Tetraploidy, aneuploidy and cancer

Ganem, Neil J.; Storchová, Zuzana; Pellman, David

doi:10.1016/j.gde.2007.02.011

Cited by 607 publications

(600 citation statements)

References 51 publications

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“…Based on these observations, it could be hypothesized that early occurrence of tetraploidization in association with duplication of the BRAF gene in pylocytic astrocytomas [43,44] could prevent histopathological grade I/II astrocytomas from evolving into an invasive phenotype and a highly progressive clinical behavior tied to aggressive histopathological features; this could be due to the fact that p16/p14 ARF and chromosome 10q losses that occur after tetraploidization would have a more limited impact in the aggressiveness of the tumor because at least one copy of each allele of these genes would still be retained. In line with this, a tetraploidy checkpoint has been associated with prevention of tumor progression among gliomas [45,46] and these cytogenetic profiles were also much less frequently observed among high-grade gliomas, where acquisition of multiple cytogenetic abnormalities leading to relatively complex cytogenetic profiles, typically preceded tetraploidization. Although early tetraploidization was associated with a significantly better clinical outcome, this could be due to its association with low-grade astrocytomas and deserves further multivariate analyses in larges series of patients to determine its potential independent prediction value.…”

Section: Discussionmentioning

confidence: 67%

Intratumoral patterns of clonal evolution in gliomas

et al. 2009

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Few studies have explored the patterns of clonal evolution in gliomas. Here, we investigate the cytogenetic patterns of intratumoral clonal evolution of gliomas and their impact on tumor histopathology and patient survival. Cytogenetic analysis of 90 gliomas was performed in individual tumor cells (>200 cells/tumor) using multicolor (N=16 probes) interphase-FISH. Overall, chromosome gains were more frequent than chromosome losses. Gains of chromosome 7 and/or EGFR amplification were detected in 91% of the cases, whereas del(9p21) (77%) and del(10q23) (78%) were the most frequent chromosome losses. Virtually, all cases (99%) showed ≥2 tumor cell clones, with higher numbers among high-versus low-grade gliomas (p=0.001). Nine different cytogenetic patterns were found in the ancestral tumor clones.In most gliomas, ancestral clones showed abnormalities of chromosome 7, 9p, and/or 10q and cytogenetic evolution consisted of acquisition of additional abnormalities followed by tetraploidization. Conversely, early tetraploidization was associated with low-grade astrocytomas-2/3 pilocytic and 3/ 6 grade II diffuse astrocytomas-and combined loss of 1p36/ 19q13 with oligodendrogliomas, respectively; both aberrations were associated with a better patient outcome (p=0.03). Overall, our results support the existence of different pathways of intratumoral evolution in gliomas

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Section: Discussionmentioning

confidence: 67%

Intratumoral patterns of clonal evolution in gliomas

et al. 2009

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“…Cytokinesis is a fundamental step of cell proliferation, and its high-fidelity completion is crucial for stable maintenance of the genome (Ganem et al, 2007;Lacroix and Maddox, 2012). Anti-parallel microtubule bundle structures such as the central spindle and the midbody play various important roles throughout cytokinesis, from positioning of cleavage furrow to final separation of the two daughter cells Glotzer, 2009;Fededa and Gerlich, 2012).…”

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confidence: 99%

Cytokinesis microtubule organisers at a glance

Lee

Davies

Mishima

2012

Journal of Cell Science

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“…Other groups reported that the cytokinesis failure process is also a programmed step in normal development (in liver and heart tissues) producing differentiated binucleated tetraploidy progenies; their findings contribute to our understanding of binucleated cells in normal tissues (Ducos et al 2007;Engel et al 2006;Guidotti et al 2003). However, aside from these physiological conditions, cytokinesis failure and the resulting tetra-and polyploidization can lead to genetically unstable states and contribute to tumorigenic transformation (Fujiwara et al 2005;Ganem et al 2007). This is the first report that binucleated HeLa cells are induced by starvation and that some binucleated cells keep the potential of proliferation.…”

Section: Discussionmentioning

confidence: 96%

Binucleated HeLa cells are formed by cytokinesis failure in starvation and keep the potential of proliferation

et al. 2015

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Many cytological studies have reported that the numbers of binucleated cells were elevated in various tumors. However, binucleated cells are observed in not only malignant tumors but also normal tissues. Thus, the clinical significance of binucleated cells is controversial. Here we attempted to elucidate the characteristics of binucleated HeLa cells using time-lapse microscopy. To examine the frequency, viability, proliferation, and formation mechanism of binucleated cells, we grew HeLa cells on chamber slides and tissue culture dishes in DMEM supplemented with (10, 3, 1 and 0.5 % media) and without fetal bovine serum (0 % medium). The proliferation was evaluated by the medium improvement examination (cultured for 2 more days in 10% medium after culturing in 0% medium; starvation). In the 0 % medium, 150 binucleated cells were formed by cytokinesis failure. There were significantly more binucleated cells in the 0 % medium than in the 10, 3, 1 and 0.5 % media. About twice the number of binucleated cells underwent mitosis in the improvement examinations than in the serum-free examination. We found here that starvation induced the binucleation of HeLa cells and that some binucleated cells can reproduce. These findings might be helpful for understanding binucleated cells in tumors.

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Tetraploidy, aneuploidy and cancer

Cited by 607 publications

References 51 publications

Intratumoral patterns of clonal evolution in gliomas

Intratumoral patterns of clonal evolution in gliomas

Cytokinesis microtubule organisers at a glance

Binucleated HeLa cells are formed by cytokinesis failure in starvation and keep the potential of proliferation

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