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Inheritance of a mutated retinoblastoma gene (Rb*) greatly increases the likelihood of developing the disease.

one hit cell remains normal one hit

CANCER

two hits senescence a state in a cell in which it will not divide again, even in the presence of growth factors apoptosis programmed cell death quickly increase the chance that a cell will become cancerous. Repair genes include those in the DNA-ligase and excision-repair gene families.

Genes Involved in Cell Mortality. A normal cell can only undergo about forty divisions, after which it dies or enters senescence. If a tumor had this limitation it would be very limited in its size, as it would reach its forty divisions relatively quickly. This process is controlled by the enzyme telomerase, which maintains the telomeres (repetitive DNA sequences at the ends of chromosomes that shorten after each round of DNA replication, until they reach a length that causes the cell to die) by not allowing them to shorten. Some cancer cells become immortal as a result of mutations in the telomerase gene, causing the telomeres to be extended indefinitely, allowing the cell to continue dividing without limit. Other mutations affect the process of apoptosis.

Cancer does not usually arise by a single event. Instead, two or more "hits" are needed to convert a well-regulated cell to a cancer cell. This is the case because each cell contains two copies of each gene, one inherited from each parent. Most cancer-causing mutations cause a loss of function in the mutated gene. Often, having only one functional copy is enough to prevent disease. Thus, two mutations are needed.

This can be illustrated by looking at retinoblastoma, a common cancer of the retina. The affected gene (called the retinoblastoma gene) is a tumor suppressor. Spontaneous mutations are rare, but since there are many millions of cells in the retina, several will develop the appropriate gene mutation over the course of a lifetime. It would be very unlikely, though, for a single cell to develop two spontaneous mutations (at least in the absence of prolonged exposure to carcinogens), and thus spontaneous retinoblastoma is very rare.

If, however, a person inherits one copy of an already-mutated gene from one parent, every cell in the eye starts life with one "hit." The chances are very high that several cells will suffer another hit sometime during their life, and so the chances are very high that the person will develop retinoblas-toma. Since inheriting a single copy of the mutated gene is so likely to lead to the disease, the gene is said to show a dominant inheritance pattern.

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