Frequent occurrence of cytogenetic abnormalities in sporadic nonmedullary thyroid carcinoma

Jenkins, Robert B.; Hay, Ian; Herath, John F.; Schultz, Cloann G.; Spurbeck, Jack L.; Grant, Clive S.; Goellner, John R.; Dewald, Gordon W.

doi:10.1002/1097-0142(19900915)66:6<1213::aid-cncr2820660622>3.0.co;2-9

Cited by 87 publications

(49 citation statements)

References 23 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: 85%

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: 85%

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

et al. 1996

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“…This patient also had nesidioblastosis, a supposedly paraneoplastic disorder of endocrine pancreatic cells that proliferate reactively in close contact with and complicating disease processes of the exocrine pancreas, e.g., pancreatic carcinomas (Eusebi et al, 1981;Kloppel & Heintz, 1984;Permert et al, 1991). Rearrangements of lOq have previously been found in, e.g., thyroid tumours -the only endocrine neoplasms that have been cytogenetically examined in any numbers -and it has been suggested that they characterize nonmedullary carcinomas, especially those whose growth pattern is papillary (Jenkins et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Karyotypic abnormalities in tumours of the pancreas

et al. 1993

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Summary Short-term cultures from 20 pancreatic tumours, three endocrine and 17 exocrine, were cytogenetically analysed. All three endocrine tumours had a normal chromosome complement. Clonal chromosome aberrations were detected in 13 of the 17 exocrine tumours: simple karyotypic changes were found in five carcinomas and numerous numerical and/or structural changes in eight. When the present findings and those previously reported by our group were viewed in conjunction, the most common numerical imbalances among the 22 karyotypically abnormal pancreatic carcinomas thus available for evaluation turned out to be, in order of falling frequency, -18, -Y, + 20, + 7, + 11 and -12. Imbalances brought about by structural changes most frequently affected chromosomes I (losses in lp but especially gains of lq), 8 (in particular 8q gains but also 8p losses), and 17 (mostly 17q gain but also loss of 17p). Chromosomal bands lp32, 1q1O, 6q21, 7p22, 8p2l, 8ql 1, 14pl 1, l5q10-1 1, and 17qll were the most common breakpoint sites affected by the structural rearrangements. Abnormal karyotypes were detected more frequently in poorly differentiated and anaplastic carcinomas than in moderately and well differentiated tumours.Pancreatic carcinoma accounts for about 10% of malignancies of the digestive organs and the outcome is fatal in more than 95% of the cases.

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“…1-6) is located on human chromosome 10q21, where potential tumor suppressor genes (TSGs) have been hypothesized to exist for prostate and other cancers (5,(7)(8)(9)(10)(11)(12)(13)(14)(15). However, the specific relevance of the ANX7 gene for cancer only became apparent after we created a knockout for this gene in the mouse (16).…”

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confidence: 99%

ANX7, a candidate tumor suppressor gene for prostate cancer

Srivastava

Bubendorf

Srikantan

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

120

101

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The ANX7 gene is located on human chromosome 10q21, a site long hypothesized to harbor a tumor suppressor gene(s) (TSG) associated with prostate and other cancers. To test whether ANX7 might be a candidate TSG, we examined the ANX7-dependent suppression of human tumor cell growth, stage-specific ANX7 expression in 301 prostate specimens on a prostate tissue microarray, and loss of heterozygosity (LOH) of microsatellite markers at or near the ANX7 locus. Here we report that human tumor cell proliferation and colony formation are markedly reduced when the wild-type ANX7 gene is transfected into two prostate tumor cell lines, LNCaP and DU145. Consistently, analysis of ANX7 protein expression in human prostate tumor microarrays reveals a significantly higher rate of loss of ANX7 expression in metastatic and local recurrences of hormone refractory prostate cancer as compared with primary tumors (P ‫؍‬ 0.0001). Using four microsatellite markers at or near the ANX7 locus, and laser capture microdissected tumor cells, 35% of the 20 primary prostate tumors show LOH. The microsatellite marker closest to the ANX7 locus showed the highest rate of LOH, including one homozygous deletion. We conclude that the ANX7 gene exhibits many biological and genetic properties expected of a TSG and may play a role in prostate cancer progression.cancer genetics ͉ chromosome 10q21 ͉ loss of heterozygosity T he gene for annexin 7 (ANX7 ‡ ‡ , synexin; refs. 1-6) is located on human chromosome 10q21, where potential tumor suppressor genes (TSGs) have been hypothesized to exist for prostate and other cancers (5, 7-15). However, the specific relevance of the ANX7 gene for cancer only became apparent after we created a knockout for this gene in the mouse (16). Although the homozygous Anx7(Ϫ͞Ϫ) deletion is embryonically lethal, the phenotype of the Anx7(ϩ͞Ϫ) heterozygote includes calcium signaling deficits and growth defects such as gigantism, and selective organomegaly. As these mice aged, we also began to observe a profoundly increased frequency of disparate spontaneous tumors in both male and female Anx7(ϩ͞Ϫ) mutants (17).Because of these observations, and the chromosomal location of the gene, we hypothesized that ANX7 might be a candidate TSG associated with 10q21 locus. Commonly, TSGs can suppress growth of tumor cells, in vitro, and are frequently inactivated by mutations, deletions, or loss of expression in tumors, in vivo. In addition, loss of heterozygosity (LOH) often is observed for these genes in clinical tumor specimens. Therefore, to test this hypothesis for the ANX7 gene, we analyzed the action of the ANX7 gene on colony formation by human tumor cell lines. We also examined the expression of the ANX7 protein in hundreds of prostate cancers by using tumor tissue microarray technology. Finally, we tested a panel of primary and metastatic prostate cancers for evidence of LOH.In this paper we show that the ANX7 gene suppresses the growth of the prostate tumor cell lines DU145 and LNCaP. Consistently, in a prostate tissue microarray, we...

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Frequent occurrence of cytogenetic abnormalities in sporadic nonmedullary thyroid carcinoma

Cited by 87 publications

References 23 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

Karyotypic abnormalities in tumours of the pancreas

ANX7, a candidate tumor suppressor gene for prostate cancer

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