Cancer (medicine)

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Tumor Suppressor Genes Stop Working

When runaway cell division occurs, it does not necessarily lead to cancer. Neighboring cells respond by excreting a growth inhibitor. This chemical binds to receptors in the malfunctioning cell, sending a signal to the nucleus that activates tumor suppressor genes. Tumor suppressor genes are like brakes for cell growth. When activated, these genes halt the cell cycle, preventing further cell division.

But if tumor suppressor genes malfunction due to mutations, the rapidly dividing cell ignores messages from its neighbors telling it to stop dividing. Malfunctioning tumor suppressor genes are not enough to cause cancer—the cell still must overcome a host of other safety mechanisms before it can cause truly significant damage.

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Cell Cycle Clock Malfunctions

The cell nucleus contains a collection of interacting proteins that control cell division. Sometimes called the cell cycle clock, this group of proteins interprets incoming messages at several checkpoints in the cell division cycle. At these checkpoints, the clock evaluates the health of the cell. If conditions are right, the clock activates certain proto-oncogenes, which produce proteins that trigger the cell to enter the next stage of the cell cycle. If conditions are not right, certain tumor suppressor genes produce proteins that prevent the cell from proceeding with cell division.

If the cell cycle clock detects DNA damage in a cell, a tumor suppressor gene called p53 prevents the cell from reproducing until the damage is repaired. If the cell is unable to repair the DNA damage, p53 instructs the cell to undergo programmed cell death, or apoptosis, putting a stop to runaway cell division before it starts. Programmed cell death is a normal part of cell life and is tightly controlled by many genes, primarily p53.

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In a cancerous cell, one or more mutations prevent these genes from doing their jobs. When mutated, p53 allows a cell to continue to divide, even with damaged DNA. This can lead to additional mutations in proto-oncogenes or tumor suppressor genes. In some cases, mutations occur in genes that produce proteins to repair damaged DNA. Such mutations can lead to yet other mutations because the faulty DNA cannot duplicate properly during cell division.

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4

Cells Achieve Immortality

A normal cell has a life span of about 40 cell divisions. This life span is controlled in part by telomeres, protective segments at the ends of the cell’s DNA. Telomeres shorten with each cell division until they can no longer protect the DNA. At this point cell division severely damages the DNA, ultimately killing the cell. This normal process ensures that older cells, which may have accumulated mutations, no longer reproduce. Cancer cells escape this protective mechanism by producing a protein called telomerase. Telomerase extends the length of telomeres indefinitely, rendering the cells immortal and capable of never-ending cell division.

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Cells Break Free and Spread

Evading the many obstacles that guard against runaway cell division is still not enough for cancer to develop. A malfunctioning cell must also skirt a number of safety mechanisms designed to prevent cells from growing where they are not supposed to in the body.

Normal cells adhere to each other and to a fibrous meshwork called an extracellular matrix. This matrix exists throughout all tissues and provides the structural support on which cells grow and form organs and other complex tissues. While a normal cell will often die if it cannot adhere to an extracellular matrix, cancer cells survive without this matrix.

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Tumor Forms

A tumor is a mass of cells not dependent upon an extracellular matrix. These cells can grow on top of each other, creating a mass of abnormal cells. Often a tumor develops its own network of tiny blood vessels to supply itself with nutrient-rich blood, a process called angiogenesis.

There are two general types of tumors. Benign tumors do not invade other tissues and are limited to one site, making surgical removal possible and the odds for a full recovery excellent. Some benign tumors are quite harmless and are not surgically removed unless they are unsightly or uncomfortable. For example, warts are benign tumors of the outer layer of the skin. Although they are usually not dangerous, warts may cause discomfort. Other benign tumors are thought to be precursors to cancerous, or malignant, tumors.

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