Malignant Brain Tumours by Mark Noble, Karen Bevan, Deon Venter (auth.), David G. T. PDF

By Mark Noble, Karen Bevan, Deon Venter (auth.), David G. T. Thomas MA, FRCP(G), FRCS Ed., David I. Graham MBBCh, PhD, FRCPath, FRS(Ed) (eds.)

"...an instance of a superb co-operation among neurosurgery and neuropathology...an first-class compendium of present proposal and perform of mind tumours...The ebook may well function a reference either for learn, perform, study and educating. it may be totally prompt" - magazine of mind examine

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E. E. , 1990). Losses of 17p are also observed in all grades of glioma, which oeeur in some patients with NF 1. , 1989). It seems unlikely that this is related to the NF 1 loeus on 17q in terms of tumorigenesis in this disease, and more complex meehanisms than the two hit system are probably operative in this context. Cytogenetic and Molecular Genetic Studies of Malignant Brain Tumours: Gliomas Several eytogenetic investigations into the ehromosome content of glioma eelis, from both fresh biopsy material and cultured eelis, have been performed, the most extensive of which is that of Bigner et al.

Br J Haem 48: 179-197 Hughes S, Lillien LE, Raff MC, Rohrer H, Sendtner M (1988) Ciliary neurotrophie faetor induees type-2 astroeyte differentiation in culture. Nature 335: 70-73 James CD, Carlborn E, Dumanski JP et al. (1988) Clonal genomie alterations in glioma malignancy stages. Caneer Res 48: 5546-5561 Jat PS, Sharp PA (1989) Cell lines established by a temperature-sensitive simian viru s 40 large-T antigen gene are growth restrieted at the nonpermissive temperature. Molee Cell Biol9: 1672-1681 Janzer R, Raff MC (1987) Astroeytes indu ee blood-brain barrier properties in endotheiial eelis.

Over 30 human oneogenes have been eharaeterized (Gilbert, 1988), and the meehanisms by whieh they eause neoplastie growth indude the produetion of abnormaI types or amounts of growth faetors or growth faetor reeeptors, or of eellular kinase enzymes. For example, a gene on the short arm of ehromosome 7 eodes for the epidermal growth faetor reeeptor (EGFR). The e-erb B oneogene produet is homologous to EGFR, but laeks its external EGF binding portion, perhaps removing the meehanism for homeostatie controI.

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