1992 Fiscal Year Final Research Report Summary
Analyses of Oncogene and Antioncogene in Childhood Cancer
| Project/Area Number |
03670477
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pediatrics
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| Research Institution | The University of Tsukuba |
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Principal Investigator |
KANEKO Michio Univ.Tsukuba Pediatr Surg Assoc Professor, 臨床医学系, 助教授 (60152807)
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| Project Period (FY) |
1991 – 1992
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| Keywords | Neuroblastoma / nm23 / N-myc / Topoisomerase / Gene amplification / in situ hybridization / Wilms' tumor |
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| Research Abstract |
1) An analysis of tumor suppressor gene Rb and WT1, transform suppressor gene Krev-1 and metastasis related gene nm23 in malignant solid tumor in childhood.
These tumor suppression related genes were analyzed by Southern and northern blotting methods in 112 childhood solid tumors and cell lines. The WT1 abnormalities could not be detected in all the specimens examined including 17 Wilms' tumors. Both alleles of the Rb gene were found defective only in one neuroblastoma tissue and osteogenic sarcoma. Krev-1 gene abnormalities were found in Ewing sarcoma, PNET and some neuroblastoma cells exclusively, suggesting the common characteristics among these tumors. The nm23 was found to be amplified and rearranged in one neuroblastoma tissue but its expression seemed to be normal.
2) Fluorescent in situ hybridization (FISH) of the N-myc gene
The FISH of the N-myc gene was performed in neuroblastoma and liposarcoma cell lines and normal lymphocyte. N-myc genes were assigned to double minutes and a chromosome in neuroblastoma cell line TS-N-2, but were assigned an HSR-like fashion on chromosomes in liposarcoma cell line TS-LS-1. The N-myc signals were dispersed in 2 clusters and 2 to 3 dots in resting cells. The FISH is a rapid and reliable method of determining N-myc copy number in clinical settings.
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