Cytogenetic study of a papillary thyroid carcinoma with a rearranged chromosome 10

Herrmann, Marille E.; Mohamed, Anwar N.; Talpos, Gary B.; Wolman, Sandra R.

doi:10.1016/0165-4608(91)90154-m

Cited by 21 publications

(6 citation statements)

References 26 publications

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“…Pooled results of an overall breakpoint analysis of the structural chromosome aberrations are summarized in Figure 3 and compared with literature data on cytogenetic changes in papillary carcinomas 6, 18–25…”

Section: Resultsmentioning

confidence: 99%

Karyotypic characterization of papillary thyroid carcinomas

Roque

Nunes

Ribeiro

et al. 2001

Cancer

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BACKGROUND Cytogenetic studies performed in papillary thyroid carcinoma (PTC) identified chromosome 10q rearrangements with breakpoints at 10q11.2 as the most frequent aberrations in these tumors. In the current study, the authors aimed to identify other chromosomal abnormalities nonrandomly associated with papillary thyroid carcinomas. METHODS Cytogenetic analysis was performed on 94 papillary thyroid carcinomas after short‐term culture of the tumors sterile fragments. RESULTS Clonal chromosomal changes were found in 37 tumors (40%). Structural cytogenetic abnormalities were observed in 18 carcinomas. Chromosomes 1, 3, 7, and 10 were the most frequently involved in rearrangements. Pooled results of the breakpoints detected in these tumors, as well as those described in the literature, allowed the authors to verify as the most common breakpoint loci 1p32‐36, 1p11‐13, 1q, 3p25‐26, 7q34‐36, and 10q11.2. The correlation between the karyotype features of the 94 PTCs and the histologic data revealed that some PTC follicular variants were characterized by chromosomal aberrations commonly found in thyroid follicular adenomas: a del(11)(q13q13), a t(2;3)(q13;p35), and gains of chromosomes 3, 5, 7, 9, 12, 14, 17, and 20. In the tall cell PTC variant group, 4 of the 7 tumors presented clonal cytogenetic changes, 3 (75%) of which were characterized by anomalies of chromosome 2 that lead to a overrepresentation of the long arm of this chromosome. Noted also in these series was an association between complex karyotypes and tumors with poorly differentiated histiotypes. CONCLUSIONS In this study, the authors report chromosome 1p32‐36, 1p11‐13, 3p25‐26, and 7q32‐36 as novel breakpoint cluster regions in PTC, and they suggest that there are cytogenetic changes preferentially associated with the follicular and tall cell PTC variants. Cancer 2001;92:2529–38. © 2001 American Cancer Society.

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Section: Resultsmentioning

confidence: 99%

Karyotypic characterization of papillary thyroid carcinomas

Roque

Nunes

Ribeiro

et al. 2001

Cancer

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“…29 Chromosomal rearrangements in epithelial tumors are well described for lesions of the thyroid including carcinomas and adenomas. 3,6,8,21,27,30 Of those, t(2;3)(q13;p25) is a recurrent finding in human follicular thyroid adenomas and carcinomas. 5,21,22,31 Fine mapping and molecular characterization of the 2q13 and 3p25 translocation breakpoint regions revealed fusion between exons 1 to 7, 1 to 8, or 1 to 9 of PAX8 (2q13) and exons 1 to 6 of PPARg (3p25).…”

Section: Discussionmentioning

confidence: 99%

Evidence for a 3p25 Breakpoint Hot Spot Region in Thyroid Tumors of Follicular Origin

Drieschner

Belge

Rippe

et al. 2006

Thyroid

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Epithelial tumors of the thyroid are cytogenetically well-investigated tumors. So far, the main cytogenetic subgroups, characterized by trisomy 7 and by rearrangements of either 19q13 or 2p21, respectively, have been described. Recently, we have been able to describe the involvement of a novel gene called THADA in benign thyroid lesions with 2p21 rearrangements. Other fusion genes found in thyroid lesions are RET/PTC and PAX8/PPAR(gamma). The latter occurs in follicular thyroid carcinomas with a t(2;3)(q13;p25). Here we present molecular-cytogenetic and cytogenetic investigations on a follicular thyroid adenoma with a t(2;20;3)(p21;q11.2; p25). In this case, an intronic sequence of PPAR(gamma) is fused to exon 28 of THADA. We used BAC clones containing the genomic sequence of PPARgamma for fluorescence in situ hybridization to confirm the localization of the breakpoint within intron 2 of PPAR(gamma) . Our findings suggest that the close surrounding of PPAR(gamma) is a breakpoint hot spot region, leading to recurrent alterations of this gene in thyroid tumors of follicular origin including carcinomas as well as adenomas with or without involvement of PAX8.

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“…Even though it usually pursues an indolent course, more aggressive tumors have been observed in some adult cases and, in particular, among the childhood cases from Belarus (Fugazzola et al, 1995;Nikiforov et al, 1995). Rearrangements of chromosomes 1 and 10 are frequently observed cytogenetic changes in PTC (Bongarzone et al, 1989(Bongarzone et al, , 1993Herrmann et al, 1991a;Jossart et al, 1995), while loss of heterozygosity (LOH) for several loci on chromosome 3 had initially been reported only in follicular TC (Herrmann et al, 1991b). Adult PTC studies revealed clonal structural chromosomal abnormalities involving chromosome 10q11.…”

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Molecular cytogenetic characterization of chromosome 9-derived material in a human thyroid cancer cell line

Tuton

Ito

Chu

et al. 2006

Cytogenet Genome Res

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The incidence of papillary thyroid carcinoma (PTC) increases significantly after exposure of the head and neck region to ionizing radiation, yet we know neither the steps involved in malignant transformation of thyroid epithelium nor the specific carcinogenic mode of action of radiation. Such increased tumor frequency became most evident in children after the 1986 nuclear accident in Chernobyl, Ukraine. In the eight years following the accident, the average incidence of childhood PTCs (chPTC) increased 70-fold in Belarus, 200-fold in Gomel, 10-fold in the Ukraine and 50-fold in Tschnigov, Kiev, Rovno, Shitomyr and Tscherkassy compared to the rate of about 1 tumor incidence per 106 children per year prior to 1986 (Likhtarev et al., 1995; Sobolev et al., 1997; Jacob et al., 1998). To study the etiology of radiation-induced thyroid cancer, we formed an international consortium to investigate chromosomal changes and altered gene expression in cases of post-Chernobyl chPTC. Our approach is based on karyotyping of primary cultures established from chPTC specimens, establishment of cell lines and studies of genotype-phenotype relationships through high resolution chromosome analysis, DNA/cDNA micro-array studies, and mouse xenografts that test for tumorigenicity. Here, we report the application of fluorescence in situ hybridization (FISH)-based techniques for the molecular cytogenetic characterization of a highly tumorigenic chPTC cell line, S48TK, and its subclones. Using chromosome 9 rearrangements as an example, we describe a new approach termed ‘BAC-FISH’ to rapidly delineate chromosomal breakpoints, an important step towards a better understanding of the formation of translocations and their functional consequences.

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Cytogenetic study of a papillary thyroid carcinoma with a rearranged chromosome 10

Cited by 21 publications

References 26 publications

Karyotypic characterization of papillary thyroid carcinomas

Karyotypic characterization of papillary thyroid carcinomas

Evidence for a 3p25 Breakpoint Hot Spot Region in Thyroid Tumors of Follicular Origin

Molecular cytogenetic characterization of chromosome 9-derived material in a human thyroid cancer cell line

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