VEGF also improved angiogenesis and tissue sparing, indicating multifaceted actions for repair of injured spinal cord. The strategy of human NSC-based VEGF delivery may have potential to be CP-690550 clinically translated for the victims of SCI. However, these HPV-induced dysplasias are asymptom-atic and most regress, demonstrating that HPV is not sufficient to result in cervical cancer. The progression of cervical dysplasias to invasive, lethal cervical cancers has been attributed to diverse factors such as immune, hormonal, and nutritional status, or co-infection with other sexually-transmitted agents, but supporting data have been equivocal. Insertional mutagenesis by HPV is another proposed tumor-promoting mechanism, but recent studies have not supported this hypothesis. No common,Evofosfamide recurring genetic alterations that cooperate with HPV to promote cervical cancer progression have been identified since Harald Zur Hausen first identified HPV as the causal transmissible agent of cervical cancer over thirty years ago. Thus, the pressing question as to the biological basis of cervical cancer progression has remained unresolved. Topo IIa inhibitors such as anthracyclines or epididophyllotox-ins are important agents in the treatment of human malignancy. These agents cause DNA damage by two mechanisms, locking Topo IIa in a cleavage complex producing DNA double-strand breaks, and inhibiting chromatid decatenation. While the former mechanism is well understood, far less is known about the latter, yet it can be just as catastrophic to the cell. Failure of decatenation results in DSBs at anaphase, and to prevent this cells probably monitor decatenation at two positions in the cell cycle, at the G2/M boundary and at the metaphase to anaphase transition. These decatentation checkpoints are activated independently of the G2/M DNA damage-dependent checkpoint. Interestingly, lung and bladder cancers proceed through the decatenation checkpoints even in the presence of high levels of Topo IIa inhibitors, and this was thought to be secondary to a failure of the cell cycle arrest machinery. We recently isolated and characterized a human protein with SET and transposase domains called Metnase. Metnase promotes non-homologous end joining DNA repair, enhances plasmid and viral DNA integration, and cleaves but does not degrade supercoiled plasmid DNA.