Tajiri T, Suita S, Shono K, Kubota M, Fujii Y, Oki E, Oda S, Maehara Y, Sugimachi K
Department of Pediatric Surgery, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Cancer Lett. 1998 Feb 13;124(1):59-63. doi: 10.1016/s0304-3835(97)00448-5.
It has recently been reported that mismatch repair enzymes, which are one type of DNA repair enzymes, are the causative genes for a major group of hereditary non-polyposis colon cancers (HNPCC). Abnormalities in the mismatch repair system can be monitored by observing instability at the microsatellite loci (MSI) in cancer cells. MSI has been reported not only in tumors associated with hereditary non-polyposis colorectal cancer but also in sporadic forms of various tumors. No correlation between pediatric malignant tumors and the mismatch repair system has yet been reported. In the present study, we examined the frequency of MSI in 21 neuroblastomas, which are the most common solid tumors in childhood, using a high resolution fluorescent microsatellite analysis. MSI on five microsatellite loci was detected in none of the 21 samples. Other mechanisms independent of mismatch repair deficiency may thus play a role in both tumorigenesis and the development of neuroblastoma.
最近有报道称，错配修复酶作为DNA修复酶的一种类型，是一大类遗传性非息肉病性结肠癌（HNPCC）的致病基因。错配修复系统的异常可以通过观察癌细胞微卫星位点（MSI）的不稳定性来监测。MSI不仅在与遗传性非息肉病性结直肠癌相关的肿瘤中被报道，也在各种肿瘤的散发性形式中被报道。儿科恶性肿瘤与错配修复系统之间的相关性尚未见报道。在本研究中，我们使用高分辨率荧光微卫星分析检测了21例神经母细胞瘤（儿童最常见的实体瘤）中MSI的频率。在21个样本中均未检测到5个微卫星位点上的MSI。因此，独立于错配修复缺陷的其他机制可能在神经母细胞瘤的肿瘤发生和发展中起作用。
