and accumulation in 5 cases (42%). One of the 2 cases that showed mutations had a mutation in the well-differentiated component; this mutation was silent. The other case had mutations that differed between the 2 components. In well-differentiated liposarcomas, mutation was not seen in any of the cases (0/18; 0%); however, accumulation was seen frequently in the sclerosing-type cases (5/8; 63%), but not in the lipoma-like cases (0/10; 0%). Malignant fibrous histiocytomas showed mutation and accumulation in 5 (56%) and 4 (44%) cases, respectively, without any exact correlation between the cases. Cases with accumulation had a higher MIB-1 labeling index than those without, among both the sclerosing-type well-differentiated liposarcomas (P < .05) and the malignant fibrous histiocytomas. Conclusions.- Our results suggest the possible involvement of β-catenin activation caused by β-catenin mutation in liposarcoma and malignant fibrous histiocytoma, but the contribution would seem to be different, depending on the tumor type. β-Catenin accumulation is also thought to be related to cell proliferation in some of the cases.

AB - Context.- β-Catenin is an adhesion molecule that also plays a role in the Wnt signaling pathway. Objective.- To analyze β-catenin mutation and accumulation in a series of liposarcomas and malignant fibrous histiocytomas. Design.- β-Catenin mutation in exon 3 was studied using polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) and direct sequencing analysis in 30 formalin-fixed, paraffin-embedded liposarcomas. The tumors included 12 dedifferentiated liposarcomas, characterized by both high-grade anaplastic components and well-differentiated liposarcoma components, plus 18 well-differentiated liposarcomas (10 lipoma-like and 8 sclerosing-type cases). The 2 components of dedifferentiated liposarcomas were analyzed independently. β-Catenin accumulation in the nuclei or cytoplasm and Ki-67 expression (cell-proliferation marker, MIB-1 labeling index) were examined immunohistochemically. Nine storiform-pleomorphic-type malignant fibrous histiocytomas were also studied. Results.- Dedifferentiated liposarcomas showed mutation in 2 cases (17%) and accumulation in 5 cases (42%). One of the 2 cases that showed mutations had a mutation in the well-differentiated component; this mutation was silent. The other case had mutations that differed between the 2 components. In well-differentiated liposarcomas, mutation was not seen in any of the cases (0/18; 0%); however, accumulation was seen frequently in the sclerosing-type cases (5/8; 63%), but not in the lipoma-like cases (0/10; 0%). Malignant fibrous histiocytomas showed mutation and accumulation in 5 (56%) and 4 (44%) cases, respectively, without any exact correlation between the cases. Cases with accumulation had a higher MIB-1 labeling index than those without, among both the sclerosing-type well-differentiated liposarcomas (P < .05) and the malignant fibrous histiocytomas. Conclusions.- Our results suggest the possible involvement of β-catenin activation caused by β-catenin mutation in liposarcoma and malignant fibrous histiocytoma, but the contribution would seem to be different, depending on the tumor type. β-Catenin accumulation is also thought to be related to cell proliferation in some of the cases.

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