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| Glioblastoma Multiforme | ||
| Etiology •The exact etiology is not known but has to do with several mutations in protooncogenes and tumor suppressor genes. •Some appear as a part of several hereditary syndromes such as neurofibromatosis or Turcot's syndrome. | ||
| Pathogenesis •The cause of the glioblastoma or any brain tumor is not known but changes or loss of chromosome 17 and inactivation of a tumor suppressor gene, p53, play a role. Thus far, we do not know what precipitates these changes., | ||
| Epidemiology •Glioblastomas are the most comman primary brain tumor. •They account for 50% of all gliomas and arise after age 50 in most patients. •Younger patients tend to have a better prognosis than the elderly. •Radiation and chemotherapy appear to extend the life of the patient. | ||
| General Gross Description •The glioblastoma multiforme has a multiform or variable appearance with evidence of old and recent hemorrhage (yellowish-brown to red), necrosis and areas of firm tissue. •Usually the glioblastoma is seen as a mass lesion involving a focal area although it may cross the corpus callosum to the other hemisphere or be multifocal. •Examples: | ||
| General Microscopic Description •Microscopically the glioblastoma has many forms as well. •Is a highly cellular tumor with pleomorphic, basophilic nuclei with indistinct cytoplasmic borders or plump pink cytoplasm and a delicate fibrillary background. •Mitoses,necrosis, and capillary endothelial proliferation are common. •Examples: | ||
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 1342-1344. • • Poirer J et.al. Manual of basic neuropathology. Philadelphia: Saunders, 1990, pp. 25-26. This link will directly take you to the relevant new literature Glioblastoma Multiforme
| Synopsis by: M. L. Grunnet M.D. (TX2000M94403)[30]
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