ZIP kinase and lung cancer
Abstracts
Initial Award Abstract |
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The numbers of cells in most tissues are controlled by a delicate balance between cell production as a results of cell division and cell loss as a result of programmed cell death. However, in lung cancers, the mechanisms responsible for cell death often become defective, contributing to malignant cell expansion. Moreover, defects in the normal cell suicide mechanisms also make it more difficult to kill cancer cells using radiotherapy or chemotherapy. I have discovered a molecule in cells called ZIP kinase that triggers tumor cells to commit suicide. The hypothesis I propose to address is that ZIP kinase can be stimulated by exogenous means to kill lung cancer cells.
The methods that will be employed include transfer of genes producing ZIP kinase or experimentially modified forms of ZIP kinase into lung cancer cells, seeking an understanding of precisely how this molecule triggers cancer cells to die. Studies will also be performed using genetically engineered mice to ask whether ZIP kinase normally helps to suppress development of lung cancer by encouraging cells to undergo programmed cell death.
Many attempts to treat lung cancer seek to somehow damage the tumor cells and thereby destroy them. However, I believe that it should be possible to trick cancer cells into killing themselves, through cell suicide. ZIP kinase is a good candidate for inducing lung cancer cells to commit suicide. Learning how to use natural programmed cell death mechanisms to fight cancer is an innovative approach that deserves to be tried. |
