Mutations associated with carcinomas arising from pleomorphic adenomas of the salivary glands

Y. Yamamoto, Y. Kishimoto, A. K. Virmani, A. Smith, F. Vuitch, J. Albores- Saavedra, A. F. Gazdar

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Abstract

Pleomorphic adenoma (PA) is the most common benign tumor of salivary glands. Carcinomas in pleomorphic adenomas (CPAs) may arise by malignant transformation of the epithelial components of PAs. Occasionally, transitional zones containing cells with histological features intermediate between those of the benign PA anti carcinomatous components of CPA are identified. After careful microdissection of archival microslides, the authors studied 12 cases of CPAs and their attendant adenomatous and transitional areas for mutations in the p$3, RB, and K-ras genes, and at chromosomal loci 5q and 9p. The authors failed to find mutations in the K- ras gene or 9p locus. A relatively high rate of mutations (loss of heterozygosity [LOH] and microsatellite alterations) at the p53 gene were detected in CPAs (58%), and at somewhat lower frequencies at the RB gene (33%) and chromosomal location 5q (17%). Mutational frequency in the associated transitional and adenomatous areas were slightly lower than in the corresponding CPAs. No mutations were detected in adenomatous or transitional areas unless they also were present in the corresponding CPAs. Mutations of these three genes were absent in four cases of CPA, and in seven PAs without malignant change. These findings indicate that most CPAs arise from adenomas as the result of mutations in the three genes, especially p53. In addition, other, as yet unidentified genes may also be involved both in the development of PA and in its malignant progression to CPA. Mutational analysis of PAs may provide information of prognostic importance.

Original languageEnglish (US)
Pages (from-to)782-786
Number of pages5
JournalHuman Pathology
Volume27
Issue number8
DOIs
StatePublished - 1996

Fingerprint

Pleomorphic Adenoma
Carcinoma
Mutation
ras Genes
p53 Genes
Pleomorphic Salivary Gland Adenoma
Genes
Microdissection
Loss of Heterozygosity
Mutation Rate
Salivary Glands
Adenoma
Microsatellite Repeats
Neoplasms

Keywords

  • chromosome 5q
  • p53 gene
  • pleomorphic adenoma
  • RB gene
  • salivary gland carcinoma

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Yamamoto, Y., Kishimoto, Y., Virmani, A. K., Smith, A., Vuitch, F., Albores- Saavedra, J., & Gazdar, A. F. (1996). Mutations associated with carcinomas arising from pleomorphic adenomas of the salivary glands. Human Pathology, 27(8), 782-786. https://doi.org/10.1016/S0046-8177(96)90449-9

Mutations associated with carcinomas arising from pleomorphic adenomas of the salivary glands. / Yamamoto, Y.; Kishimoto, Y.; Virmani, A. K.; Smith, A.; Vuitch, F.; Albores- Saavedra, J.; Gazdar, A. F.

In: Human Pathology, Vol. 27, No. 8, 1996, p. 782-786.

Research output: Contribution to journalArticle

Yamamoto, Y, Kishimoto, Y, Virmani, AK, Smith, A, Vuitch, F, Albores- Saavedra, J & Gazdar, AF 1996, 'Mutations associated with carcinomas arising from pleomorphic adenomas of the salivary glands', Human Pathology, vol. 27, no. 8, pp. 782-786. https://doi.org/10.1016/S0046-8177(96)90449-9
Yamamoto Y, Kishimoto Y, Virmani AK, Smith A, Vuitch F, Albores- Saavedra J et al. Mutations associated with carcinomas arising from pleomorphic adenomas of the salivary glands. Human Pathology. 1996;27(8):782-786. https://doi.org/10.1016/S0046-8177(96)90449-9
Yamamoto, Y. ; Kishimoto, Y. ; Virmani, A. K. ; Smith, A. ; Vuitch, F. ; Albores- Saavedra, J. ; Gazdar, A. F. / Mutations associated with carcinomas arising from pleomorphic adenomas of the salivary glands. In: Human Pathology. 1996 ; Vol. 27, No. 8. pp. 782-786.
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abstract = "Pleomorphic adenoma (PA) is the most common benign tumor of salivary glands. Carcinomas in pleomorphic adenomas (CPAs) may arise by malignant transformation of the epithelial components of PAs. Occasionally, transitional zones containing cells with histological features intermediate between those of the benign PA anti carcinomatous components of CPA are identified. After careful microdissection of archival microslides, the authors studied 12 cases of CPAs and their attendant adenomatous and transitional areas for mutations in the p$3, RB, and K-ras genes, and at chromosomal loci 5q and 9p. The authors failed to find mutations in the K- ras gene or 9p locus. A relatively high rate of mutations (loss of heterozygosity [LOH] and microsatellite alterations) at the p53 gene were detected in CPAs (58{\%}), and at somewhat lower frequencies at the RB gene (33{\%}) and chromosomal location 5q (17{\%}). Mutational frequency in the associated transitional and adenomatous areas were slightly lower than in the corresponding CPAs. No mutations were detected in adenomatous or transitional areas unless they also were present in the corresponding CPAs. Mutations of these three genes were absent in four cases of CPA, and in seven PAs without malignant change. These findings indicate that most CPAs arise from adenomas as the result of mutations in the three genes, especially p53. In addition, other, as yet unidentified genes may also be involved both in the development of PA and in its malignant progression to CPA. Mutational analysis of PAs may provide information of prognostic importance.",
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AU - Kishimoto, Y.

AU - Virmani, A. K.

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AU - Albores- Saavedra, J.

AU - Gazdar, A. F.

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N2 - Pleomorphic adenoma (PA) is the most common benign tumor of salivary glands. Carcinomas in pleomorphic adenomas (CPAs) may arise by malignant transformation of the epithelial components of PAs. Occasionally, transitional zones containing cells with histological features intermediate between those of the benign PA anti carcinomatous components of CPA are identified. After careful microdissection of archival microslides, the authors studied 12 cases of CPAs and their attendant adenomatous and transitional areas for mutations in the p$3, RB, and K-ras genes, and at chromosomal loci 5q and 9p. The authors failed to find mutations in the K- ras gene or 9p locus. A relatively high rate of mutations (loss of heterozygosity [LOH] and microsatellite alterations) at the p53 gene were detected in CPAs (58%), and at somewhat lower frequencies at the RB gene (33%) and chromosomal location 5q (17%). Mutational frequency in the associated transitional and adenomatous areas were slightly lower than in the corresponding CPAs. No mutations were detected in adenomatous or transitional areas unless they also were present in the corresponding CPAs. Mutations of these three genes were absent in four cases of CPA, and in seven PAs without malignant change. These findings indicate that most CPAs arise from adenomas as the result of mutations in the three genes, especially p53. In addition, other, as yet unidentified genes may also be involved both in the development of PA and in its malignant progression to CPA. Mutational analysis of PAs may provide information of prognostic importance.

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