Kawaguchi T, Miyaki M, Masui T, Watanabe M, Ohta H, Maruyama M, Utakoji T, Kitagawa T
Department of Pathology, Cancer Institute, Tokyo.
Jpn J Cancer Res. 1991 Feb;82(2):138-41. doi: 10.1111/j.1349-7006.1991.tb01820.x.
An epithelial cell line designated FPCK-1 has been established from a tubular adenoma developing in a male familial polyposis coli (FPC) patient. The FPCK-1 cells grow very slowly with abundant mucus production and have been maintained stably for 3 years in culture. No growth was evident either in soft agar or nude mice. FPCK-1 cells present a normal male karyotype and do not show loss of specific loci on chromosomes 5, 17, 18, and 22 which have been reported to be lost frequently in human colon carcinomas. The cells have neither a point mutation on codon 12 of K-ras gene nor gene amplification of myc, c-H-ras, and/or c-K-ras genes. These results thus suggest the existence of hitherto unknown causative event(s) underlying adenoma development in FPC patients. The FPCK-1 cell line should prove useful for further analytical investigation of the multiple steps involved in human colon carcinogenesis.
一种名为FPCK-1的上皮细胞系,是从一名男性家族性结肠息肉病(FPC)患者所患的管状腺瘤中建立的。FPCK-1细胞生长非常缓慢,会产生大量黏液,并且已在培养物中稳定保存3年。在软琼脂或裸鼠中均未观察到明显生长。FPCK-1细胞呈现正常男性核型,在5号、17号、18号和22号染色体上未显示特定基因座的缺失,而据报道这些基因座在人类结肠癌中经常丢失。这些细胞在K-ras基因的第12密码子上既没有点突变,也没有myc、c-H-ras和/或c-K-ras基因的扩增。因此,这些结果表明FPC患者腺瘤发生的潜在原因是迄今未知的事件。FPCK-1细胞系对于进一步分析人类结肠癌发生过程中涉及的多个步骤应是有用的。