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Positivity of the proliferation marker Ki-67 in noncycling cells.

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TLDR
It is found that cycle-arrested osteosarcoma cells are positive for Ki-67 even when they are arrested in G1/S or G2/M by using synchronizing inhibitors, by inducing p21(Waf1/Cip1) in a tetracycline-regulated expression system or by inducing wild type p53 and p21 after inflicting DNA damage.
Abstract
Ki-67 is a proliferation marker that is often used to estimate the growth fraction of tumors and other tissues. This antigen is expressed during all phases of the cell cycle but not in quiescent G0 cells. Many studies fail to indicate that the Ki-67 antigen can be expressed even when DNA synthesis is blocked. We studied the expression of the antigen Ki-67 in cycle-arrested osteosarcoma cells. We found that these cells are positive for Ki-67 even when they are arrested in G1/S or G2/M by using synchronizing inhibitors, by inducing p21(Waf1/Cip1) in a tetracycline-regulated expression system or by inducing wild type p53 and p21 after inflicting DNA damage. Our results show that not all cells containing the Ki-67 antigen are actively proliferating cells and we advise against the use of Ki-67 in studies on cells that overexpress p53 or p21.

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Journal ArticleDOI

The Ki‐67 protein: From the known and the unknown

TL;DR: Although the Ki‐67 protein is well characterized on the molecular level and extensively used as a proliferation marker, the functional significance still remains unclear; there are indications, however, that Ki‐ 67 protein expression is an absolute requirement for progression through the cell‐division cycle.
Journal ArticleDOI

Progression From Compensated Hypertrophy to Failure in the Pressure-Overloaded Human Heart Structural Deterioration and Compensatory Mechanisms

TL;DR: These structure-function correlations confirm the hypothesis that transition to HF occurs by fibrosis and myocyte degeneration partially compensated by hypertrophy involving DNA synthesis and transcription.
Journal ArticleDOI

Cyclin-dependent kinase pathways as targets for cancer treatment.

TL;DR: Current work is focusing on overcoming pharmacokinetic barriers that hindered development of flavopiridol, a pan-cdk inhibitor, as well as assessing novel classes of compounds potently targeting groups of cell cycle cdks (cdk4/6 or cdk2/1) with variable effects on the transcriptional cdks 7 and 9.
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