Intrinsic brain tumors, those that originate from neural cells within the brain and spinal cord, occur more frequently in older adults and children than they do in the general population. The main feature that makes intrinsic brain tumors different from cancers arising from other organs in the body is the fact that they rarely, if ever, metastasize outside the brain. Some cells in brain tumors do, however, stop dividing long enough to migrate a few millimeters away from the parent tumor to form new intracranial tumors. The most malignant of these is called glioblastoma multiforme (GBM).
In men and women less than 20 years old, brain cancer is, after leukemia, the next most prevalent cause of cancer deaths. Apart from leukemia, intracranial-derived tumors are the next leading cause of fatality in men between the ages of 20 and 30. In females between 20 and 39 years old, brain tumors are the fifth most prevalent cause of cancer deaths.
The incidence of GBM is very low, between two and three new cases per 100,000. Because of their ability to migrate away from the parent tumor and start new growths, complete surgical excision is impossible. Try scraping off all of the butter from your next slice of toast.
The type of cell that gives rise to GBM is the glial cell, of which there are three types. Nerve cells lose their ability to divide once they have reached terminal differentiation. Glial cells, on the other hand, are able to divide throughout the life of the individual. Evidence from both in vivo studies in the '60s and in vitro studies in the '90s and early 21st century support the hypothesis that most, if not all, intrinsic brain tumors begin forming in the developing fetus.
Glial cells come in three different forms: microglia, astrocytes and oligodendrocytes. Of these, astrocytes and astrocytic tumors, are the most common. The nastiest, most malignant and most deadly variant of astrocytoma is the GBM, which has a median time of survival without treatment of less than five months.
Astrocytes are characterized by their starry morphology and the presence of glial fibrillary acidic protein (GFAP). The normal function of astrocytes is to supply nutrients to nerve cells, support the vascular cells that comprise the blood brain barrier and repair damaged cells following trauma. New studies suggest that they communicate with neuronal cells by secreting glutamate, the brain's main excitatory neurotransmitter.
Other glial cells include the oligodendrocytes. These have fewer 'arms' than do astrocytes. The primary function of the oligodendrocytes is to form the myelin sheath that insulates nerve cells and accelerates the rate of neural transmission. One oligodendrocyte can insulate up to 50 separate neuronal cells. The myelin sheath is subject to attack by the immune system in the chronic and debilitation condition, multiple sclerosis (MS).
Microglia are the smallest members of the glial cell team. Their main function is to provide a rapid response to invading foreign bodies and prepare them for slaughter by T-cells. They do this by engulfing foreign matter in a process called phagocytosis. Resting microglia are the prettiest, and look like tiny astrocytes. Activated microglial cells look more bulbous with the processes less prominent.
In men and women less than 20 years old, brain cancer is, after leukemia, the next most prevalent cause of cancer deaths. Apart from leukemia, intracranial-derived tumors are the next leading cause of fatality in men between the ages of 20 and 30. In females between 20 and 39 years old, brain tumors are the fifth most prevalent cause of cancer deaths.
The incidence of GBM is very low, between two and three new cases per 100,000. Because of their ability to migrate away from the parent tumor and start new growths, complete surgical excision is impossible. Try scraping off all of the butter from your next slice of toast.
The type of cell that gives rise to GBM is the glial cell, of which there are three types. Nerve cells lose their ability to divide once they have reached terminal differentiation. Glial cells, on the other hand, are able to divide throughout the life of the individual. Evidence from both in vivo studies in the '60s and in vitro studies in the '90s and early 21st century support the hypothesis that most, if not all, intrinsic brain tumors begin forming in the developing fetus.
Glial cells come in three different forms: microglia, astrocytes and oligodendrocytes. Of these, astrocytes and astrocytic tumors, are the most common. The nastiest, most malignant and most deadly variant of astrocytoma is the GBM, which has a median time of survival without treatment of less than five months.
Astrocytes are characterized by their starry morphology and the presence of glial fibrillary acidic protein (GFAP). The normal function of astrocytes is to supply nutrients to nerve cells, support the vascular cells that comprise the blood brain barrier and repair damaged cells following trauma. New studies suggest that they communicate with neuronal cells by secreting glutamate, the brain's main excitatory neurotransmitter.
Other glial cells include the oligodendrocytes. These have fewer 'arms' than do astrocytes. The primary function of the oligodendrocytes is to form the myelin sheath that insulates nerve cells and accelerates the rate of neural transmission. One oligodendrocyte can insulate up to 50 separate neuronal cells. The myelin sheath is subject to attack by the immune system in the chronic and debilitation condition, multiple sclerosis (MS).
Microglia are the smallest members of the glial cell team. Their main function is to provide a rapid response to invading foreign bodies and prepare them for slaughter by T-cells. They do this by engulfing foreign matter in a process called phagocytosis. Resting microglia are the prettiest, and look like tiny astrocytes. Activated microglial cells look more bulbous with the processes less prominent.
About the Author:
When you are looking for information about glioblastoma, pay a visit to the web pages online here today. You can see details at http://www.megapedia.net now.
No comments:
Post a Comment