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Molecular Cancer Therapeutics
Molecular Cancer Therapeutics

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Article

Cross-talk between DNA damage and cell survival checkpoints during G2 and mitosis: pharmacologic implications

Przemyslaw Bozko, Michal Sabisz, Annette K. Larsen and Andrzej Skladanowski
Przemyslaw Bozko
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Michal Sabisz
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Annette K. Larsen
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Andrzej Skladanowski
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DOI: 10.1158/1535-7163.MCT-05-0138 Published December 2005
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    Figure 1.

    DNA histograms of MOLT-4 cells treated with 2 μg/mL melphalan for 18 h and postincubated in the absence or presence of 1 mmol/L caffeine (A) or with nocodazole in the absence or presence of 1 mmol/L caffeine (B).

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    Figure 2.

    Western blot analysis of Cdk1 phosphorylation, cyclin B1 expression, and presence of the mitotic MPM-2 phosphoepitope in MOLT-4 cells treated with 2 μg/mL melphalan for 18 h and postincubated in the absence or presence of 1 mmol/L caffeine (A) or with a combination of 1 mmol/L caffeine and 50 ng/mL nocodazole (B and C).

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    Figure 3.

    A, nuclear morphology of MOLT-4 cells treated with 2 μg/mL melphalan for 18 h and postincubated in the absence or presence of 1 mmol/L caffeine or with a combination of 1 mmol/L caffeine and 50 ng/mL nocodazole (caff+noco) as well as 1 mmol/L caffeine and 10 μmol/L taxol (caff+taxol). B and C, changes in the number of mitotic (B) and apoptotic (C) cells in cell populations of MOLT-4 cells treated with 2 μg/mL melphalan for 18 h and postincubated in the absence or presence of 1 mmol/L caffeine or with a combination of 1 mmol/L caffeine and 50 ng/mL nocodazole as well as 1 mmol/L caffeine and 10 μmol/L taxol.

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    Figure 4.

    Analysis of nuclear morphology (A) and DNA fragmentation (B and C) and in MOLT-4 cells treated with 2 μg/mL melphalan for 18 h and postincubated in the absence or presence of 1 mmol/L caffeine.

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    Figure 5.

    A, changes in mitochondrial membrane potential in MOLT-4 cells treated with 2 μg/mL melphalan for 18 h and postincubated in the absence or presence of 1 mmol/L caffeine as determined by 3,3'-dihexyloxacarbocyanine iodide (DiOC6) and PI staining and analyzed by flow cytometry. B, Western blot analysis of survivin expression, caspase-3 activation, and apoptosis-associated poly(ADP-ribose) polymerase cleavage in MOLT-4 cells. Cells were treated with 2 μg/mL melphalan for 18 h and postincubated in the absence or presence of 1 mmol/L caffeine, combination of 1 mmol/L caffeine and 50 ng/mL nocodazole, or combination of 1 mmol/L caffeine and 10 μmol/L taxol. C, caspase-3 activation as determined by an enzymatic activity assay. MOLT-4 cells were treated with 2 μg/mL melphalan for 18 h and postincubated in the absence (•) or presence (▴) of 1 mmol/L caffeine, combination of 1 mmol/L caffeine and 50 ng/mL nocodazole (⧫), or combination of 1 mmol/L caffeine and 10 μmol/L taxol (□). Nocodazole (○) and taxol (▵) alone had only minor effect on caspase-3 activation in melphalan-treated cells in the absence of caffeine. SD is not shown for clarity but was never higher than 5%.

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    Figure 6.

    A model for the cellular response of tumor cells progressing through G2 and M with a damaged genome in the presence of microtubule-stabilizing or microtubule-destabilizing drugs. When cells enter mitosis with damaged DNA due to weak DNA damage checkpoints or to checkpoint abrogation, mitotic cell death is favored if microtubules are destabilized, whereas cell survival may be observed when microtubules are stabilized due to active survivin signaling.

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Molecular Cancer Therapeutics: 4 (12)
December 2005
Volume 4, Issue 12
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Cross-talk between DNA damage and cell survival checkpoints during G2 and mitosis: pharmacologic implications
Przemyslaw Bozko, Michal Sabisz, Annette K. Larsen and Andrzej Skladanowski
Mol Cancer Ther December 1 2005 (4) (12) 2016-2025; DOI: 10.1158/1535-7163.MCT-05-0138

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Cross-talk between DNA damage and cell survival checkpoints during G2 and mitosis: pharmacologic implications
Przemyslaw Bozko, Michal Sabisz, Annette K. Larsen and Andrzej Skladanowski
Mol Cancer Ther December 1 2005 (4) (12) 2016-2025; DOI: 10.1158/1535-7163.MCT-05-0138
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Molecular Cancer Therapeutics
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