Mitotic modifications and aberrations in human cervical cancer

Therman, Eeva; Buchler, Dolores A.; Nieminen, U; Timonen, S

doi:10.1016/0165-4608(84)90113-4

Cited by 29 publications

(22 citation statements)

References 11 publications

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“…As such, our findings describe a novel source of DNA damage. Second, because cancer cells frequently contain mitotic defects that induce arrest (1,18), and because DNA breaks can promote tumorigenesis (17), our findings suggest that one way mitotic arrest may promote tumorigenesis is through DNA damage. Along these lines, it is interesting to note that inactivation of the tumor suppressor hCDC4 and oncogenic overexpression of MAD2 are accompanied not only by prolongation of mitosis and aneuploidy but also by evidence of DNA damage (3,4).…”

Section: Dna Damage and Mitotic Arrestmentioning

confidence: 88%

Human Cancer Cells Commonly Acquire DNA Damage during Mitotic Arrest

et al. 2007

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The mitotic checkpoint is a mechanism that arrests the progression to anaphase until all chromosomes have achieved proper attachment to mitotic spindles. In cancer cells, satisfaction of this checkpoint is frequently delayed or prevented by various defects, some of which have been causally implicated in tumorigenesis. At the same time, deliberate induction of mitotic arrest has proved clinically useful, as antimitotic drugs that interfere with proper chromosome-spindle interactions are effective anticancer agents. However, how mitotic arrest contributes to tumorigenesis or antimitotic drug toxicity is not well defined. Here, we report that mitotic chromosomes can acquire DNA breaks during both pharmacologic and genetic induction of mitotic arrest in human cancer cells. These breaks activate a DNA damage response, occur independently of cell death, and subsequently manifest as karyotype alterations. Such breaks can also occur spontaneously, particularly in cancer cells containing mitotic spindle abnormalities. Moreover, we observed evidence of some breakage in primary human cells. Our findings thus describe a novel source of DNA damage in human cells. They also suggest that mitotic arrest may promote tumorigenesis and antimitotic toxicity by provoking DNA damage. [Cancer Res 2007;67(24):11487-92]

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Section: Dna Damage and Mitotic Arrestmentioning

confidence: 88%

Human Cancer Cells Commonly Acquire DNA Damage during Mitotic Arrest

et al. 2007

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“…Previous studies have described metaphases with lagging chromosomes in cervical intraepithelial neoplasia (CIN) and cervical carcinoma (Therman et al, 1984). A greater severity of CIN coincides with increased proliferation and increased numbers of mitosis with lagging chromosomes.…”

Section: Discussionmentioning

confidence: 99%

The human papillomavirus type 16 E6 oncogene induces premature mitotic chromosome segregation

Plug-Demaggio

McDougall

2002

Oncogene

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Expression of the human papillomavirus type 16 E6 and E7 oncogenes initiates and maintains abnormal cell replication, by interacting with the p53 and retinoblastoma (Rb) gene products. Subsequent changes in host cell gene expression, as a consequence of genetic instability, can result in progression to invasive carcinoma. In addition to previously described effects of these viral oncogenes on centrosome synthesis, primarily associated with the expression of E7, the results described herein demonstrate that the E6 oncogene can induce premature chromosome segregation in human cells.

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“…The occurrence of non-random MSEs which are dependent upon total cellular DNA content, and which were actually observed for the MCa-11 line, had the result that 73% of the daughter Te-cells had DNA contents within 3 pg of the modal peak. This process allows continuous input by non-modal, outlying cells to the genetic diversity of the modal peak, and it may help to maintain the modal chromosome number and DNA content peaks of heteroploid cell populations over many generations (5,8,(11)(12)(13)17,20,21,26).…”

Section: Discussionmentioning

confidence: 99%

Non‐random distribution of abnormal mitoses in heteroploid cell lines

Dooley

Allison

1992

Cytometry

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We have performed absorption-cytometric DNA measurements of the DNA contents of the GdG,, G,, metaphase, and telophase cells of the heteroploid MCa-11 and HL-60 lines, as well as the WCHE-5 line which has a narrowly restricted number of chromosomes. We found that morphologically unbalanced mitoses occurred much more frequently in telophase-cell pairs of the heteroploid MCa-11 and HL-60 lines than in those of the chromosomally stable WCHE-5 line. Furthermore, the morphologically unbalanced mitoses represented unequal segregation of DNA into each of the daughter telophase nuclei. Such mitotic segregation errors (MSE) occurred almost exclusively in telophase cells with DNA contents which were above, or below, the DNA content of the modal telophase population. The net effect of these non-random, unbalanced divisions of heteroploid cells with non-modal DNA contents is to produce one daughter cell with a DNA content that tends to return to the modal DNA content peak. 0 1992 Wiley-Liss, Inc.

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Mitotic modifications and aberrations in human cervical cancer

Cited by 29 publications

References 11 publications

Human Cancer Cells Commonly Acquire DNA Damage during Mitotic Arrest

Human Cancer Cells Commonly Acquire DNA Damage during Mitotic Arrest

The human papillomavirus type 16 E6 oncogene induces premature mitotic chromosome segregation

Non‐random distribution of abnormal mitoses in heteroploid cell lines

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