Use a Common Cold Virus to Target and Disrupt Cancer Cell?

Researchers from the Salk Institute have published a paper describing findings into how adenovirus controls crucial cell death mechanisms that are also knocked out in cancer cells. The research has been published in the 26th August edition of Nature here.

The research looked into a viral protein that interfered with the p53 gene by compressing it's code thereby inactivating it. This novel mechanism used by adenovirus to sidestep the cell's suicide program, could go a long way to explain how tumor suppressor genes are silenced in tumor cells and pave the way for a new type of targeted cancer therapy.

When a cell is under stress, the tumor suppressor p53 springs into action activating an army of foot soldiers that initiate a built-in "auto-destruct" mechanism that eliminates virus-infected or otherwise abnormal cells from the body. Just like tumor cells, adenoviruses, which cause upper-respiratory infections, need to get p53 out of the way to multiply successfully.

"Instead of inactivating p53 directly, adenovirus renders the 'guardian of the genome' powerless by targeting the genome itself," explains Clodagh O'Shea, Ph.D., an assistant professor in the Molecular and Cell Biology Laboratory, who led the study. "It literally creates zip files of p53 target genes by compressing them till they can no longer be read."

The p53 tumor suppressor pathway is inactivated in almost every human cancer, allowing cells to escape normal growth controls. Yet there is still no rationally designed targeted cancer therapy to treat patients based on the loss of p53.

Article sourced from Science Daily.