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来自结肠癌的两个细胞系中扩增的c-myb癌基因的异常表达。

Aberrant expression of an amplified c-myb oncogene in two cell lines from a colon carcinoma.

作者信息

Alitalo K, Winqvist R, Lin C C, de la Chapelle A, Schwab M, Bishop J M

出版信息

Proc Natl Acad Sci U S A. 1984 Jul;81(14):4534-8. doi: 10.1073/pnas.81.14.4534.

Abstract

Two cell lines (COLO 201 and COLO 205) derived independently from a single adenocarcinoma of the human colon each harbored an approximately 10-fold amplification of the cellular oncogene c-myb and a proportional abundance of the 4-kilobase mRNA derived from c-myb. By contrast, expression of c-myb could not be detected in cells from a variety of other solid tumors, including other colon carcinomas. Analysis of the amplified DNA with restriction endonucleases failed to reveal any topographical abnormalities within c-myb. Neither COLO 201 nor COLO 205 carry the double minute chromosomes and homogeneously staining regions of chromosomes that frequently serve as karyotypic signatures of amplified DNA. Instead, amplified c-myb is carried on what appear to be disomic or trisomic copies of the same anomalous marker chromosome that is characteristic of both COLO 201 and COLO 205. The karyological origin of this abnormal chromosome is not presently apparent. Our findings show c-myb expression by cells outside of the hemopoietic lineage, raise the possibility that amplification and/or ectopic expression of c-myb may have contributed to the genesis of the tumor from which the cells of COLO 201 and COLO 205 arose, and suggest that amplification of cellular oncogenes may be a more common factor in tumorigenesis than might have been suspected from available karyological data.

摘要

从人类结肠的单一腺癌独立衍生出的两个细胞系(COLO 201和COLO 205),各自含有细胞癌基因c-myb约10倍的扩增以及源自c-myb的4千碱基mRNA的相应丰度。相比之下,在包括其他结肠癌在内的多种其他实体瘤的细胞中未检测到c-myb的表达。用限制性内切酶分析扩增的DNA未能揭示c-myb内的任何拓扑异常。COLO 201和COLO 205均未携带常作为扩增DNA核型特征的双微小染色体和染色体均匀染色区。相反,扩增的c-myb位于似乎是二体或三体拷贝的同一条异常标记染色体上,这是COLO 201和COLO 205共有的特征。这条异常染色体的核型起源目前尚不清楚。我们的研究结果显示造血谱系以外的细胞表达c-myb,增加了c-myb的扩增和/或异位表达可能促成了COLO 201和COLO 205细胞所源自的肿瘤发生的可能性,并表明细胞癌基因的扩增可能是肿瘤发生中比现有核型数据所推测的更为常见的因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fea/345625/5352b14bf81c/pnas00615-0302-a.jpg

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