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. 2009 Mar 16;4(3):e4849. doi: 10.1371/journal.pone.0004849

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Gemenetzidis et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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(A) FOXM1 expression is upregulated early during the progression from dysplasia to HNSCC malignancy. Nicotine may promote tumour development by synergising with the upregulation of FOXM1 during oncogenesis. (B) Oncogenic 1^st hit represents overexpression of FOXM1 which directly activates CEP55 but indirectly activates HELLS expressions. This may destabilise the genome through aberrant mitotic division/cytokinesis and/or epigenetic modification events induced by CEP55 and HELLS, respectively. Oncogenic 2^nd hit represents the subsequent accumulation of further genomic instability (for example 10q23 amplification) which promotes oncogenesis.