Mutation cause changes in signal molecules?

Answer 1

Releasing the brakes. Once it reaches the nucleus, an everyday "divide" signal induces the cell to divide by temporarily overriding a set of division suppressors that otherwise prevent division from occuring. For cancer to occur, it is necessary to permanently blow away these division suppressors, called "tumor suppressors." Like letting up on the brakes of a speeding car, decreasing the activity of tumor suppressors speeds up the cell division process.

1. Unleashing the copy signal. In healthy cells the primary brake on cell division is a tumor suppressor protein called pRB. pRB acts by blocking the signal which directs the cell to copy its DNA. Normal cell division is triggered to begin when pRB is inhibited, unleashing the "copy" signal. Mutations which destroy pRB release the signal from its control completely, leading to ceaseless cell division. 40% of all cancers have a defective form of pRB.

2. Killing the guardian angel. Before it divides, a healthy cell checks to ensure that it's DNA is undamaged. This job is carried out by a remarkable tumor suppressor protein called p53, sometimes called the "Guardian Angel" of the cell. p53 inspects the DNA, and when it detects damaged DNA it stops cell division and activates the cell's DNA repair systems. If the damage doesn't get repaired in a reasonable time, p53 pulls the plug, triggering events that kill the cell. In this way, mutations such as those that cause cancer are either repaired or the cells containing them eliminated. If p53 is itself destroyed by mutation, future damage accumulates unrepaired. Among this damage are mutations that lead to cancer, mutations that would have been repaired by a healthy p53. Over 50% of all cancers have a disabled p53. Fully 80% of lung cancers have a mutant inactive p53 the chemical benzo (a) pyrene in cigarette smoke is a potent mutangen of the p53 gene.

3. Removing the limit on a cell's life span. In healthy cells another tumor suppressor inhibits production of a special enzyme called telomerase. Without this enzyme, a cell's chromosomes loose material from their tips, called telomeres. Every time a chromosome is copied as the cell prepares to divide, more of the tip is lost. After some thirty divisions, so much is lost that copying is no longer possible. Cells in the tissues of an adult human have typically undergone twenty five or more divisions. Cancer can't get very far with only the five remaining cell divisions, so inhibiting telomerase is a very effective natural brake on the cancer process. Any mutation that destroys this telomerase inhibitor releases that brake, making cancer possible. It is thought that almost all cancers involve such a release of telomerase production.

This knowledge about how cancer is caused, obtained in many dozens of laboratories, is at last providing researchers with the weapons we need to attempt to cure cancer.