Lymphoma development in mice and humans: diversity of initiation is followed by convergent cytogenetic evolution.

Lymphoma development in mice and humans: diversity of initiation is followed by convergent cytogenetic evolution.
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小鼠和人类淋巴瘤的发展:起始的多样性随后是趋同的细胞遗传学进化。

DOI:
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发表时间:
1979
影响因子:
11.1
通讯作者:
G. Klein
G. Klein
中科院分区:
综合性期刊1区
文献类型:
--
作者:
G. Klein

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人B细胞淋巴瘤和鼠T细胞白血病可由几种药剂引发。本文阐述了细胞遗传学变化在随后的肿瘤过程中的作用的一些想法。启动产生长寿命的癌前细胞。在某些方面,它们与维持二倍体核型并且在体内不致瘤的体外转化(“永生化”)细胞系相当。致瘤性(“自主”)克隆的发展取决于遗传水平上的额外变化。在人类B和小鼠T细胞淋巴瘤中,存在特征性的非随机染色体改变。14 q+标记物似乎在人类B细胞淋巴瘤中起关键作用。伯基特淋巴瘤中的相互8;14易位是这一类别中的一个专门亚类。在小鼠T细胞白血病中,15三体是主要的变化。这些非随机变化的集群肿瘤来源于某种细胞类型,而不是由一个给定的病原体诱导的肿瘤有重要的意义,为理解的遗传控制细胞的反应,在体内的生长调节力量。
Human B cell lymphoma and murine T cell leukemia can be initiated by several agents. The present paper formulates some thoughts on the role of cytogenetic changes in the subsequent neoplastic process. Initiation creates long-lived preneoplastic cells. In some respects, they are comparable to in vitro-transformed ("immortalized") cell lines that maintain a diploid karyotype and are not tumorigenic in vivo. The development of a tumorigenic ("autonomous") clone is dependent on additional changes at the genetic level. In human B and murine T cell lymphoma, there are characteristic nonrandom chromosomal changes. The 14q+ marker appears to play a key role in human B cell lymphomas. The reciprocal 8;14 translocation in Burkitt lymphoma is a specialized subclass within this category. In murine T cell leukemia, trisomy 15 is the predominant change. The clustering of these nonrandom changes to tumors derived from a certain cell type rather than to tumors induced by a given etiological agent has important implications for the understanding of the genetic control of cellular responsiveness to growth-regulating forces in vivo.