1989 Fiscal Year Final Research Report Summary
DEVELOPMENT OF DIAGNOSIS FOR PEDIATRIC CANCER WITH ANTI N-MYC ANTIBODY
| Project/Area Number |
63570459
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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 | TOHO UNIVERSITY SCHOOL OF MEDICINE |
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Principal Investigator |
SHIMATAKE Hiroyuki TOHO UNIVERSITY SCHOOL OF MEDICINE, ASSOCIATE PROFESSOR, 医学部, 助教授 (40010110)
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| Co-Investigator(Kenkyū-buntansha) |
AOKI Tsugutoshi TOHO UNIVERSITY SCHOOL OF MEDICINE, PROFESSOR, 医学部, 教授 (50057585)
KIKICHI Takanobu TOHO UNIVERSITY SCHOOL OF MEDICINE, RESEARCH ASSISTANT, 医学部, 助手 (50177797)
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| Project Period (FY) |
1988 – 1989
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| Keywords | PEDIATRIC CANCER / ANTI N-MYC ANTIBODY / N-MYC PROTEIN / NEUROBLASTOMA / RETINOBLASTOMA / IMMUNOHISTOCHEMISTRY / WESTERN BLOTTING / N-MYC GENE AMPLIFICATION |
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| Research Abstract |
The N-myc gene belongs to the myc oncogene family and is known to express in certain pediatric cancers, including neuroblastoma and retinoblastoma. In particular, neuroblastoma is known for the amplification of the gene. There exists positive correlation between its amplification and clinical course of the disease. There have been discovered, however, cases in which the N-myc gene was not amplified, yet they took unfavorable courses. It seemed more likely that the expression of the N-myc gene was more important rather than the amplification per se to evaluate the degree of malignancy of these diseases.
We have experienced a malignant case of neuroblastoma which showed no sign of N-myc gene amplification on Southern blot analysis. This case, however, showed an evidence of N-myc protein expression. This suggested that an increased expression of the N-myc protein was caused not only by the amplification mechanism alone. It also suggested that tests for N-myc gene amplification was not enough to evaluate malignancy of neuroblastoma cases and that it would be necessary to test an amount of N-myc protein expression as well. We also examined six cases of retinoblastomas. In all cases examined, N-myc protein was expressed even in the absence of the N- myc gene amplification. It was revealed that clinical retinoblastomas were represented by very few involvement of the N-myc gene amplification compared to clinical neuroblastomas (30%).
In addition, we have engineered pan-myc antigen in order to raise anti pan-myc antibody as well as N-pan-myc fusion protein for the standard protein, which are intended for clinical tests to evaluate the extent of the N-myc gene expression in clinical situations. These proteins were produced in the E. coli expression vector system (pCA221, pCA216), purified and used to raise the antibody. New methods to quantitate the amount of the N-myc protein will be shortly available.
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