Nagai H, Kinoshita T, Imamura J, Murakami Y, Hayashi K, Mukai K, Ikeda S, Tobinai K, Saito H, Shimoyama M
Virology Division, National Cancer Center Research Institute, Tokyo.
Jpn J Cancer Res. 1991 Dec;82(12):1421-7. doi: 10.1111/j.1349-7006.1991.tb01815.x.
Abnormalities of p53 mRNA in adult T-cell leukemia (ATL) were analyzed using reverse transcription-polymerase chain reaction-single strand conformation polymorphism analysis. Mutations were present in two of 12 ATL patients studied, but not in 3 cell lines immortalized by human T cell leukemia virus type 1 (HTLV-1) infection in vitro. Direct sequencing analysis of the p53 gene from these two patients revealed missense point mutations at codon 153 (arginine to histidine) or codon 220 (cysteine to tyrosine), respectively. Immunohistochemical analysis revealed the elevated expression of p53 proteins in ATL cells from a patient carrying the mutated p53 gene at codon 158. Neither gross rearrangement of p53 gene nor abnormal size of mRNA for the gene was demonstrated by Southern or Northern blot analyses. Thus, there is a mutated p53 in some patients with ATL. The involvement of abnormalities in some suppressor oncogenes may play a role in the development of ATL.
采用逆转录-聚合酶链反应-单链构象多态性分析法分析成人T细胞白血病（ATL）中p53 mRNA的异常情况。在研究的12例ATL患者中，有2例存在突变，但在3株经1型人类T细胞白血病病毒（HTLV-1）体外感染而永生化的细胞系中未发现突变。对这2例患者的p53基因进行直接测序分析，分别在密码子153（精氨酸突变为组氨酸）或密码子220（半胱氨酸突变为酪氨酸）发现错义点突变。免疫组织化学分析显示，在密码子158携带突变p53基因的患者的ATL细胞中，p53蛋白表达升高。Southern印迹分析和Northern印迹分析均未显示p53基因有大片段重排或该基因mRNA大小异常。因此，部分ATL患者存在p53突变。某些抑癌基因异常的参与可能在ATL的发生发展中起作用。
