Mühlbauer K-R, Gröne H-J, Ernst T, Gröne E, Tschada R, Hergenhahn M, Hollstein M
Department of Genetic Alterations in Carcinogenesis, German Cancer Research Center (Deutsches Krebsforschungszentrum), D-69120 Heidelberg, Germany.
Br J Cancer. 2003 Aug 18;89(4):687-90. doi: 10.1038/sj.bjc.6601164.
A recent report suggests that the KLF6 gene encoding the Krüppel-like factor 6 protein is a frequently mutated, putative tumour suppressor gene in prostate cancer. The aims of the present study were to confirm these initial findings by determining the frequency of exon2 KLF6 mutations in a cohort of European prostate cancer patients, and to investigate whether there was evidence for mutational inactivation of both the KLF6 and TP53 tumour suppressor loci in some tumours. We examined 32 primary prostate tumours and three prostate tumour cell lines for mutations by PCR amplification and direct dideoxy sequencing (KLF6), and by oligonucleotide microarray (p53GeneChip) analysis and dideoxy sequencing (TP53). Whereas TP53 mutations typical of prostate cancer were found at a frequency consistent with the literature, no KLF6 mutations were found in any of the tumour samples nor in the three prostate cancer cell lines.
最近的一份报告表明，编码Krüppel样因子6蛋白的KLF6基因是前列腺癌中一种频繁突变的假定肿瘤抑制基因。本研究的目的是通过确定一组欧洲前列腺癌患者中外显子2 KLF6突变的频率来证实这些初步发现，并调查在某些肿瘤中是否存在KLF6和TP53肿瘤抑制基因座突变失活的证据。我们通过PCR扩增和直接双脱氧测序（KLF6）以及寡核苷酸微阵列（p53基因芯片）分析和双脱氧测序（TP53）来检测32个原发性前列腺肿瘤和3个前列腺肿瘤细胞系中的突变。虽然前列腺癌典型的TP53突变频率与文献一致，但在任何肿瘤样本或三个前列腺癌细胞系中均未发现KLF6突变。
