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【答案】应助回帖
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suqingru: 金币+5, 翻译EPI+1 2013-06-23 09:50:52
先把原文贴在这里供大家参考，然后我再说。
Although the two canonical suppressors of proliferation—
TP53 and RB—have preeminent importance in regulating cell
proliferation, various lines of evidence indicate that each oper-
ates as part of a larger network that is wired for functional redun-
dancy. For example, chimeric mice populated throughout their
bodies with individual cells lacking a functional Rb gene are
surprisingly free of proliferative abnormalities, despite the expec-
tation that loss of RB function would allow continuous firing of the
cell division cycle in these cells and their lineal descendants;
some of the resulting clusters of Rb null cells should, by all rights,
progress to neoplasia. Instead, the Rb null cells in such chimeric
mice have been found to participate in relatively normal tissue
morphogenesis throughout the body; the only neoplasia
observed was in the development of pituitary tumors late in life
(Lipinski and Jacks, 1999). Similarly, TP53 null mice develop nor-
mally, show largely proper cell and tissue homeostasis, and
again develop abnormalities later in life, in the form of leukemias
and sarcomas (Ghebranious and Donehower, 1998). Both exam-
ples must reflect the operations of redundantly acting mecha-
nisms that serve to constrain inappropriate replication of cells
lacking these key proliferation suppressors.
字面翻译是“由此产生的某些Rb基因缺失的细胞团无论如何也应该发展为肿瘤”。Rb null cells是Rb-null的细胞，跟null cells无关。
这是根据对肿瘤抑制基因旧的认识所产生的推论（expectation）之一。但是（Instead），这种认识被嵌合体小鼠( chimeric mice)研究所颠覆。BTW，其实整段的关键词是redundancy-就是一种功能由多种基因或机制调控。嵌合体小鼠研究的贡献就在于此。 |
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