Mechanism of T-cell lymphomagenesis: transformation of growth-factor-dependent T-lymphoblastoma cells to growth-factor-independent T-lymphoma cells.
Mechanism of T-cell lymphomagenesis: transformation of growth-factor-dependent T-lymphoblastoma cells to growth-factor-independent T-lymphoma cells.
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T细胞淋巴瘤发生机制：生长因子依赖性T淋巴细胞瘤细胞向生长因子非依赖性T淋巴瘤细胞的转化。
DOI：
10.1073/pnas.81.6.1742
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发表时间：
1984
影响因子：
11.1
通讯作者：
Jones,OW
中科院分区：
文献类型：
--
作者：
Haas,M;Altman,A;Rothenberg,E;Bogart,MH;Jones,OW
在以前的一篇论文中，我们描述了两类淋巴T细胞肿瘤的诱导：第一类，命名为T细胞淋巴母细胞瘤(TCLB)，由生长因子依赖的整二倍体细胞组成，它位于脾内，注射到同基因小鼠体内会引起脾肿瘤；第二类，命名为T细胞淋巴瘤(TCL)，由生长因子非依赖性非整倍体或假二倍体细胞组成，在皮下注射部位产生局部肿瘤。本文描述了将生长因子依赖的二倍体TCLB细胞注入胸腺后，产生一族非生长因子非整倍体或假二倍体的TCL细胞。与供体TCLB细胞相比，所获得的TCL细胞可以在半固体介质中克隆，在皮下注射部位产生局部肿瘤，并在体外以不依赖生长因子的方式增殖。诱导的生长因子非依赖性TCL细胞在染色体和表型上都是不稳定的，并在体内和体外继续进化。在胸腺中繁殖后，细胞除了出现非整倍体外，还表现出稳定的易位。我们认为，胸腺中生长因子依赖的TCLB细胞在增殖过程中引起的染色体异常构成了肿瘤细胞从生长因子依赖向独立发展的一般机制。
In a previous paper we described the induction by x-irradiation or radiation-induced leukemia virus-inoculation of two classes of lymphoid T-cell neoplasms: The first class, designated T-cell lymphoblastoma (TCLB), consists of growth-factor-dependent eudiploid cells that home to the spleen and give rise to splenic tumors on injection into syngeneic mice; the second class, designated T-cell lymphoma (TCL), consists of growth-factor-independent aneuploid or pseudodiploid cells that give rise to local tumors at the site of subcutaneous injection. This paper describes the generation of a family of growth-factor-independent aneuploid or pseudodiploid TCL cells after the injection into the thymus of growth-factor-dependent diploid TCLB cells. In contrast to the donor TCLB cells, the resulting TCL cells could be cloned in semisolid medium, produced local tumors at the site of subcutaneous injection, and proliferated in a growth-factor-independent fashion in vitro. The induced growth-factor-independent TCL cells were chromosomally and phenotypically unstable and continued to evolve both in vivo and in vitro. After propagation in the thymus, the cells often showed stable translocations in addition to the evolving aneuploidy. We propose that the chromosome abnormalities induced during the proliferation of growth-factor-dependent TCLB cells in the thymus constitute a general mechanism by which neoplastic cells progress from growth-factor dependency to independency.