Cytogenetic studies on 19 papillary thyroid carcinomas

Antonini, P.; Venuat, A.M.; Caillou, Bernard; Berger, Roland; Schlumberger, Martin; Bernheim, Alain; Parmentier, C

doi:10.1002/gcc.2870050306

Cited by 20 publications

(11 citation statements)

References 27 publications

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“…Previous studies have addressed papillary, follicular, and anaplastic thyroid carcinomas individually for the presence of genome-wide abnormalities and confirm that thyroid cancers are commonly characterized by chromosomal instability. [11][12][13][14][15][16][17] However, these reports show a wide variation in the detection rate of abnormalities and suggest that rates of chromosomal complexity are similar between papillary, follicular, and anaplastic carcinomas. Since none of these studies performed a detailed histopathological appraisal, the inclusion of morphologically heterogeneous study populations likely confounds the data presented.…”

Section: Discussionmentioning

confidence: 93%

“…[11][12][13][14][15][16][17] However, since none of these studies have meticulously categorized the morphological phenotypes of the investigated specimens, a comparison of the chromosomal constitution of WDTC, PDTC, and ATC is currently unavailable. Comparative genomic hybridization (CGH), known for its genome-wide detection of chromosomal gains, losses, and amplifications, is a particularly attractive method to study chromosomal abnormalities.…”

Section: (Am J Pathol 2002 161:1549 -1556)mentioning

confidence: 99%

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Genome-Wide Appraisal of Thyroid Cancer Progression

Wreesmann

Ghossein

Patel

et al. 2002

The American Journal of Pathology

155

118

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Several lines of evidence suggest that follicular cellderived thyroid cancers represent a continuum of disease that progresses from the highly curable welldifferentiated thyroid cancers to the universally fatal anaplastic cancers. However, the genetic mechanisms underlying thyroid cancer progression remain ill defined. We compared the molecular-cytogenetic profiles derived from comparative genomic hybridization (CGH) analysis of major histological variants of thyroid cancer to define genetic variables associated with progression. Overall, a sequential increase in chromosomal complexity was observed from welldifferentiated papillary thyroid cancer to poorly differentiated and anaplastic carcinomas, both in terms of the presence of CGH detectable abnormalities (P ‫؍‬ 0.003) and the median number of abnormalities per case (P < 0.001). The presence of multiple abnormalities common to all thyroid cancer variants, including gains of 5p15, 5q11-13, 19p, and 19q and loss of 8p, suggests that these tumors are derived from a common genetic pathway. Gains of 1p34 -36, 6p21, 9q34, 17q25, and 20q and losses of 1p11-p31, 2q32-33, 4q11-13, 6q21, and 13q21-31 may represent secondary events in progression, as they were only detected in poorly differentiated and anaplastic carcinomas. Finally, recurrent gains at 3p13-14 and 11q13, and loss of 5q11-31 were unique to anaplastic carcinomas, suggesting they may be markers for anaplastic transformation. Our data suggests that the development of chromosomal instability underlies the progression to more aggressive phenotypes of thyroid cancer and sheds light on the possible genomic aberrations that may be selected for during this process.

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Section: Discussionmentioning

confidence: 93%

Section: (Am J Pathol 2002 161:1549 -1556)mentioning

confidence: 99%

Genome-Wide Appraisal of Thyroid Cancer Progression

Wreesmann

Ghossein

Patel

et al. 2002

The American Journal of Pathology

155

118

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“…1991). Characteristic cytogenetic abnormalities of chromosome 10 have also been described in papillary thyroid carcinomas (Antonini et al, 1992;Sozzi et al. 1992).…”

Section: Discussionmentioning

confidence: 97%

Analysis of nuclear and mitochondrial DNA alterations in thyroid and renal oncocytic tumors

Tallini

Ladanyi

Rosaí

et al. 1994

Cytogenet Genome Res

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The search for mitochondrial DNA (mtDNA) defects in oncocytic neoplasms has been the subject of several recent studies. We have performed qualitative and quantitative analysis of nuclear and mitochondrial DNAs in a series of 19 renal and 12 thyroid oncocytic tumors to identify specific alterations that might predict the clinical and biological behavior of these tumors. Allelic losses were seen in 2 of 19 renal tumors and 5 of 12 thyroid tumors. Among all loci (3p, 3q, 9q, 10q, 11p, 17p, and 17q) that showed losses, losses at 10q (one renal tumor and three thyroid tumors) were significantly higher (P < 0.05) than expected. Analysis of the COX I region previously reported to be altered in oncocytomas and the delta-loop region of mtDNA showed no detectable abnormalities in the restriction pattern in 10 renal and five thyroid tumors. PCR analysis of the commonly deleted 4,977-bp region failed to detect an increased frequency of mtDNA deletions in tumors compared to the controls. In addition, segmental amplification of the complete mtDNA from a renal oncocytoma using nine sets of primers revealed no gross alteration in mtDNA. Oncocytic tumors showed a mean 5-fold increase in mitochondrial DNA, which was significant (P < 0.001) when compared to corresponding controls. The relative increase in the cellular content of mtDNA may be associated with alterations in the normal coordinated interaction between the nuclear and mitochondrial genomes. Allelic deletions at 1 Oq may be significant in the biology of oncocytic tumors, and their impact on the clinical behavior of these tumors warrants further investigation.

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“…Other nonrandom chromosomal alterations in papillary carcinoma have also been described, e.g. involving chromosomes 7 and 17 (Antonini et al ., 1992). Studies of allelic loss in thyroid tumours indicate that papillary carcinoma in contrast to follicular and anaplastic carcinoma show a low rate of loss of heterozygosity (LOH) at the chromosomal sites tested (Ward et al ., 1998; Trovato et al ., 1999).…”

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confidence: 99%

A novel chromosomal translocation t(3;5)(q12;p15.3) and loss of heterozygosity on chromosome 22 in a multifocal follicular variant of papillary thyroid carcinoma presenting with skin metastases

Smit¹,

Zelderen-Bhola

Merx

et al. 2001

Clinical Endocrinology

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Classic genetic rearrangements in papillary carcinoma of the thyroid involve the RET- or TRK proto-oncogenes. We report a novel chromosomal translocation t(3;5)(q12;p15.3), confirmed by fluorescence in situ hybridization, in a multifocal follicular variant of a papillary carcinoma of the thyroid in a 79-year-old woman, with skin metastases as a presenting symptom. Three years earlier, another cutaneous metastasis on her scalp was misdiagnosed as hidradenoma. Four tumour foci were recognized in the thyroid, two with a follicular variant of papillary carcinoma. To detect loss of heterozygosity, 14 chromosomes were investigated with 59 microsatellite markers. A clonal relationship was detected between the two foci of tumour in the thyroid gland containing follicular variant of papillary carcinoma and one of the skin lesions tested, all demonstrating loss of heterozygosity (LOH) in the same region of chromosome 22. Based on earlier reports, the low rate of LOH detected is in agreement with the diagnosis papillary carcinoma of the thyroid. Whole body scintigraphy performed after ablative therapy with radioiodine revealed multiple metastases in the lungs and skeleton. After repeated radioiodine therapy, thyroglobulin under thyroxine suppression became undetectable and post-therapeutic scintigraphy revealed important regression of metastases.

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Cytogenetic studies on 19 papillary thyroid carcinomas

Cited by 20 publications

References 27 publications

Genome-Wide Appraisal of Thyroid Cancer Progression

Genome-Wide Appraisal of Thyroid Cancer Progression

Analysis of nuclear and mitochondrial DNA alterations in thyroid and renal oncocytic tumors

A novel chromosomal translocation t(3;5)(q12;p15.3) and loss of heterozygosity on chromosome 22 in a multifocal follicular variant of papillary thyroid carcinoma presenting with skin metastases

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