간모세포종에서 p73, APC, p53 이형접합성의 소실 ( Loss of Heterozygosity of p73, APC, and p53 in Hepatoblastoma ) |
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Loss of Heterozygosity of p73, APC, and p53 in Hepatoblastoma |
Han Seong Kim,Young Mi Jung,Mi Ran Kim,Jung Young Lee,Mi Sook Lee,Ja June Jang |
Department of P athology, Seoul National University College of Medicine
and Catholic Univers ity Medical College1, Seoul, Korea |
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ABSTRACT |
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Background/Aims : The status of tumor suppression gene can be assessed indirectly by analyzing the loss
of heterozygosity. Hepatoblastoma is a malignant liver tumor in childhood. To find the molecular carcinogenetic
mechanism of hepatoblastoma, loss of heterozygosity (LOH) of p73, APC and p53 was studied. Materials and
methods : Hepatoblastoma tissues from thirty- three cases were collected by lobectomy or tumorectomy. On
H- E stained sections, normal and tumor cells were microdissected separately and LOH analysis was perfomed
using 8 markers: six of p73, one of APC and one of p53. Results : Number of cases showing at least one LOH
in six p73 markers was four out of twenty- six (15.4%): each LOH frequencies in D1S160, D1S170, D1S199,
D1S228, D1S243 and D1S253 were in order of 7.7%, 0%, 9.1%, 0%, 12.5% and 0%. LOH frequency of APC was
41.7% and that of p53 was 13.3%. Conclus ion : Low LOH frequency of p73 related markers indicates that p73
gene may not be implicated in carcinogenesis of hepatoblastoma. (Korean J Hepatol 1999;5:43-49) |
KeyWords:
Hepatoblastoma, loss of heterozygosity, p73, APC, p53, |
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