About Cellular Stress
Cells have evolved highly sensitive mechanisms to recognize the warning signs of excess cellular stress that occur during viral infections and the development of cancer. For example, during a viral infection, intrinsic pathways within the host cell sense the presence of viral RNA or DNA, triggering the cell to arrest its replication machinery and prevent the virus from replicating. As part of this intrinsic response, immune system pathways are activated to recognize infected cells and mount a robust attack to eliminate those cells. By efficiently detecting these warning signs, the infected cell and the immune system are able to cooperatively respond to cellular stress that arises not only from viral infections, but also from many other sources of cellular stress that are common in cancer.
A common feature of many cancer cells is that they are under continuous cellular stress caused by many factors including genomic instability, alterations in protein expression and metabolism, nutrient deprivation and hypoxia, which is the deprivation of adequate oxygen supply at the tissue level, and mechanical stress imposed by altered tissue architecture. In order for these cancer cells to survive in the presence of stress conditions, they must be able to balance these stresses by utilizing stress support pathways. Cancer cells hijack alternative pathways, not required by healthy cells, and use them as stress support pathways, allowing cancer cells to proliferate and evade the antitumor response of the immune system. We believe these stress support pathways represent novel cancer vulnerabilities that have been previously underexploited.