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T51B大鼠肝细胞在缺钙培养基中的集落形成、在软琼脂中的集落形成与肿瘤形成之间的关系。

Relation between colony formation in calcium-deficient medium, colony formation in soft agar, and tumor formation by T51B rat liver cells.

作者信息

Boynton A L, Kleine L P, Whitfield J F

出版信息

Cancer Lett. 1984 Jan;21(3):293-302. doi: 10.1016/0304-3835(84)90008-9.

DOI:10.1016/0304-3835(84)90008-9
PMID:6692347
Abstract

T51B rat liver cells and several carcinogen-treated, carcinogen + saccharin-treated, or spontaneously altered clones of T51B cells were tested for their abilities to form colonies in calcium-deficient medium and soft agar and to produce tumors in athymic nude mice. Most (10 out of 11) of the clones which were derived from colonies in calcium-deficient medium were unable to form colonies in soft agar and 8 out of 11 were non-tumorigenic. Conversely, 6 out of 9 clones derived from colonies in soft agar were unable to multiply significantly in calcium-deficient medium and 5 of these 6 clones were also non-tumorigenic. Two of these 9 soft agar-growing clones were tumorigenic, one of which also proliferated in calcium-deficient medium, and the other of which acquired the ability to proliferate in calcium-deficient medium after it became able to form tumors in athymic nude mice. Thus, T51B rat liver cells gain the ability to grow in calcium-deficient medium and soft agar independently during the process of neoplastic transformation and neither characteristic by itself reliably predicts tumorigenicity.

摘要

对T51B大鼠肝细胞以及几个经致癌物处理、致癌物+糖精处理或自发改变的T51B细胞克隆,检测它们在缺钙培养基和软琼脂中形成集落的能力以及在无胸腺裸鼠体内产生肿瘤的能力。大多数(11个中的10个)从缺钙培养基中的集落衍生而来的克隆无法在软琼脂中形成集落,11个中有8个无致瘤性。相反,从软琼脂中的集落衍生而来的9个克隆中有6个在缺钙培养基中无法显著增殖,这6个克隆中的5个也无致瘤性。这9个在软琼脂中生长的克隆中有2个具有致瘤性,其中一个在缺钙培养基中也能增殖,另一个在无胸腺裸鼠中能够形成肿瘤后获得了在缺钙培养基中增殖的能力。因此,T51B大鼠肝细胞在肿瘤转化过程中独立获得了在缺钙培养基和软琼脂中生长的能力,且这两种特性本身都不能可靠地预测致瘤性。

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Relation between colony formation in calcium-deficient medium, colony formation in soft agar, and tumor formation by T51B rat liver cells.T51B大鼠肝细胞在缺钙培养基中的集落形成、在软琼脂中的集落形成与肿瘤形成之间的关系。
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Neoplastic transformation of rat liver epithelial cells is enhanced by non-transferrin-bound iron.
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