| Project/Area Number |
04454276
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pediatrics
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| Research Institution | University of Tokyo Hospital, Faculty of Medicine, University of Tokyo |
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Principal Investigator |
BESSHO Fumio University of Tokyo Hospital, Faculty of Medicine, University of Tokyo, Associate Professor, 医学部(病), 助教授 (40010285)
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| Co-Investigator(Kenkyū-buntansha) |
HIRAI Hisamaru University of Tokyo Hospital, Faculty of Medicine, University of Tokyo, Assistan, 医学部(病), 講師 (90181130)
KAMOSHITA Shigehiko University of Tokyo Hospital, Faculty of Medicine, University of Tokyo, Professo, 医学部(病), 教授 (60048973)
HAYASHI Yasuhide University of Tokyo Hospital, Faculty of Medicine, University of Tokyo, Assistan, 医学部(病), 講師 (30238133)
小島 美由紀 (小林 美由紀) 東京大学, 医学部(病), 助手 (60205391)
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| Project Period (FY) |
1992 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥6,300,000 (Direct Cost: ¥6,300,000)
Fiscal Year 1994: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1993: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1992: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Cancer high risk / tumor suppressor gene / p53 gene / p16 gene / p15 gene / epidemilogy / cancer clustering / childhood cancer / Rb遺伝子 / DCC遺伝子 / DAN遺伝子 / 神経芽腫 / homozygous deletion / 高危険体質 / 癌抑制遺伝子 / P53遺伝子 / RB遺伝子 / 多重がん / 点突然変異 / 小児固型腫瘍 / 小児白血病 / がん発生体質 / t(li19) / ユーイング肉腫 / 細胞株 |
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| Research Abstract |
Several anti-oncogenes were studied for common childrhood cancers. Anti-oncogenes studied included p53 gene, p16/15 genes, Rb gene, DCC gene and NF1 gene. Generally, these genes tend to be mutated or deleted in cell lines more often than fresh tumor cells and in tumor cells of advanced stages and of relapsed cases. However, frequency of abnormalities of these genes varied among different tumor types. In spite of neural crest origin of both tumors, abnormalities of p53 genes were frequent seen in Ewing sarcoma but not in neuroblastoma. Abnormalities of p16/p15 genes were more frequently seen in common ALL antigen-positive acute lymphoblatic leukemia (ALL) without chromosome transloction, t (1 ; 19), than in ALL with this translocation. These abnormalies were also commn in T-ALL.
Materials of non-Hodgkin lymphoma developed in 3 siblings and lung cancer in 11-year-old boy were negative for abnormalities of p53 gene. In these patients other tumor suppressor genes might be responsible for familial or rare development of their cancers.
In addition to molecular study, epidemiological study was performed to find out familial clustering of common childhood cancers and constitutional factors affecting development of these cancers, using data of Japan Children's Cancer Registry (JCCR). We found that distribution of tumor types among family of children with cancer was different from that of general population. Brain tumor was more often seen in family of cancer, but colon cancer, lung cancer and cancer of bile duct were less often seen. Distribution of cancer types among parents and siblings whose family had cancers in 3 consecutive generations was different from cancer types of general population only in female and breast cancer and uterus cancer were more frequently seen.
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