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TUMOR SUPPRESSOR GENES IN HUMAN HEPATOCELLULAR CARCINOMA

TUMOR SUPPRESSOR GENES IN HUMAN HEPATOCELLULAR CARCINOMA
人类肝细胞癌中的抑癌基因
批准号:
3774899
负责人:
E TABOR
金额:
$0.0万
依托单位国家:
美国
项目类别:
财政年份:
--
资助国家:
美国
项目状态:
未结题
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中文摘要
翻译
抑癌基因p53和RB在7例人肺癌组织中的表达 肝细胞癌和肝母细胞瘤细胞系通过以下方法进行评价 北方和western印迹和免疫组织化学。 p53的表达 是异常的,如缺乏可检测的p53 RNA或 p53蛋白在7个细胞系中的5个中过表达; 过表达的p53蛋白似乎是突变p53基因的产物。 尽管RB RNA在所有7个细胞系中都可检测到,但RB蛋白在所有细胞系中都可检测到。 在三种细胞系中检测不到,但在另一种细胞系中检测到 四 免疫组化检测RB抑癌基因产物 来自中国的14例人类肝癌的冰冻切片。 B型肝炎表面 在所有14例患者的邻近非肿瘤肝中均检测到HBsAg HCC患者。 RB蛋白在3/14(21%)的HCC细胞中缺失。 RB基因的缺失在外显子12-23内通过单克隆抗体分析。 链构象多态性(SSCP),使用5个重叠片段, 每个129至337个核苷酸。 从人HCC衍生的五种细胞系是 研究了 (All其他文献中报告的RB基因突变或缺失 人类癌症包括外显子12-23的部分。 中的缺失 在两个细胞系的外显子17-21中发现RB cDNA,在两个细胞系的外显子17-21中发现RB cDNA,在两个细胞系的外显子17 - 21中发现RB cDNA。 20-21在第三细胞系中。 外显子检查是正常的, 剩余的细胞系。 通过免疫组织化学方法检测肝肿瘤组织中的p53, 被认为是HCC的可能前体,以及HCC, 匈牙利患者 16例HCC中8例检出突变型p53, 23例良性肝肿瘤。
英文摘要
The expression of the p53 and RB tumor suppressor genes in seven human hepatocellular carcinoma and hepatoblastoma cell lines was evaluated by northern and western blot and immunohistochemistry. The expression of p53 was abnormal as indicated by the absence of detectable p53 RNA or the overexpression of p53 protein in five of the seven cell lines; the overexpressed p53 protein appeared to be the product of a mutant p53 gene. Although RB RNA was detectable in all seven cell lines, RB protein was undetectable in three of the cell lines but was detectable in the other four. The RB tumor suppressor gene product was examined by immunohistochemistry in frozen sections from 14 human HCCs from China. Hepatitis B surface antigen (HBsAg) was detectable in adjacent nontumorous liver from all 14 HCC patients. RB protein was absent from HCC cells of 3/14 (21%) HCCs. Abnormalities of the RB gene were analyzed within exons 12-23 by single- strand conformation polymorphism (SSCP) using five overlapping segments of 129 to 337 nucleotides each. Five cell lines derived from human HCCs were studied. (All mutations or deletions of the RB gene reported in other human cancers have encompassed portions of exons 12-23. Deletions in the RB cDNA were found in exons 17-21 in two of the cell lines, and in exons 20-21 in the third cell line. The exons examined were normal in the remaining cell lines. p53 was examined by immunohistochemistry in tissues of liver tumors that are thought to be possible precursors of HCC, as well as HCCs, from Hungarian patients. Mutant p53 was detected in 8 of 16 HCCs and in none of 23 benign liver tumors.
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