Wagata T, Ishizaki K, Imamura M, Shimada Y, Ikenaga M, Tobe T
Radiation Biology Center, Kyoto University, Japan.
Cancer Res. 1991 Apr 15;51(8):2113-7.
We have analyzed allelic deletion at 23 loci on 18 different chromosomes in 35 esophageal squamous cell carcinoma tissues by using restriction fragment length polymorphism markers. Loss of heterozygosity was detected on chromosomes 2, 3, 6, 7, 11-14, 16-18, 21, and 22, while no loss was detected on chromosomes 1, 4, and 8-10. Only the loss of chromosome 17p was detected with high frequency (45%), and losses on other chromosomes had frequencies of less than 22%. These losses with low frequencies might be random losses caused by chromosomal rearrangement during the course of tumor development and progression. On the contrary, the loss of 17p might play an important role in the development of esophageal squamous cell carcinoma, such as inactivation of a tumor suppressor gene. Amplification of the int-2 gene was observed in 39% of the tumors. However, no significant relationship between int-2 amplification and the deletion of any chromosome was detected.
我们利用限制性片段长度多态性标记，对35例食管鳞状细胞癌组织中18条不同染色体上的23个位点进行了等位基因缺失分析。在2号、3号、6号、7号、11 - 14号、16 - 18号、21号和22号染色体上检测到杂合性缺失，而在1号、4号以及8 - 10号染色体上未检测到缺失。仅17号染色体短臂缺失的检测频率较高（45%），其他染色体缺失的频率均低于22%。这些低频缺失可能是肿瘤发生发展过程中染色体重排导致的随机缺失。相反，17号染色体短臂缺失可能在食管鳞状细胞癌的发生发展中起重要作用，比如导致肿瘤抑制基因失活。在39%的肿瘤中观察到int - 2基因扩增。然而，未检测到int - 2基因扩增与任何染色体缺失之间存在显著关联。
