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11号染色体的肿瘤抑制作用并非源于细胞衰老。

Tumor suppression by chromosome 11 is not due to cellular senescence.

作者信息

Ning Y, Shay J W, Lovell M, Taylor L, Ledbetter D H, Pereira-Smith O M

机构信息

Roy M. and Phyllis Gough Huffington Center on Aging, Baylor College of Medicine, Houston, Texas 77030.

出版信息

Exp Cell Res. 1991 Jan;192(1):220-6. doi: 10.1016/0014-4827(91)90179-x.

Abstract

Previous hybrid studies involving fusion of normal with immortal human cells indicated that the phenotype of cellular senescence is dominant and that immortality results from recessive changes in normal growth regulatory genes. We have further assigned 28 different immortal human cell lines to at least four complementation groups for indefinite division. In order to identify the chromosomes involved in regulating cell proliferation, we have introduced single human chromosomes by microcell fusion into immortal human cells representative of the different complementation groups. Our results demonstrate that the introduction of chromosome 11, implicated in tumor suppression, does not cause cellular senescence in three different immortal human cell lines tested.

摘要

先前涉及正常人类细胞与永生人类细胞融合的杂交研究表明,细胞衰老的表型是显性的,而永生是正常生长调节基因隐性变化的结果。我们进一步将28种不同的永生人类细胞系至少分为四个互补组以进行无限分裂。为了确定参与调节细胞增殖的染色体,我们通过微细胞融合将单个人类染色体引入代表不同互补组的永生人类细胞中。我们的结果表明,在测试的三种不同永生人类细胞系中,引入与肿瘤抑制相关的11号染色体不会导致细胞衰老。

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