Cancer is the result of a rupture of the exquisite equilibrium established between the proliferation of the cells and their death. A cell should exclusively divide when the conditions require that it does, and this is signaled through a battery of messengers called growth factors. Even in the presence of those factors, a very complex control mechanism checks whether the moment for division is appropriate, and every step of replication of the cell is followed by checkpoints that determine if it has been successfully completed.
Under normal conditions, an alteration detected at any of these checkpoints
results in the immediate destruction of the cell (see Figure 1) Such a complex
mechanism can fail either if cell starts the division without an external signal
and any of the checkpoints fail to detect the error, or if the mechanisms
designed to delete the abnormal cell fail. For this reason, virtually all of the
proteins implicated in these processes can, when altered, be the cause of cancer. They are then called protooncogenes in their normal form, and
oncogenes in their altered manifestation. This alteration can be caused by a
mutation of the protein itself, inducing a greater activity in those genes
implicated in growth stimulation or a decreased activity in those implicated in
cell death. Alternatively, the regulation of the expression of the protein can
be altered. The expression (conversion of information from the gene into a
functional protein) of every gene is tightly regulated and varies depending on
many factors, such as the developmental stage of a particular cell, its location
and its type. A protein is expressed only where and when it is needed. The
expression out of time or out of place results in an altered function, although
the structure of the protein can be normal. It is easy to imagine that, since
all cells have to divide and eventually die sooner or later, the presence of the
proteins implicated in cell cycle control is universal in all ti
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Contact: Luis A. Pardo,Max Planck Institute for Experimental Medicine
lpardo@gwdg.de
49-551-3899-643
Max-Planck-Gesellschaft
15-Oct-1999