1. A Safety System Fails: While each human cell performs its own specialized function, it also exerts influence on the cells around it. Cells communicate with one another via receptors, protein molecules on the cell surface. A cell releases chemical messages, which fit into the surface receptors of cells nearby, much as a key fits into a lock. A cell may instruct other cells in its neighborhood to divide, for example, by releasing a growth-promoting signal, or growth factor. The growth factor binds to receptors on adjacent cells, activating a message within each individual cell. This message travels to the nucleus, where a cell’s genes are located. 2. Proto-Oncogenes
Become Oncogenes: When the growth factor message reaches the cell nucleus, it activates genes called proto-oncogenes. These genes produce proteins that stimulate the cell to divide. In cancerous cells, mutations in proto-oncogenes cause these genes to malfunction. When a proto-oncogene mutates, it becomes an oncogene—a gene that instructs the cell to grow and divide repeatedly without stimulation from neighboring cells. Some oncogenes overproduce growth factors, causing the cell to divide too often. Other oncogenes stimulate the cell to reproduce even when no growth factor is present. Cancer researchers have identified about 100 different types of proto-oncogenes and their cancer-causing oncogene counterparts.
3. 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. 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. 5. Cells Break Free and Spread: 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. http://www.adhitz.com/en/Publishers-Generate_Code?pid=25286
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