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Early G2/M checkpoint failure as a molecular mechanism underlying etoposide-induced chromosomal aberrations
Shinichiro Nakada, … , Johji Inazawa, Shuki Mizutani
Shinichiro Nakada, … , Johji Inazawa, Shuki Mizutani
Published August 1, 2006
Citation Information: J Clin Invest. 2006;116(8):2306-2307. https://doi.org/10.1172/JCI25716E1.
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Erratum

Early G2/M checkpoint failure as a molecular mechanism underlying etoposide-induced chromosomal aberrations

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Abstract

Authors

Shinichiro Nakada, Yoko Katsuki, Issei Imoto, Tetsuji Yokoyama, Masayuki Nagasawa, Johji Inazawa, Shuki Mizutani

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Figure 3

FISH analysis for chromosome 11.

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FISH analysis for chromosome 11.

                        (A) Representa...
(A) Representative image of metaphase ATM-deficient fibroblasts hybridized with the CH11C probe (green) and MLL probes (green and red overlap). Chromosomes were stained by DAPI. The arrows indicate overlapping MLL signals. (B) Representative image of metaphase ATM-deficient fibroblasts hybridized with probes for whole chromosome 11 (red) and MLL (green and red overlap). (C) Flow diagram of the cell fractionation procedure. (D) Etoposide-treated postmitotic G1 phase ATM-deficient fibroblasts with 1 (upper panel) and 3 (lower panel) centromeric 11q23 signals. (E) Proportion of metaphase and postmitotic G1 phase cells with gain (red) and loss (blue) of CH11C (left) or centromeric 11q23 (right) probe signals.n > 250 for each. *Odds ratio (OR) for etoposide treatment. **P = 0.77 and †P < 0.0001, differences in OR between postmitotic G1 and metaphase cells when cells were hybridized with CH11C and centromeric 11q23 probes, respectively (P for interaction term of cell cycle phase × treatment by a logistic regression model). (F) Micronuclei containing centromeric 11q23 signals (arrows). Cells were hybridized with centromeric 11q23 probes. Original magnification of FISH images, ×600.

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