And the big paper is in press

Our manuscript is accepted in the Biochemical Journal.  It is a too brief moment of satisfaction of completing a project.  A special thanks to the experimentalists who succeeded in converting the complex problem of cell division with damaged DNA into a powerful experimental model. Of the cell lines we tested, HT-29 cells have features that provide a window of the key transition point of entry into mitosis after a checkpoint. 
What's next - we have developed a non-radioisotope assay to measure enzyme activity in mitotic cells; we are testing how to block checkpoint adaptation, and we are looking very closely at the DNA in cancer cells that survive checkpoint adaptation. 
If interested, please feel free to contact us for questions, reagents or a copy of the paper.

Mitosis or apoptosis (life or death)

Our laboratory has invested much time and effort in developing an experimental model of how human cells can divide even when they have damaged DNA.  The efforts are beginning to pay off.  Recently we found that when cells enter mitosis with damaged chromosomes, they can inactivate apoptosis.  Perhaps this should not be too surprising because mitosis should cause all the alarms to sound (loss of contact, changes in organelles, DNA everywhere).  The rub is to know if cancer cells use this as another mechanism to survive.  We are now examining the pathways that might provide survival.  A new area for us, which was illuminated by our model and a pharmacological approach.