Deletion of 3p25→pter in a primary follicular thyroid carcinoma and its metastasis

Roque, Lúcia; Castedo, Sérgio; Clode, A.; Soares, Jorge

doi:10.1002/gcc.2870080311

Cited by 39 publications

(25 citation statements)

References 8 publications

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“…We used four markers at chromosome 3p25-14. LOH was found in 20% of the tumors, but only a single tumor showed LOH at this location and not on chromosome lOq, which is in contrast to earlier reports (Jenkins et al 1990;Herrmann et al 1991;Roque et al 1993). Although small interstitial deletions cannot be excluded, we conclude that LOH on 3p is probably not a prerequisite for development of follicular thyroid carcinomas.…”

Section: Discussioncontrasting

confidence: 87%

“…Former studies of thyroid tumors have implicated LOH at chromosome Ilql3 in follicular adenomas (Matsuo et al 1991), at chromosome 3p in follicular carcinomas (Herrmann et al 1991;Roque et al 1993), and at chromosome lOq in atypical adenomas and carcinomas (Zedenius et al 1995a). However, the number of carcinomas was small in the latter study.…”

Section: Discussionmentioning

confidence: 67%

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Deletions of the long arm of chromosome 10 in progression of follicular thyroid tumors

et al. 1996

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Previous studies of follicular thyroid tumors have shown loss of heterozygosity (LOH) on the short arm of chromosome 3 in carcinomas, and on chromosome 10 in atypical adenomas and carcinomas, but not in common adenomas. We studied LOH on these chromosomal arms in 15 follicular thyroid carcinomas, 19 atypical follicular adenomas and 6 anaplastic (undifferentiated) carcinomas. Deletion mapping of chromosome 10 using 15 polymorphic markers showed that 15 (37.5%) of the tumors displayed LOH somewhere along the long arm. Thirteen of these tumors showed deletions involving the telomeric part of chromosome lOq, distal to D10S187. LOH on chromosome 3p was found in 8 (20%) cases. Seven of these also showed LOH on chromosome lOq. In eight cases LOH was seen on chromosome lOq but not 3p. In comparison, the retinoblastoma gene locus at chromosome 13q showed LOH in 22% of the tumors. Most of these also had deletions on chromosome lOq. The results indicate that a region at the telomeric part of 1 Oq may be involved in progression of follicular thyroid tumors.

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Section: Discussioncontrasting

confidence: 87%

Section: Discussionmentioning

confidence: 67%

Deletions of the long arm of chromosome 10 in progression of follicular thyroid tumors

et al. 1996

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“…11-14,24 -26 The short arm of chromosome 3 has been reported to contain rearrangements, and a minimal common deleted region at 3p25-pter has been detected. 14,25 Jenkins et al 12 reported aberrations that were mainly deletions in three follicular carcinomas investigated, and we found a loss of chromosome 22 in 7 of the 13 follicular carcinomas studied. 27 Similarly, only few anaplastic carcinomas with an abnormal karyotype have been described, 12,28 and the molecular mechanisms involved in the genesis of this type of thyroid carcinoma are unknown.…”

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confidence: 76%

DNA Copy Number Changes in Thyroid Carcinoma

Hemmer¹,

Wasenius²,

Knuutila

et al. 1999

The American Journal of Pathology

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The genetic changes leading to thyroid cancer are poorly characterized. We studied DNA copy number changes by comparative genomic hybridization (CGH) in 69 primary thyroid carcinomas. In papillary carcinoma , DNA copy number changes were rare (3 of 26 , 12%). The changes were all gains , and they were associated with old age (P ‫؍‬ 0.01) and the presence of cervical lymph node metastases at presentation (P ‫؍‬ 0.08). DNA copy number changes were much more frequent in follicular carcinoma (16 of 20, 80%) than in papillary carcinoma (P < 0.0001), and follicular carcinomas had more often deletions (13/20 versus 0/26 , P < 0.0001). Loss of chromosome 22 was common in follicular carcinoma (n ‫؍‬ 7 , 35%) , it was more often seen in widely invasive than in minimally invasive follicular carcinoma (54% versus 0% , P ‫؍‬ 0.04) , and it was associated with old age at presentation (P ‫؍‬ 0.01). In three of the four patients with follicular carcinoma who died of cancer , the tumor had loss of chromosome 22. DNA copy number changes were found in 5 (50%) of the 10 medullary carcinomas studied. Four of these five carcinomas had deletions , and in two of them there was deletion of chromosome 22. Eleven (85%) of the thirteen anaplastic carcinomas investigated had DNA copy number changes , of which five had deletions , and one had deletion of chromosome 22. The most common gains in anaplastic carcinoma were in chromosomes 7p (p22-pter , 31%) , 8q (q22-qter , 23%) , and 9q (q34-qter , 23%). We conclude that DNA copy number changes are frequent in follicular , medullary, and anaplastic thyroid carcinoma but rare in papillary carcinoma when studied by CGH. Loss of chromosome 22 is particularly common in follicular carcinoma , and it is associated with the widely invasive type. (Am J Pathol 1999, 154:1539 -1547)The great majority of all thyroid cancers are either papillary, follicular, or anaplastic carcinomas, which are thought to be derived from follicular cells. Only 5% to 10% are medullary carcinomas, which originate from the C-cells.1 This histopathological classification of thyroid carcinomas into four major subtypes has been considered as established, and each of the four entities have typical clinical features. Papillary carcinoma frequently gives rise to cervical lymph node metastases, but distant metastases are rare. This pattern is reversed in follicular carcinoma, which often has distant bone metastases, but cervical lymph node metastases are rare. Papillary and follicular carcinoma are frequently found in the same thyroid as anaplastic carcinoma, suggesting that some anaplastic carcinomas originate from pre-existing differentiated carcinoma. 2,3The molecular genetic events in the evolution of different types of thyroid carcinomas are poorly characterized. However, the central role of mutations in the RET protooncogene, located at 10q11.2, in the genesis of hereditary medullary thyroid carcinoma is now well recognized, and used in screening of this disorder. More than 95% of patients with MEN 2A have missense germ line mu...

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“…This pattern appears different from the single pathway of step-wise genetic progression envisioned for colorectal and pancreatic carcinomas, which nearly all contain APC 10,42,43 or KRAS 44 mutations, respectively. Although PPAR␥ rearrangement and aneuploidy appear to arise independently in early follicular carcinomas, they can co-exist 16,18 (TG Kroll and JA Fletcher, unpublished data). In two such published cases, PPAR␥ rearrangement and aneuploidy appeared together in recurrent 16 and metastatic 18 follicular cancers.…”

Section: Discussionmentioning

confidence: 99%

“…15,[17][18][19]21,22 Recent studies have shown that t(2;3)(q13;p25) forms a PAX8-PPAR␥ gene fusion 21 that is present in a subset of follicular carcinomas. 21,30,31 Here, we used interphase FISH with probes flanking the PPAR␥ gene to investigate these 3p25 rearrangements.…”

Section: Detection Of 3p25/ppar␥ Rearrangement and 3p25 Aneusomymentioning

confidence: 99%