Carcinogenesis and molecular genetics

All tissues have a rate at which cells naturally die, while other cells divide to take their place. The skin, for example, consists of large numbers of cells that are dying or dead and are constantly sloughed off, while new layers of skin regenerate by cell division beneath the cell surface. Maintaining the homeostatic balance of cell loss and cell gain is crucial to the health and survival of the tissue and organism, and so the balance is tightly regulated in all tissues throughout the body. Disturbing this balance of cell loss and cell proliferation can lead to disease. Tumor formation occurs when cell division exceeds cell death. This happens in one of two ways: either cell proliferation is increased so that it occurs faster than cell death or cell death is prevented or slowed so that it no longer keeps up with cell division. The progression of cellular changes leading to this excess growth and formation of a malignant tumor is the process known as multistage carcinogenesis. Most, if not all, of the morphological and biochemical characteristics of malignant cells have as their source either genetical or epigenetical alterations in gene expression. Therefore, the controls that usually tightly regulate the cell growth and death processes on a molecular level must be examined and manipulated in order to fully understand multistage carcinogenesis. Many factors can contribute to carcinogenesis, including viruses, chemicals, radiation, diet, hormones, and genetical predisposition.

Duke Scholars

Author Steven Patierno Medicine, Medical Oncology