Kadota Masao, Tamaki Yasuhiro, Sekimoto Mitsugu, Fujiwara Yoshiyuki, Aritake Noriko, Hasegawa Seiichi, Kobayashi Tetsuro, Ikeda Takayuki, Horii Akira, Monden Morito
Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine, Japan.
Oncol Rep. 2003 Jan-Feb;10(1):35-8.
The aim of this study was to clarify the genetic alterations in anaplastic transformation of the thyroid cancer. A total of 17 thyroid cancers including 7 anaplastic and 10 papillary cancers were analyzed for loss of heterozygosity (LOH) on chromosome 16p and 18q. All the samples from anaplastic cancer showed LOH at one or more loci out of ten markers on 16p, and only two showed one LOH at two loci out of five markers on 18q. No LOH was found on either 16p or 18q in papillary cancers. D16S423, D16S418 and D16s406 on 16p13.3 were the most frequently deleted loci in anaplastic cancers, and the region around these may harbor the putative tumor suppressor gene related to anaplastic transformation of thyroid cancer.
本研究的目的是阐明甲状腺癌间变性转化中的基因改变。对总共17例甲状腺癌进行分析，其中包括7例间变性癌和10例乳头状癌，检测其16号染色体短臂（16p）和18号染色体长臂（18q）上的杂合性缺失（LOH）情况。所有间变性癌样本在16p上的10个标记中的一个或多个位点显示出杂合性缺失，而在18q上的5个标记中只有两个样本在两个位点显示出一个杂合性缺失。在乳头状癌的16p或18q上均未发现杂合性缺失。16p13.3上的D16S423、D16S418和D16S406是间变性癌中最常缺失的位点，这些位点周围的区域可能含有与甲状腺癌间变性转化相关的假定肿瘤抑制基因。
