Cancer is uncontrolled cell division. A normal cell becomes a cancer cell when it loses its ability to stop at inter phase of the cell cycle. Most cancers arise from just one aberrant cell. The original cancer cell produces daughter cells with the same defect, and these daughter cells divide to form more cancer cells. (At some point, a cancer cell also acquires the ability to metastasize—to burrow its way into a blood
vessel or lymph vessel and invade other parts of the body. A cancer that has metastasized can no longer be eliminated by surgery because its cells are too widely dispersed throughout the body. Cancer cells continue to multiply, in various parts of the body, until they interfere with normal body functions by monopolizing nutrients and pressing on blood vessels.
When a critical function fails, the person dies. Cancer kills one out of every five adult Americans. Cancer cells behave abnormally even under laboratory conditions. Normal cells, when grown in a dish, multi-ply until the cells cover the bottom of the dish with a single layer—no more. The physical contact of one cell with other cells signals the cell to stop dividing. This phenomenon is known as contact inhibition. Cancer cells, by contrast, continue to divide even after they contact one another. They pile up, layer after layer, within the dish.
Another abnormality seen,'n laboratory-grown cells is that a line'uf cancer cells can live forever. Normal cells are programmed to divide only a certain number of times. Certain cells in an embryo, for example, always divide just fifty times. They then remain in interphase until they die. Cancer cells, by contrast, continue to divide and divide; the line of cells does not die out. One line of cancer cells—the so-called HeLa cells (removed from a patient named Henrietta Lacks)—have been dividing continuously since 1951. The cells appear to be immortal.
Cancer begins when something goes wrong with the genes that regulate the cell cycle. Two sets of genes appear to be involved: genes that stimulate cell division and genes that sup-press cell division. Whether a cell divides or remains in interphase depends on the relative activity of these two sets of genes. Normal genes that stimulate cell division are called protooncogenes. They become oncogenes, and cause cancer, when too many copies of their proteins are synthesized.
The excess proteins dominate the cell, ordering it to continue immediately into mitosis rather than to stop at interphase. The best-known oncogene codes for the Ras protein, which forms part of a pathway that re-lays signals between the plasma membrane and the nucleus. When a signal from this pathway reaches the nucleus, it activates genes that trigger cell division. About 15% of all human cancers synthesize too much of the Ras protein. Genes that inhibit cell division are called suppressor genes. They normally switch off cell division so that the cell spends most of its time in interphase. In a cancer cell these genes fail to produce enough of their proteins to stop the cell cycle at interphase. Consequently, the cell moves directly from one cell division to the next.
The best-known suppressor gene is p53, which codes for a protein that blocks cell division. Its mutated form does not produce its protein, and so the cell does not stop at interphase. Roughly half of all human cancers contain the mutated form of p53. A cancer cell is the outcome of a series of genetic accidents—perhaps as many as fifteen changes in the genes that control the cell cycle. Some of these changes may be inherited; others occur during the lifetime of the individual as the DNA is damaged by radiation or chemicals in the environment, such as tobacco smoke, smog, and pesticides.
In addition to damage to the genes that control the cell cycle, the development of a cancer cell may also require damage to the genes that pro-mote DNA repair. These genes code for proteins that recognize and correct errors in the DNA molecule. If they did not function correctly, the cell would accumulate mutations rapidly. A person's cells undergo about 1016 cell divisions during their lifetime. Cancer can develop anytime one of these cell cycles gets stuck in the "on" position. Most likely, these cell divisions often generate cancer cells, but they are destroyed by the immune system (white blood cells and antibodies) before they have time to proliferate into a tumor. Cancer appears to develop from both a series of altered genes and a weakened or abnormal immune system.
Wednesday, October 5, 2016
Cancer effects and the Cell Cycle
would you like to know how dose the Cancer effects the Cell Cycle?
Cancer is uncontrolled cell division. A normal cell becomes a cancer cell when it loses its ability to stop at inter phase of the cell cycle. Most cancers arise from just one aberrant cell. The original cancer cell produces daughter cells with the same defect, and these daughter cells divide to form more cancer cells. (At some point, a cancer cell also acquires the ability to metastasize—to burrow its way into a blood
vessel or lymph vessel and invade other parts of the body. A cancer that has metastasized can no longer be eliminated by surgery because its cells are too widely dispersed throughout the body. Cancer cells continue to multiply, in various parts of the body, until they interfere with normal body functions by monopolizing nutrients and pressing on blood vessels.
When a critical function fails, the person dies. Cancer kills one out of every five adult Americans. Cancer cells behave abnormally even under laboratory conditions. Normal cells, when grown in a dish, multi-ply until the cells cover the bottom of the dish with a single layer—no more. The physical contact of one cell with other cells signals the cell to stop dividing. This phenomenon is known as contact inhibition. Cancer cells, by contrast, continue to divide even after they contact one another. They pile up, layer after layer, within the dish.
Another abnormality seen,'n laboratory-grown cells is that a line'uf cancer cells can live forever. Normal cells are programmed to divide only a certain number of times. Certain cells in an embryo, for example, always divide just fifty times. They then remain in interphase until they die. Cancer cells, by contrast, continue to divide and divide; the line of cells does not die out. One line of cancer cells—the so-called HeLa cells (removed from a patient named Henrietta Lacks)—have been dividing continuously since 1951. The cells appear to be immortal.
Cancer begins when something goes wrong with the genes that regulate the cell cycle. Two sets of genes appear to be involved: genes that stimulate cell division and genes that sup-press cell division. Whether a cell divides or remains in interphase depends on the relative activity of these two sets of genes. Normal genes that stimulate cell division are called protooncogenes. They become oncogenes, and cause cancer, when too many copies of their proteins are synthesized.
The excess proteins dominate the cell, ordering it to continue immediately into mitosis rather than to stop at interphase. The best-known oncogene codes for the Ras protein, which forms part of a pathway that re-lays signals between the plasma membrane and the nucleus. When a signal from this pathway reaches the nucleus, it activates genes that trigger cell division. About 15% of all human cancers synthesize too much of the Ras protein. Genes that inhibit cell division are called suppressor genes. They normally switch off cell division so that the cell spends most of its time in interphase. In a cancer cell these genes fail to produce enough of their proteins to stop the cell cycle at interphase. Consequently, the cell moves directly from one cell division to the next.
The best-known suppressor gene is p53, which codes for a protein that blocks cell division. Its mutated form does not produce its protein, and so the cell does not stop at interphase. Roughly half of all human cancers contain the mutated form of p53. A cancer cell is the outcome of a series of genetic accidents—perhaps as many as fifteen changes in the genes that control the cell cycle. Some of these changes may be inherited; others occur during the lifetime of the individual as the DNA is damaged by radiation or chemicals in the environment, such as tobacco smoke, smog, and pesticides.
In addition to damage to the genes that control the cell cycle, the development of a cancer cell may also require damage to the genes that pro-mote DNA repair. These genes code for proteins that recognize and correct errors in the DNA molecule. If they did not function correctly, the cell would accumulate mutations rapidly. A person's cells undergo about 1016 cell divisions during their lifetime. Cancer can develop anytime one of these cell cycles gets stuck in the "on" position. Most likely, these cell divisions often generate cancer cells, but they are destroyed by the immune system (white blood cells and antibodies) before they have time to proliferate into a tumor. Cancer appears to develop from both a series of altered genes and a weakened or abnormal immune system.
Cancer is uncontrolled cell division. A normal cell becomes a cancer cell when it loses its ability to stop at inter phase of the cell cycle. Most cancers arise from just one aberrant cell. The original cancer cell produces daughter cells with the same defect, and these daughter cells divide to form more cancer cells. (At some point, a cancer cell also acquires the ability to metastasize—to burrow its way into a blood
vessel or lymph vessel and invade other parts of the body. A cancer that has metastasized can no longer be eliminated by surgery because its cells are too widely dispersed throughout the body. Cancer cells continue to multiply, in various parts of the body, until they interfere with normal body functions by monopolizing nutrients and pressing on blood vessels.
When a critical function fails, the person dies. Cancer kills one out of every five adult Americans. Cancer cells behave abnormally even under laboratory conditions. Normal cells, when grown in a dish, multi-ply until the cells cover the bottom of the dish with a single layer—no more. The physical contact of one cell with other cells signals the cell to stop dividing. This phenomenon is known as contact inhibition. Cancer cells, by contrast, continue to divide even after they contact one another. They pile up, layer after layer, within the dish.
Another abnormality seen,'n laboratory-grown cells is that a line'uf cancer cells can live forever. Normal cells are programmed to divide only a certain number of times. Certain cells in an embryo, for example, always divide just fifty times. They then remain in interphase until they die. Cancer cells, by contrast, continue to divide and divide; the line of cells does not die out. One line of cancer cells—the so-called HeLa cells (removed from a patient named Henrietta Lacks)—have been dividing continuously since 1951. The cells appear to be immortal.
Cancer begins when something goes wrong with the genes that regulate the cell cycle. Two sets of genes appear to be involved: genes that stimulate cell division and genes that sup-press cell division. Whether a cell divides or remains in interphase depends on the relative activity of these two sets of genes. Normal genes that stimulate cell division are called protooncogenes. They become oncogenes, and cause cancer, when too many copies of their proteins are synthesized.
The excess proteins dominate the cell, ordering it to continue immediately into mitosis rather than to stop at interphase. The best-known oncogene codes for the Ras protein, which forms part of a pathway that re-lays signals between the plasma membrane and the nucleus. When a signal from this pathway reaches the nucleus, it activates genes that trigger cell division. About 15% of all human cancers synthesize too much of the Ras protein. Genes that inhibit cell division are called suppressor genes. They normally switch off cell division so that the cell spends most of its time in interphase. In a cancer cell these genes fail to produce enough of their proteins to stop the cell cycle at interphase. Consequently, the cell moves directly from one cell division to the next.
The best-known suppressor gene is p53, which codes for a protein that blocks cell division. Its mutated form does not produce its protein, and so the cell does not stop at interphase. Roughly half of all human cancers contain the mutated form of p53. A cancer cell is the outcome of a series of genetic accidents—perhaps as many as fifteen changes in the genes that control the cell cycle. Some of these changes may be inherited; others occur during the lifetime of the individual as the DNA is damaged by radiation or chemicals in the environment, such as tobacco smoke, smog, and pesticides.
In addition to damage to the genes that control the cell cycle, the development of a cancer cell may also require damage to the genes that pro-mote DNA repair. These genes code for proteins that recognize and correct errors in the DNA molecule. If they did not function correctly, the cell would accumulate mutations rapidly. A person's cells undergo about 1016 cell divisions during their lifetime. Cancer can develop anytime one of these cell cycles gets stuck in the "on" position. Most likely, these cell divisions often generate cancer cells, but they are destroyed by the immune system (white blood cells and antibodies) before they have time to proliferate into a tumor. Cancer appears to develop from both a series of altered genes and a weakened or abnormal immune system.
Subscribe to:
Post Comments (Atom)
No comments:
Post a Comment