Literature DB >> 12114777

Clonality Analysis of Benign Parathyroid Lesions by Human Androgen Receptor (HUMARA) Gene Assay.

Xavier Sanjuan, Bonita R. Bryant, Mark E. Sobel, Maria I. Merino.   

Abstract

Benign conditions of the parathyroid gland have been classified as adenomas and hyperplasias. These entities however are difficult to distinguish when only a single gland is enlarged. Adenomas are defined as neoplastic clonal growths whereas hyperplasias are considered to be reactive processes of polyclonal origin. In order to analyze the clonal pattern of these lesions, we have studied hyperplasias and adenomas of parathyroid glands from women by the human androgen receptor (HUMARA) assay, a recently reliable and highly-lnformative technique based on the X-chromosome inactivation pattern in females. Samples consisted of formalin-fixed as well as frozen tissues. Informativeness with HUMARA marker was 87% (13/15 cases). All hyperplasias (5/5) and 6/8 adenomas yielded polyclonal results, since two alleles of similar intensity appeared when the lesion was HpaIl-digested. Two parathyroid adenomas had a loss of one X-alIeIe for the HUMARA gene and they were interpreted as monoclonal. These results show that parathyroid hyperplasias and adenomas, considered as multigland or monogland involvement diseases respectively, may be both polyclonal in origin, and that only a small subset of adenomas is found to be clonal. Consequently, clonality analysis cannot allow a clear distinction between these two entities as classically diagnosed. A different approach should be considering hyperplasia or adenoma when a polyclonal or monoclonal result has been obtained by clonality analysis.

Entities:  

Year:  1998        PMID: 12114777     DOI: 10.1007/bf02739689

Source DB:  PubMed          Journal:  Endocr Pathol        ISSN: 1046-3976            Impact factor:   3.943


  26 in total

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Journal:  Genomics       Date:  1992-09       Impact factor: 5.736

2.  Clonality in myeloproliferative disorders: analysis by means of the polymerase chain reaction.

Authors:  D G Gilliland; K L Blanchard; J Levy; S Perrin; H F Bunn
Journal:  Proc Natl Acad Sci U S A       Date:  1991-08-01       Impact factor: 11.205

3.  The Pathology of the Parathyroid Gland in Hyperparathyroidism: A Study of 25 Cases.

Authors:  B Castleman; T B Mallory
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4.  Clonal analysis of nodular parathyroid hyperplasia in renal hyperparathyroidism.

Authors:  Y Tominaga; S Kohara; Y Namii; T Nagasaka; T Haba; K Uchida; M Numano; Y Tanaka; H Takagi
Journal:  World J Surg       Date:  1996-09       Impact factor: 3.352

5.  Comparative analysis of clonality and pathology in primary and secondary hyperparathyroidism.

Authors:  L Shan; M Nakamura; Y Nakamura; D Inoue; S Morimoto; T Yokoi; K Kakudo
Journal:  Virchows Arch       Date:  1997-03       Impact factor: 4.064

6.  X-chromosome inactivation in the Wiskott-Aldrich syndrome: a marker for detection of the carrier state and identification of cell lineages expressing the gene defect.

Authors:  W L Greer; P C Kwong; M Peacocke; P Ip; L A Rubin; K A Siminovitch
Journal:  Genomics       Date:  1989-01       Impact factor: 5.736

7.  PCR bias in amplification of androgen receptor alleles, a trinucleotide repeat marker used in clonality studies.

Authors:  G L Mutter; K A Boynton
Journal:  Nucleic Acids Res       Date:  1995-04-25       Impact factor: 16.971

8.  Adrenoleukodystrophy: evidence for X linkage, inactivation, and selection favoring the mutant allele in heterozygous cells.

Authors:  B R Migeon; H W Moser; A B Moser; J Axelman; D Sillence; R A Norum
Journal:  Proc Natl Acad Sci U S A       Date:  1981-08       Impact factor: 11.205

9.  Langerhans'-cell histiocytosis (histiocytosis X)--a clonal proliferative disease.

Authors:  C L Willman; L Busque; B B Griffith; B E Favara; K L McClain; M H Duncan; D G Gilliland
Journal:  N Engl J Med       Date:  1994-07-21       Impact factor: 91.245

10.  Analysis of clonality by amplification of short tandem repeats. Carcinomas of the female reproductive tract.

Authors:  T Enomoto; M Fujita; M Inoue; O Tanizawa; T Nomura; K R Shroyer
Journal:  Diagn Mol Pathol       Date:  1994-12
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  5 in total

Review 1.  Different clonal origin of bilateral papillary thyroid carcinoma, with a review of the literature.

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2.  Polyclonal origin of parathyroid tumors is common and is associated with multiple gland disease in primary hyperparathyroidism.

Authors:  Yuhong Shi; Pedram Azimzadeh; Sarada Jamingal; Shannon Wentworth; Janice Ferlitch; James Koh; Nariman Balenga; John A Olson
Journal:  Surgery       Date:  2018-01       Impact factor: 3.982

Review 3.  Intratumor heterogeneity in human parathyroid tumors.

Authors:  C Verdelli; G S Tavanti; S Corbetta
Journal:  Histol Histopathol       Date:  2020-05-29       Impact factor: 2.303

Review 4.  Potential applications of molecular biology in neuroendocrine tumors.

Authors:  Tommaso Emmer; Marco Volante; Alberto Pagani; Elena Allia; Pellegrino Crafa; Gianni Bussolati
Journal:  Endocr Pathol       Date:  2003       Impact factor: 3.943

5.  Functional and genetic studies of isolated cells from parathyroid tumors reveal the complex pathogenesis of parathyroid neoplasia.

Authors:  Yuhong Shi; Joyce Hogue; Darshana Dixit; James Koh; John A Olson
Journal:  Proc Natl Acad Sci U S A       Date:  2014-02-07       Impact factor: 11.205

  5 in total

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