| Project/Area Number |
11470427
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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 |
Surgical dentistry
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
NOTANI Ken-ichi Hokkaido Univ., Grad. School of Dental Medicine, 大学院・歯学研究科, 助教授 (70113602)
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| Co-Investigator(Kenkyū-buntansha) |
CHIBA Itsuo Hokkaido Univ., Grad. School of Dental Medicine, 歯学部・附属病院, 講師 (50250460)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥7,800,000 (Direct Cost: ¥7,800,000)
Fiscal Year 2001: ¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 2000: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1999: ¥3,500,000 (Direct Cost: ¥3,500,000)
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| Keywords | secondary primary tumors / Multiple Cancer / oral squamous cell carcinoma / precancerous lesion / field cancerization theory / p53 genene / clonality / field cancerlzation theory / p53遺伝子 |
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| Research Abstract |
The development of second primary tumors (SPTs) in patients with head and neck squamous cell carcinoma (HNSCC) has become increasingly important in treatment of the disease. The determination of SPTs is currently based on clinical and histologic parameters. However, the genetic origin in some SPTs has been challenged recently. Evidence has been accumulated to indicate a common clonal origin of SPTs as the primary index tumors in upper aerodigestive tract. To determine genetic relationship between multiple oral cancerous and precancerous lesions (MOC&P), we analyzed 102 MOC＆P (synchronous and metachronous) from 26 Japanese patients (average 4 lesions/patient) for patterns of microsatellite alterations (MA) using 7 markers at chromosomes 3pl4, 9p21, and 17pl3 where MA occurs early in oral carcinogenesis. Loss of heterozygosity was found in 50 % (39/79), 57 % (56/99), and 37 % (30/81) MOC＆P at 3p14, 9p21, and 17p13 respectively.
Microsatellite instability was observed in 33 % of the lesions in at least on marker. Patterns of MA were distinct in all cases with multiple precancerous lesions, suggesting most of these lesions develop independently. However, in 6 patients with multiple invasive cancerous lesions, three had identical MA patterns in at least one locus, suggesting possibility of same clonal origin in these tumors from the patients. Our data support the hypothesis that multiple cancers in oral cavity are genetically related in some patients but multiple clonal origins also exist in patients with HNSCC. Furthermore, the data indicate that multiple oral precancerous leasions are mainly multiple clonal.
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