Cytogenetic and molecular genetic studies of follicular and papillary thyroid cancers.

Herrmann, Marie A.; Hay, Ian; Bartelt, Duane; Ritland, S; Dahl, Richard J.; Grant, Clive S.; Jenkins, Robert B.

doi:10.1172/jci115472

Cited by 133 publications

(92 citation statements)

References 52 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: 88%

“…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%

“…To investigate further the frequency of 3p and lOq deletions in malignant follicular thyroid tumors and their putative impact on tumor progression, we studied LOH in several atypical adenomas, follicular carcinomas, and anaplastic carcinomas. In the study of Herrmann et al (1991), all six carcinomas investigated showed deletions of chromosome 3p, mainly involving large parts of the arm. We used four markers at chromosome 3p25-14.…”

Section: Discussionmentioning

confidence: 96%

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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: 88%

Section: Discussionmentioning

confidence: 67%

Section: Discussionmentioning

confidence: 96%

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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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“…Mutations activating the RAS proto-oncogenes represent an early step in the pathway of follicular thyroid tumorigenesis (Lemoine et al, 1989), whereas translocations involving the RET and TRK oncogenes, with consequent expression of aberrant fusion proteins as well as amplification and overexpression of the MET oncogene, have been implicated in papillary thyroid carcinogenesis (Bongarzone et al, 1989;Di Renzo et al, 1992). A role for tumoursuppressor genes has also been evidenced: anaplastic carcinomas have a high frequency of point mutations of the p53 gene, and deletions of chromosome 3p22 have been found in follicular carcinomas (Fagin et al, 1993;Hermann et al, 1996). Very recently, involvement of the PTEN/MMAC1 tumour-suppressor gene has been linked to the 10q22-23 loss of heterozygosity (LOH) observed in thyroid tumours of follicular histotype associated with Cowden's syndrome (Liaw et al, 1997).…”

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confidence: 99%

Microsatellite instability in thyroid tumours and tumour-like lesions

et al. 1998

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Summary Fifty-one thyroid tumours and tumour-like lesions were analysed for instability at ten dinucleotide microsatellite loci and at two coding mononucleotide repeats within the transforming growth factor β (TGF-β) type II receptor (TβRII) and insulin-like growth factor II (IGF-II) receptor (IGFIIR) genes respectively. Microsatellite instability (MI) was detected in 11 out of 51 cases (21.5%), including six (11.7%) with MI at one or two loci and five (9.8%) with Ml at three or more loci (RER + phenotype). No mutations in the TβRII and IGFIIR repeats were observed. The overall frequency of MI did not significantly vary in relation to age, gender, benign versus malignant status and tumour size. However, widespread MI was significantly more frequent in follicular adenomas and carcinomas than in papillary and Hürthle cell tumours: three out of nine tumours of follicular type (33.3%) resulted in replication error positive (RER + ), versus 1 out of 29 papillary carcinomas (3.4%, P = 0.01), and zero out of eight Hürthle cell neoplasms. Regional lymph node metastases were present in five MI-negative primary cancers and resulted in MI-positive in two cases.

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“…Allelotyping and LOH studies have shown that allele loss in FTC is frequently observed on chromosomes 3p, 3q, 10q, 11p, 11q, 13q, and 22q Herrmann et al, 1991;Matsuo et al, 1991;Zedenius et al, 1996). One candidate gene is the FHIT gene at 3p14.2 Sozzi et al, 1996) and may be the target of chromosomal 3p loss seen in these tumors.…”

Section: Discussionmentioning

confidence: 99%

Differential loss of heterozygosity at 7q31.2 in follicular and papillary thyroid tumors

et al. 1998

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We analysed 42 di erentiated thyroid tumors including 15 follicular adenomas (FA), 13 papillary thyroid cancers (PTC) and 14 follicular thyroid carcinomas (FTC) with 13 microsatellite markers speci®c for the long arm of human chromosome 7 within 7q31; this region is deleted frequently in several other tumor types. Overall, 20 of the 42 samples analysed (48%) displayed LOH with one or more of the markers tested. LOH was detected most frequently (78%) in FTC, the most malignant of the thyroid tumors. A smallest common deleted region (SCDR) was de®ned in this tumor typē anked by markers D7S480 and D7S490. This SCDR is distinct from D7S522, the most commonly deleted locus in many other tumors, which was deleted in only one FTC. D7S522 did show LOH in two of six informative PTCs. None of the PTC and only two of the FAs showed LOH in the FTC SCDR. Since FA is considered a premalignant stage of FTC, our results suggest that inactivation of a putative tumor suppressor at 7q31.2 may be acquired during adenoma to carcinoma progression. The absence of LOH at this locus amongst PTC suggests that inactivation of this tumor suppressor is speci®c for FTC. In conclusion, LOH at 7q31 is a frequent event in di erentiated thyroid cancer, and we have de®ned a 2 cM SCDR speci®c for FTC.

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Cytogenetic and molecular genetic studies of follicular and papillary thyroid cancers.

Abstract: Cytogenetic studies have shown frequent clonal abnormalities in papillary carcinoma (PFC)

Cited by 133 publications

References 52 publications

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

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

Microsatellite instability in thyroid tumours and tumour-like lesions

Differential loss of heterozygosity at 7q31.2 in follicular and papillary thyroid tumors

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