Analysis of Parathyroid Neoplasms by Interphase Fluorescence In Situ Hybridization

Lori A. Erickson, Syed M. Jalal, Aaron Harwood, Brandon Shearer, Long Jin, Ricardo V. Lloyd

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Recent studies have indicated that numerical chromosomal abnormalities, including changes in cyclin D1 and p53, may be involved in parathyroid tumorigenesis. We analyzed a series of parathyroid neoplasms with DNA fluorescent probes to evaluate the diagnostic and prognostic utility of numerical abnormalities of chromosomes 1, 6, 9, 11, 13, 15, 17, and 22 and cyclin D1 and p53 gene loci. Interphase fluorescence in situ hybridization (FISH) analysis was performed on paraffin-embedded tissue sections from 15 parathyroid adenomas and 18 parathyroid carcinomas. Directly labeled fluorescent DNA probes for the centromere region of chromosomes 1, 6, 9, 11, 15, and 17, and locus-specific probes for chromosome 22 and chromosome 13 and for cyclin D1 and p53 gene loci were used for dual-probe hybridization. Sixty-seven percent (10 of 15) parathyroid adenomas and 78% (14 of 18) of parathyroid carcinomas showed chromosome gains. Seventy-three percent (11 of 15) of parathyroid adenomas and 33% (6 of 18) of parathyroid carcinomas showed chromosome losses. Normal parathyroid tissues used as controls showed no chromosomal abnormalities. Parathyroid hyperplasias averaged 1.8 gains and 0.2 losses per case. Parathyroid adenomas averaged 2.8 gains and 0.8 losses per case, and parathyroid carcinomas averaged 3.6 gains and 0.6 losses per case. In summary, chromosome abnormalities, both gains and losses, are common in parathyroid adenomas and carcinomas. Parathyroid carcinomas tend to show gains of more chromosome than adenomas. Chromosome 11 was the most frequent chromosome loss identified in parathyroid adenomas and a frequent chromosomal gain in parathyroid carcinomas. These results indicate that gain of chromosome 11 is associated with more aggressive biologic behavior in parathyroid neoplasms.

Original languageEnglish (US)
Pages (from-to)578-584
Number of pages7
JournalAmerican Journal of Surgical Pathology
Volume28
Issue number5
StatePublished - May 2004

Fingerprint

Parathyroid Neoplasms
Interphase
Fluorescence In Situ Hybridization
Chromosomes
bcl-1 Genes
Chromosome Aberrations
Chromosomes, Human, Pair 11
Chromosomes, Human, Pair 6
Chromosomes, Human, Pair 1
p53 Genes
DNA Probes
Fluorescent Dyes
Neoplasm DNA
Chromosomes, Human, Pair 22
Chromosomes, Human, Pair 13
Centromere
Cyclin D1
Adenoma
Paraffin

Keywords

  • Fluorescence in situ hybridization
  • Parathyroid

ASJC Scopus subject areas

  • Anatomy
  • Pathology and Forensic Medicine

Cite this

Erickson, L. A., Jalal, S. M., Harwood, A., Shearer, B., Jin, L., & Lloyd, R. V. (2004). Analysis of Parathyroid Neoplasms by Interphase Fluorescence In Situ Hybridization. American Journal of Surgical Pathology, 28(5), 578-584.

Analysis of Parathyroid Neoplasms by Interphase Fluorescence In Situ Hybridization. / Erickson, Lori A.; Jalal, Syed M.; Harwood, Aaron; Shearer, Brandon; Jin, Long; Lloyd, Ricardo V.

In: American Journal of Surgical Pathology, Vol. 28, No. 5, 05.2004, p. 578-584.

Research output: Contribution to journalArticle

Erickson, LA, Jalal, SM, Harwood, A, Shearer, B, Jin, L & Lloyd, RV 2004, 'Analysis of Parathyroid Neoplasms by Interphase Fluorescence In Situ Hybridization', American Journal of Surgical Pathology, vol. 28, no. 5, pp. 578-584.
Erickson LA, Jalal SM, Harwood A, Shearer B, Jin L, Lloyd RV. Analysis of Parathyroid Neoplasms by Interphase Fluorescence In Situ Hybridization. American Journal of Surgical Pathology. 2004 May;28(5):578-584.
Erickson, Lori A. ; Jalal, Syed M. ; Harwood, Aaron ; Shearer, Brandon ; Jin, Long ; Lloyd, Ricardo V. / Analysis of Parathyroid Neoplasms by Interphase Fluorescence In Situ Hybridization. In: American Journal of Surgical Pathology. 2004 ; Vol. 28, No. 5. pp. 578-584.
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abstract = "Recent studies have indicated that numerical chromosomal abnormalities, including changes in cyclin D1 and p53, may be involved in parathyroid tumorigenesis. We analyzed a series of parathyroid neoplasms with DNA fluorescent probes to evaluate the diagnostic and prognostic utility of numerical abnormalities of chromosomes 1, 6, 9, 11, 13, 15, 17, and 22 and cyclin D1 and p53 gene loci. Interphase fluorescence in situ hybridization (FISH) analysis was performed on paraffin-embedded tissue sections from 15 parathyroid adenomas and 18 parathyroid carcinomas. Directly labeled fluorescent DNA probes for the centromere region of chromosomes 1, 6, 9, 11, 15, and 17, and locus-specific probes for chromosome 22 and chromosome 13 and for cyclin D1 and p53 gene loci were used for dual-probe hybridization. Sixty-seven percent (10 of 15) parathyroid adenomas and 78{\%} (14 of 18) of parathyroid carcinomas showed chromosome gains. Seventy-three percent (11 of 15) of parathyroid adenomas and 33{\%} (6 of 18) of parathyroid carcinomas showed chromosome losses. Normal parathyroid tissues used as controls showed no chromosomal abnormalities. Parathyroid hyperplasias averaged 1.8 gains and 0.2 losses per case. Parathyroid adenomas averaged 2.8 gains and 0.8 losses per case, and parathyroid carcinomas averaged 3.6 gains and 0.6 losses per case. In summary, chromosome abnormalities, both gains and losses, are common in parathyroid adenomas and carcinomas. Parathyroid carcinomas tend to show gains of more chromosome than adenomas. Chromosome 11 was the most frequent chromosome loss identified in parathyroid adenomas and a frequent chromosomal gain in parathyroid carcinomas. These results indicate that gain of chromosome 11 is associated with more aggressive biologic behavior in parathyroid neoplasms.",
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