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Cancer as a genetic disease
8/6/00. By Giles Newton
The transition from a normal cell to a malignant cancer is driven by changes to the cell's DNA.
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Cancer is the most common human genetic disease. Approximately one in three individuals in Europe and North America develops one of the approximately 200 different types of cancer, and it the cause of death of one in five. So what is going wrong?
The cells in the human body work together, dividing and reproducing in a strictly controlled and coordinated fashion. This collaboration keeps each tissue at the size, shape and architecture appropriate to the needs of the body.
Cancer cells violate this collaborative ethos, becoming 'rogue traders' that pursue their own agendas for proliferation. Such uncontrolled reproduction leads to the formation of a tumour, which is not necessarily dangerous to the body. But if the tumour becomes more advanced, acquiring nutrients by plumbing into the body's blood supply and then developing the ability to
invade other tissues or colonise other parts of the body, the cancer becomes very hard to stop.
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A growth control gene is mutated in a single cell. Excessive growth begins.
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Further mutations in tumour suppressor genes allow the tumour to resist signals to undergo programmed cell death.
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The tumour reaches a limit in its size, where it cannot acquire sufficient nutrients to grow larger.
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Other mutations promote angiogenesis - new blood vessels grow to the tumour, providing nutrients and allowing further growth.
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Metastasis - mutations allow the cancer cells to colonize other parts of the body.
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These events - the transition from a normal cell to a malignant cancer - are driven by changes to the cell's DNA. All cells acquire mutations over their lifetime, but most are quickly repaired by the cell's maintenance machinery. The machinery is not foolproof, however, and if mutations are missed in two classes of gene that control growth - proto-oncogenes and tumour
suppressor genes - the cancer cycle can begin.
To become fully cancerous, it is thought that a cell must acquire mutations in a number of growth-controlling genes, as well as in other genes that enable it to become invasive or to spread in the body.
But cancer cannot be blamed entirely on leaky repair systems. Some people inherit a predisposition to cancer (often to a certain form of cancer such as colon cancer) in the form of a faulty gene. Tumour development is accelerated because one of the early, slowly occurring steps is already in place. The risk of cancer is much higher, as fewer new mutations are required, and the
cancer will tend to 'run' in the family.
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