The origin, or etiology of cancer can be approached from many different perspectives. What follows below is a summary of several different lines of scientific inquiry into the cause of cancer. One or all of these theories may explain the development of any given cancer.
 Cell dynamic theories
 Cell division or cell proliferation is a physiological process that occurs in almost all tissues and under many circumstances. Normally the balance between proliferation and apoptosis, or programmed cell death, is tightly regulated to ensure the integrity of organs and tissues. Imbalances in the rates of cell division and cell death can lead to tumor growth in a tissue. Other events are usually required before metastasis can occur. Locally expansile tumors can also cause severe problems when they grow in certain locations, such as the head or airway.
 Natural selection and cancer
 The process of malignancy can be explained from an evolutionary perspective. Millions of years of biological evolution insure that the cellular metabolic changes that enable cancer to grow occur only very rarely. Most changes in cellular metabolism that allow cells to grow in a disorderly fashion lead to cell death. For example, the regulatory tumor suppressor gene, p53, causes the cell to enter programmed cell death when DNA damage occurs. Usually, the aquisition of multiple changes is necessary for a cell to enter a malignant state, such as metastasis-enabling DNA damage in the context of faulty p53. Considering the number of cell division events throughout the human lifetime, the number of errors that occur that lead to cancer is vanishingly slim. Cancer cells undergo a natural selection process, acquiring metabolic alterations so they can outcompete normal body cells for nutrients and oxygen. Tumors are thought to be clonal, in the sense that they probably start from a single, disorderly cell. The tumor continues to evolve due to chemotherapy treatments, and on occasion aberrant cells may acquire resistance to particular anti-cancer pharmaceuticals.