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Cancer mechanisms

Why does radiation cause excess cancers among atomic-bomb survivors?

Cancer is the general name for a group of diseases in which normal homeostatic cellular control is lost and cells grow continuously, invading, crowding, and overwhelming the surrounding normal tissues. If left unchecked, this unregulated growth results in the death of the organism. It is generally accepted that carcinogenesis, the process that transforms a normal cell into a cancer cell, is multistaged. In other words, in a cell, any single event by itself is not sufficient to turn a normal cell into a cancer cell. Only when the correct number, combination, and types of aberrant alterations have accumulated in one cell will a cancer cell develop. Normal living (for example, oxygen consumption, tobacco smoking, ultraviolet light exposure) produces a variety of damage to the cell that slowly accumulates throughout the life of an individual. This is the reason most cancers occur late in life. The identities of these crucial steps are still not completely clear, but there are a number of good candidates.
Among the major steps toward malignancy are alterations in the DNA. (See The human genome at four levels of detail.) More specifically, the key genes that control certain aspects of cellular activity and well-being, such as growth, repair, energy production, senesence, and cell suicide are affected. Genes, all of which make up the genome, are particular areas of the DNA that hold the information that is used by the cell to produce proteins, which are required for carrying out the assorted functions of the cell. It is suspected that ionizing radiation damages some of these genes through its ability to deposit molecular-bond-breaking energy, which results in altered or nonfunctional genes and gene products, ie, mutation. Once a gene has been damaged by ionizing radiation, the cell may repair it, the cell may die, or the cell may retain it. In the last scenario, depending on the gene that is damaged, the cell may attain a new character, such as some sort of survival advantage over its neighboring undamaged or repaired cells. Such cells are one step closer to becoming cancerous. As time passes, other alterations occur and accumulate, and if a critical number of events happens, cancer develops.
As far as common cancers are concerned, such as cancers of the lung, stomach, female breast, and colon, radiation exposure probably increases the risk of developing cancer by adding one more step at some point in the sequence of events occurring in those cells--cells that could have remained noncancerous if radiation exposure had not occurred. This is why no specific kinds of cancer only occur among radiation-exposed persons. This also would explain why the risk of cancer among survivors of radiation exposure is not 100 or 1000 times greater than among nonexposed persons. Usually, the cancer risk (except for leukemia) is, at most, five times greater after exposure to a whole-body radiation dose that is barely survivable.
Why do some tissues appear to be more radiosensitive?
Genes that promote tumors. What turns them on?
Genes that suppress tumors. What turns them off?