2007 Fiscal Year Final Research Report Summary
Diagnostic demonstration of telomere measurement anaplastic cancer arose from differentiated cancer in the thyroid by tissue quantitative fluorescence in situ hybridization
| Project/Area Number |
18591432
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Nihon University (2007)
The University of Tokyo (2006) |
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Principal Investigator |
KAMMORI Makoto Nihon University, School of Medicine, Concurrent Assistant Professor (50292868)
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| Co-Investigator(Kenkyū-buntansha) |
AMANO Sadao Nihon University, School of Medicine, Associate Professor (80159459)
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| Project Period (FY) |
2006 – 2007
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| Keywords | tissue O-FISE / Thyroid / Telomere / テロメラーゼ |
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| Research Abstract |
We have developed a novel method for evaluating telomere length using tissue quantitative fluorescence in situ hybridization (Q-FISH). Our method can be used to distinguish between benign and malignant tissue in esophageal lesions (Oncology, 2006). We demonstrated to evaluate telomere length in papillary carcinoma and normal thyroid tissue by Q-FISH. The average TCR in the papillary carcinoma cell was significantly lower than that in the follicular epithelial cell and fibroblast cells in the thyroid (P<0.05). The advanced papillary carcinoma of more than T2 (more than 2 cm) and Nlb (lateral area of metastasis of lymph-node) was significantly lower telomere length than the early papillary carcinoma of less than T2 and Nlb. These results suggested our TCR method can be used to distinguish between advanced and early carcinoma of the thyroid. On the other hand, one of the most aggressive human malignancies, anaplastic thyroid carcinoma (ATC), has an extremely poor prognosis that may be exp
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lained by its genomic instability. We hypothesized that the very rapid cell turnover observed in ATC might accelerate telomere shortening and chromosomal instability associated with tumor cell malignancy. To compare and measure chromosomal aberrations and telomere shortening in an anaplastic thyroid cancer cell line, OCUT-1, we applied quantitative fluorescence in situ hybridization (Q-FISH) techniques. OCUT-1 cells display several chromosomal abnormalities, but have a near-normal chromosome complement of 46, XX, making it easy to analyze the karyotype. The karyotype showed 50, XX, +7, +11, der(11)t(3 ; 11)(q23 ; q23)x2, del(12)(p11.2p12), +20, +1mar. We analyzed carefully the abnormalities in karyotype of OCUT-1 associated with telomere shortening on each chromosomes and expression of subtelomeres. Subtelomeres on the abnormal chromosome der(11)t(3 ; 11)(q23 ; q23)x2 also showed loss of signals on 11p, but there was no loss of signals in the cytogenetically normal trisomies 7 and 20 or the abnormal chromosome del(12)(p11.2p12). Subtelomeres of 3q had eight signals, one pair remaining in place on 3q and another pair on the abnormal 11p. Our findings suggest that telomere shortening and subtelomere loss are correlated with genetic instability in this anaplastic thyroid carcinoma cell line. Less
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Research Products
(10 results)
