how to create barcode in using c# INTRACRANIAL NEOPLASMS AND PARANEOPLASTIC DISORDERS in Microsoft Office


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The above model is well illustrated by consideration of the astrocytoma Among the rst detectable changes are mutations that inactivate the tumor suppressor gene, p53 on chromosome 17p; over 50 percent of astrocytomas have deletions encompassing this gene Other early changes include overexpression of growth factors or their receptors as noted below After the tumor develops, progression to a more malignant grade of astrocytoma or to a glioblastoma may be triggered by defects in the p16-retinoblastoma gene signaling pathway, loss of chromosome 10 (seen in about 90 percent of high-grade gliomas), or overexpression of the epidermal growth factor gene In fact, it is striking that analysis of the patterns of these defects correlates accurately with the staging and aggressive characteristics of these tumors Knowledge of the molecular signatures of certain other tumors has immense clinical value For example, as discussed further on, oligodendrogliomas that have combined deletions in chromosomes 1p and 19q respond well to chemotherapy, and this property may increase survival by more than 10 years This type of information may spare the nonresponsive patient from ineffective, sometimes toxic therapy (see Reifenberger and Louis; Louis et al) Much of the modern genetic classi cation of brain tumors is derived from the technical tour de force of gene microarrays The patterns of these multiple gene analyses are able to distinguish some types of medulloblastomas from the similar-appearing primitive neuroectodermal tumors; the medulloblastomas express classes of genes that are characteristic of cerebellar granule cells, suggesting they arise from these cells Also, these gene expression signatures confer useful prognostic information in a more general way than noted above for oligodendroglioma For example, medulloblastomas that express genes indicative of cerebellar differentiation are associated with longer survival than those expressing genes related to cell division (Pomeroy et al) Furthermore, as alluded to earlier, in about 50 percent of gliomas there is an overexpression or a mutant form of epidermal growth factor (EGF) and of transforming growth factor alpha (TGF- ), suggesting a role for these in the progression of certain tumor types Other trophic factors are overexpressed in yet other brain neoplasms and perhaps contribute to their morphology and growth pattern; for example, VEGF is found in extremely high concentrations in meningiomas, which are highly vascular by nature These ndings, taken together, suggest an autocrine stimulation of growth by these factors and possibly an interaction with some of the aforementioned gene defects However, having emphasized molecular and chromosomal changes, it is not yet clear if any of them is truly causative (the currently favored hypothesis) or if they simply re ect an aberrant genetic process that accompanies the dedifferentiation of tumor growth and progression On the basis of this new molecular information, our views of the pathogenesis of neoplasia are being cast along new lines Some of the speci cs of these new data are presented in the following discussions of particular tumor types A more extensive review can be found in the article by Osborne and colleagues, including the heterogeneity of ndings that suggests polygenic changes in most gliomas
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contained therein the brain (about 1200 to 1400 mL), cerebrospinal uid (CSF; 70 to 140 mL), and blood (150 mL) are relatively incompressible, particularly the brain substance, and each is subject to displacement by a localized mass lesion According to the Monro-Kellie doctrine, the total bulk of the three elements is at all times constant, and any increase in the volume of one of them must be at the expense of one or both of the others discussed in Chap 30 A tumor growing in one part of the brain therefore compresses the surrounding brain tissue and displaces CSF and blood; once the limit of this accommodation is reached, the intracranial pressure (ICP) rises The elevation of the ICP and perioptic pressure impair axonal transport in the optic nerve and the venous drainage from the optic nerve head and retina, manifesting itself in papilledema It must be pointed out, however, that only some brain tumors cause papilledema and that many others often quite as large do not Thus one may question whether the Monro-Kellie doctrine, and its simple implied relationships of intracranial volume and CSF pressure, fully accounts for the development of raised ICP and papilledema with brain tumors This discrepancy is in part because, in a slow process such as tumor growth, brain tissue is to some degree compressible, as one might suspect from the large indentations of brain produced by massive meningiomas Presumably, with tumor growth, the venules in the cerebral tissue adjacent to the tumor are compressed, with resulting elevation of capillary pressure, particularly in the cerebral white matter The slow growth of most tumors permits accommodation of the brain to changes in cerebral blood ow and ICP Only in the advanced stages of tumor growth do the compensatory mechanisms fail and CSF pressure and ICP rise, with consequences described in Chap 30 Once pressure is raised in a particular compartment of the cranium, the tumor begins to displace tissue at rst locally and at a distance from the tumor, resulting in a number of false localizing signs including coma, described in Chap 17 Indeed, the transtentorial herniations, the paradoxical corticospinal signs of Kernohan and Woltman, sixth and third nerve palsies, occipital lobe infarcts, midbrain hemorrhages, and secondary hydrocephalus were all originally described in tumor cases (see further on, under Brain Displacements and Herniations ) Brain Edema This is a most important aspect of tumor growth, but it also assumes importance in cerebral trauma, infarction, abscess, hypoxia, and other toxic and metabolic states Brain edema is such a prominent feature of cerebral neoplasm that this is a suitable place to summarize what is known about it For a long time it has been recognized that conditions leading to peripheral edema, such as hypo-albuminemia and increased systemic venous pressure, do not have a similar effect on the brain By contrast, lesions that alter the blood-brain barrier cause rapid swelling of brain tissue Klatzo speci ed two categories of edema, vasogenic and cytotoxic Fishman adds a third, which he calls interstitial edema An example of the latter is the edema that occurs with obstructive hydrocephalus, especially when the ependymal lining is lost and CSF seeps into the periventricular tissues in the spaces between cells and myelin Most neuropathologists use the term interstitial to refer to any increase in the extravascular intercellular compartment of the brain; this would include both vasogenic and Fishman s interstitial edema Vasogenic edema is the type seen in the vicinity of tumor growths and other localized processes as well as in more diffuse injury to the blood vessels (eg, lead encephalopathy, malignant
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