1996 Fiscal Year Final Research Report Summary
Analysis of Genomic Imprinting in Human Testicular Tumors
| Project/Area Number |
07457370
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Urology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
OGAWA Osamu Kyoto Univ.Urology, Instructor, 医学研究科, 助手 (90260611)
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| Co-Investigator(Kenkyū-buntansha) |
TERAI Akito Kyoto Univ.Urology, Instructor, 医学研究科, 助手 (50243019)
KAKEHI Yoshiyuki Kyoto Univ.Urology, Assistet Professor, 医学研究科, 講師 (20214273)
TERACHI Toshiro Kyoto Univ.Urology, Assistet Professor, 医学研究科, 講師 (50207487)
YOSHIDA Osamu Kyoto Univ.Urology, Professor, 医学研究科, 教授 (70025584)
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| Project Period (FY) |
1995 – 1996
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| Keywords | Testicular Tumor / Gemomic Imprinting |
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| Research Abstract |
Recent molecular analyzes have demonstrated that epigenetic alterations such as genomic imprinting might have an important role in human tumorigenesis in addition to specific genetic alterations. In order to clarify the role of genetic and/or epigenetic alterations in the tumorigenesis of testicular germ cell tumors (GCTs), 42 primary testicular GCTs were analyzed with regard to specific chromosomal losses and their parental origin. High incidence of loss of heterozygosity (LOH) were demonstrated on chromosomes 1p, 3p, 11p, and 17p : 9/19 (47%), 18/39 (46%), 13/40(33%) and 20/36 (56%), respectively. No correlation, however, was found between the frequency of LOH on any chromosomes and clinicopathological features. Regarding the parental origin of the lost allele at these chromosomes, preferential loss was not demonstrated in the present study. To clarify the imprinting status in GCTs, allele-specific expression of H19 gene, which is a paternally imprinted gene on chromosome 11p, was analyzed. All of 11 tumors without LOH at this locus showed biallelic expression of H19. Based on the recent study demonstrating the biallelic expression of H19 in primordial germ cells and spermatogonias in the mouse germ line, these results might suggest that biallelic expression of H19 in testicular GCTs simply reflect the characteristics of original germ cells in which the imprinting marking has been erased and not been newly established rather than because of loss of imprinting during the tumorigenesis.
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