Hsieh L L, Chen H J, Hsieh J T, Jee S H, Chen G S, Chen C J
Department of Public Health, Chang Gung Medical College, Taiwan, R.O.C.
Cancer Lett. 1994 Oct 28;86(1):59-65. doi: 10.1016/0304-3835(94)90180-5.
We have investigated point mutations of codons 12, 13, and 61 in H-, K-, and N-ras oncogenes as well as p53 tumour suppressor gene exon 5 through exon 9 by PCR-SSCP analysis in 26 skin biopsy tissues from 16 arsenic-related Bowen's disease patients and 6 skin samples from 4 paraquat manufacturing workers. No mutation was found. These results are different from findings with UV associated skin cancers. Interestingly, a silent change at codon 27 of H-ras in one allele was detected in all 4 paraquat manufacturing workers and in 2 of 16 arsenic-related Bowen's disease patients. It is likely that the molecular mechanisms involved in arsenic and paraquat induced skin cancers differ from sunlight-related skin malignancies.
我们通过聚合酶链反应-单链构象多态性分析（PCR-SSCP），研究了16例砷相关鲍恩病患者的26份皮肤活检组织以及4名百草枯制造工人的6份皮肤样本中H-ras、K-ras和N-ras癌基因密码子12、13和61的点突变，以及p53肿瘤抑制基因第5外显子至第9外显子。未发现突变。这些结果与紫外线相关皮肤癌的研究结果不同。有趣的是，在所有4名百草枯制造工人以及16例砷相关鲍恩病患者中的2例中，均检测到一个等位基因的H-ras密码子27处发生沉默变化。砷和百草枯诱发皮肤癌的分子机制可能与阳光相关的皮肤恶性肿瘤不同。
