p55 mutation and MDM2 amplification in inflammatory myofibroblastic tumours

Hidetaka Yamamoto, Yoshinao Oda, T. Saito, A. Sakamoto, K. Miyajima, S. Tamiya, Masazumi Tsuneyoshi

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Abstract

Aims: The pathogenic mechanism and predictive indicators of biological behaviour of inflammatory myofibroblastic tumour are poorly understood. We investigated molecular abnormalities of p53 and MDM2 in order to assess whether these play an important role in pathogenesis, and whether they also contribute to clinicopathological aggressive phenotype in inflammatory myofibroblastic tumour. Methods and results: We compared the immunohistochemical expression of calponin, h-caldesmon, ALK, and p53 gene mutation and MDM2 gene amplification with clinicopathological findings in 15 cases of inflammatory myofibroblastic tumour. Histologically, cellular atypia was observed in five (33.3%) out of 15 cases, Local recurrences were observed in two (14.3%) of 14 informative cases, but no distant metastasis was observed. The expression of calponin (9/14; 64%) but not h-caldesmon (0/14; 0%) was seen, which suggested myofibroblastic differentiation. ALK expression was seen in eight (53.3%) out of 15 cases, particularly in patients under 40 years old. Nuclear expression of p53 protein was recognized in only one (6.7%) of 15 cases, and polymerase chain reaction single-strand conformation polymorphism followed by direct sequencing revealed 1953 gene missense mutations in two (13.3%) of 15 cases. Nuclear expression of MDM2 was seen in four (26.7%) of 15 cases, and the MDM2 gene amplification was observed in two of the four cases. Conclusion: Inflammatory myofibroblastic tumour shows a wide spectrum of cellular atypia and biological behaviour with p53 and MDM2 expression. However, the alterations in the p53 pathway seem not to play a major role in the pathogenesis of inflammatory myofibroblastic tumour.

Original languageEnglish
Pages (from-to)431-439
Number of pages9
JournalHistopathology
Volume42
Issue number5
DOIs
Publication statusPublished - May 1 2003

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Mutation
Calmodulin-Binding Proteins
Gene Amplification
Neoplasms
p53 Genes
Missense Mutation
Neoplasm Metastasis
Phenotype
Recurrence
Polymerase Chain Reaction
Genes
Proteins
calponin

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine
  • Histology

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p55 mutation and MDM2 amplification in inflammatory myofibroblastic tumours. / Yamamoto, Hidetaka; Oda, Yoshinao; Saito, T.; Sakamoto, A.; Miyajima, K.; Tamiya, S.; Tsuneyoshi, Masazumi.

In: Histopathology, Vol. 42, No. 5, 01.05.2003, p. 431-439.

Research output: Contribution to journalArticle

Yamamoto, H, Oda, Y, Saito, T, Sakamoto, A, Miyajima, K, Tamiya, S & Tsuneyoshi, M 2003, 'p55 mutation and MDM2 amplification in inflammatory myofibroblastic tumours', Histopathology, vol. 42, no. 5, pp. 431-439. https://doi.org/10.1046/j.1365-2559.2003.01611.x
Yamamoto, Hidetaka ; Oda, Yoshinao ; Saito, T. ; Sakamoto, A. ; Miyajima, K. ; Tamiya, S. ; Tsuneyoshi, Masazumi. / p55 mutation and MDM2 amplification in inflammatory myofibroblastic tumours. In: Histopathology. 2003 ; Vol. 42, No. 5. pp. 431-439.
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AU - Tamiya, S.

AU - Tsuneyoshi, Masazumi

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N2 - Aims: The pathogenic mechanism and predictive indicators of biological behaviour of inflammatory myofibroblastic tumour are poorly understood. We investigated molecular abnormalities of p53 and MDM2 in order to assess whether these play an important role in pathogenesis, and whether they also contribute to clinicopathological aggressive phenotype in inflammatory myofibroblastic tumour. Methods and results: We compared the immunohistochemical expression of calponin, h-caldesmon, ALK, and p53 gene mutation and MDM2 gene amplification with clinicopathological findings in 15 cases of inflammatory myofibroblastic tumour. Histologically, cellular atypia was observed in five (33.3%) out of 15 cases, Local recurrences were observed in two (14.3%) of 14 informative cases, but no distant metastasis was observed. The expression of calponin (9/14; 64%) but not h-caldesmon (0/14; 0%) was seen, which suggested myofibroblastic differentiation. ALK expression was seen in eight (53.3%) out of 15 cases, particularly in patients under 40 years old. Nuclear expression of p53 protein was recognized in only one (6.7%) of 15 cases, and polymerase chain reaction single-strand conformation polymorphism followed by direct sequencing revealed 1953 gene missense mutations in two (13.3%) of 15 cases. Nuclear expression of MDM2 was seen in four (26.7%) of 15 cases, and the MDM2 gene amplification was observed in two of the four cases. Conclusion: Inflammatory myofibroblastic tumour shows a wide spectrum of cellular atypia and biological behaviour with p53 and MDM2 expression. However, the alterations in the p53 pathway seem not to play a major role in the pathogenesis of inflammatory myofibroblastic tumour.

AB - Aims: The pathogenic mechanism and predictive indicators of biological behaviour of inflammatory myofibroblastic tumour are poorly understood. We investigated molecular abnormalities of p53 and MDM2 in order to assess whether these play an important role in pathogenesis, and whether they also contribute to clinicopathological aggressive phenotype in inflammatory myofibroblastic tumour. Methods and results: We compared the immunohistochemical expression of calponin, h-caldesmon, ALK, and p53 gene mutation and MDM2 gene amplification with clinicopathological findings in 15 cases of inflammatory myofibroblastic tumour. Histologically, cellular atypia was observed in five (33.3%) out of 15 cases, Local recurrences were observed in two (14.3%) of 14 informative cases, but no distant metastasis was observed. The expression of calponin (9/14; 64%) but not h-caldesmon (0/14; 0%) was seen, which suggested myofibroblastic differentiation. ALK expression was seen in eight (53.3%) out of 15 cases, particularly in patients under 40 years old. Nuclear expression of p53 protein was recognized in only one (6.7%) of 15 cases, and polymerase chain reaction single-strand conformation polymorphism followed by direct sequencing revealed 1953 gene missense mutations in two (13.3%) of 15 cases. Nuclear expression of MDM2 was seen in four (26.7%) of 15 cases, and the MDM2 gene amplification was observed in two of the four cases. Conclusion: Inflammatory myofibroblastic tumour shows a wide spectrum of cellular atypia and biological behaviour with p53 and MDM2 expression. However, the alterations in the p53 pathway seem not to play a major role in the pathogenesis of inflammatory myofibroblastic tumour.

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