Secondary malignant giant-cell tumour of bone: Molecular abnormalities of p53 and H-ras gene correlated with malignant transformation

Y. Oda, A. Sakamoto, T. Saito, S. Matsuda, K. Tanaka, Y. Iwamoto, M. Tsuneyoshi

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

Aims: We report two cases of secondary malignant giant-cell tumour occurring without irradiation therapy. To elucidate the mechanism of malignant transformation in this tumour, we searched for the molecular abnormalities of p53, MDM2 and the H-ras genes. Methods and results: These cases were retrieved after a review of 103 cases of primary giant-cell tumour of bone, registered in our institute. One case occurred in the distal femur of a 42-year-old female after surgical curettage, while the other arose in the acetabulum of a 25-year-old male after en bloc resection. Microscopically, the malignant tumour in the distal femur was composed of a proliferation of ovoid or fusiform cells arranged in fascicles with high mitotic activities. The malignant transformed tumour in the acetabulum was made up of pleomorphic tumour cells with atypical mitoses. In the tumour of the distal femur, both p53 and H-ras mutations were detected. Abnormal nuclear accumulation of p53 protein and c-myc expression were also revealed by immunohistochemistry. In both cases, the recurrent malignant tumour over-expressed MMP-9 and revealed a higher MIB-1-labelling index compared with the primary conventional giant-cell tumour. Conclusions: Our results suggest that multiple oncogene or tumour suppressor gene mutations may play an important role during malignant transformation in conventional giant-cell tumours.

Original languageEnglish
Pages (from-to)629-637
Number of pages9
JournalHistopathology
Volume39
Issue number6
DOIs
Publication statusPublished - Dec 1 2001

Fingerprint

Giant Cell Tumor of Bone
ras Genes
Giant Cell Tumors
Femur
Neoplasms
Acetabulum
Proto-Oncogene Proteins c-myc
Genetic Suppression
Curettage
Tumor Suppressor Genes
Matrix Metalloproteinases
Oncogenes
Mitosis
Immunohistochemistry
Mutation

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine
  • Histology

Cite this

Secondary malignant giant-cell tumour of bone : Molecular abnormalities of p53 and H-ras gene correlated with malignant transformation. / Oda, Y.; Sakamoto, A.; Saito, T.; Matsuda, S.; Tanaka, K.; Iwamoto, Y.; Tsuneyoshi, M.

In: Histopathology, Vol. 39, No. 6, 01.12.2001, p. 629-637.

Research output: Contribution to journalArticle

Oda, Y. ; Sakamoto, A. ; Saito, T. ; Matsuda, S. ; Tanaka, K. ; Iwamoto, Y. ; Tsuneyoshi, M. / Secondary malignant giant-cell tumour of bone : Molecular abnormalities of p53 and H-ras gene correlated with malignant transformation. In: Histopathology. 2001 ; Vol. 39, No. 6. pp. 629-637.
@article{7837679167624c2eba6d65cfef563538,
title = "Secondary malignant giant-cell tumour of bone: Molecular abnormalities of p53 and H-ras gene correlated with malignant transformation",
abstract = "Aims: We report two cases of secondary malignant giant-cell tumour occurring without irradiation therapy. To elucidate the mechanism of malignant transformation in this tumour, we searched for the molecular abnormalities of p53, MDM2 and the H-ras genes. Methods and results: These cases were retrieved after a review of 103 cases of primary giant-cell tumour of bone, registered in our institute. One case occurred in the distal femur of a 42-year-old female after surgical curettage, while the other arose in the acetabulum of a 25-year-old male after en bloc resection. Microscopically, the malignant tumour in the distal femur was composed of a proliferation of ovoid or fusiform cells arranged in fascicles with high mitotic activities. The malignant transformed tumour in the acetabulum was made up of pleomorphic tumour cells with atypical mitoses. In the tumour of the distal femur, both p53 and H-ras mutations were detected. Abnormal nuclear accumulation of p53 protein and c-myc expression were also revealed by immunohistochemistry. In both cases, the recurrent malignant tumour over-expressed MMP-9 and revealed a higher MIB-1-labelling index compared with the primary conventional giant-cell tumour. Conclusions: Our results suggest that multiple oncogene or tumour suppressor gene mutations may play an important role during malignant transformation in conventional giant-cell tumours.",
author = "Y. Oda and A. Sakamoto and T. Saito and S. Matsuda and K. Tanaka and Y. Iwamoto and M. Tsuneyoshi",
year = "2001",
month = "12",
day = "1",
doi = "10.1046/j.1365-2559.2001.01275.x",
language = "English",
volume = "39",
pages = "629--637",
journal = "Histopathology",
issn = "0309-0167",
publisher = "Wiley-Blackwell",
number = "6",

}

TY - JOUR

T1 - Secondary malignant giant-cell tumour of bone

T2 - Molecular abnormalities of p53 and H-ras gene correlated with malignant transformation

AU - Oda, Y.

AU - Sakamoto, A.

AU - Saito, T.

AU - Matsuda, S.

AU - Tanaka, K.

AU - Iwamoto, Y.

AU - Tsuneyoshi, M.

PY - 2001/12/1

Y1 - 2001/12/1

N2 - Aims: We report two cases of secondary malignant giant-cell tumour occurring without irradiation therapy. To elucidate the mechanism of malignant transformation in this tumour, we searched for the molecular abnormalities of p53, MDM2 and the H-ras genes. Methods and results: These cases were retrieved after a review of 103 cases of primary giant-cell tumour of bone, registered in our institute. One case occurred in the distal femur of a 42-year-old female after surgical curettage, while the other arose in the acetabulum of a 25-year-old male after en bloc resection. Microscopically, the malignant tumour in the distal femur was composed of a proliferation of ovoid or fusiform cells arranged in fascicles with high mitotic activities. The malignant transformed tumour in the acetabulum was made up of pleomorphic tumour cells with atypical mitoses. In the tumour of the distal femur, both p53 and H-ras mutations were detected. Abnormal nuclear accumulation of p53 protein and c-myc expression were also revealed by immunohistochemistry. In both cases, the recurrent malignant tumour over-expressed MMP-9 and revealed a higher MIB-1-labelling index compared with the primary conventional giant-cell tumour. Conclusions: Our results suggest that multiple oncogene or tumour suppressor gene mutations may play an important role during malignant transformation in conventional giant-cell tumours.

AB - Aims: We report two cases of secondary malignant giant-cell tumour occurring without irradiation therapy. To elucidate the mechanism of malignant transformation in this tumour, we searched for the molecular abnormalities of p53, MDM2 and the H-ras genes. Methods and results: These cases were retrieved after a review of 103 cases of primary giant-cell tumour of bone, registered in our institute. One case occurred in the distal femur of a 42-year-old female after surgical curettage, while the other arose in the acetabulum of a 25-year-old male after en bloc resection. Microscopically, the malignant tumour in the distal femur was composed of a proliferation of ovoid or fusiform cells arranged in fascicles with high mitotic activities. The malignant transformed tumour in the acetabulum was made up of pleomorphic tumour cells with atypical mitoses. In the tumour of the distal femur, both p53 and H-ras mutations were detected. Abnormal nuclear accumulation of p53 protein and c-myc expression were also revealed by immunohistochemistry. In both cases, the recurrent malignant tumour over-expressed MMP-9 and revealed a higher MIB-1-labelling index compared with the primary conventional giant-cell tumour. Conclusions: Our results suggest that multiple oncogene or tumour suppressor gene mutations may play an important role during malignant transformation in conventional giant-cell tumours.

UR - http://www.scopus.com/inward/record.url?scp=0035667318&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035667318&partnerID=8YFLogxK

U2 - 10.1046/j.1365-2559.2001.01275.x

DO - 10.1046/j.1365-2559.2001.01275.x

M3 - Article

C2 - 11903582

AN - SCOPUS:0035667318

VL - 39

SP - 629

EP - 637

JO - Histopathology

JF - Histopathology

SN - 0309-0167

IS - 6

ER -