Biology of Brain Tumour: Proceedings of the Second by John Paul (auth.), Michael D. Walker M.D, David G. T. Thomas

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By John Paul (auth.), Michael D. Walker M.D, David G. T. Thomas MRCP, FRCSE (eds.)

This quantity includes the complaints of the second one foreign Symposium on Biology of mind Tumour. the 1st Symposium used to be held in 1979 at Gardonne Riviera, Italy. This assembly was once deliberate to be able to coincide with the lOOth Anniversary of the 1st stated operation for glioma in London on November 25, 1884. because the first assembly, the sphere of neuro-oncology has made outstanding development in realizing either uncomplicated and scientific components of importance to sufferers with mind tumor. whereas the sooner assembly dealt to a wide volume with clinically orientated experiences, this symposium used to be extra seriously weighted towards the biology of mind tumour and bettering our figuring out on the physiologic, biochemical, pharmacologic, and mobile point. The assembly used to be divided in accordance with medical content material into displays and discussions in addition to posters for extra leisurely viewing, in order to permit the most topics of the assembly to sequentially improve. the 1st consultation dealt widely with neuro-oncology on the molecular point and integrated significant discus­ sion of fabric regarding the babic biochemical milieu within which tumors originate, proliferate, and finally ruin the mind. vintage neuropathology has been the mainstay of tumor identity and characteriza­ tion, although, the method of class has develop into even more advanced. the supply of numerous new instruments has allowed research into the validity of the extra conventional type platforms in addition to the advance of more moderen biologically comparable concepts.

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Additional info for Biology of Brain Tumour: Proceedings of the Second International Symposium on Biology of Brain Tumour (London, October 24–26, 1984)

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Chemical agents/drugs used. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 00() xg spnt. Dil. 05tLg/ml 15tLglmi Concentrations of drugs were selected according to the following criteria. (4,5,8,10) ID,{) from cloning glioma. (9) cytostatic (DNA synth. ) wlo cell death. (6) Morphological response in normal and malignant glia. ). (2) GFAP induction in C 6 maximum induction of plating efficiency in human glioma cclllines. 37 400 %Incr. D. OX RA IFN PBE Me MNU 25 DX RA IFN PBE NMA Me MNU Fig. 1. Effect of six of the agents tested on high affinity uptake of Fig.

Semi Neuroll: 181-187. 1981 2. Patel AJ, Lewis PD: Effects on cell proliferatiorr of pharmacological agents acting on the central nervous system. In: KN Prasad and A Vernadakis (eds) Mechanisms of actions of neurotoxic substances. Raven Press. New York, 1982, pp 181-218 3. Thomas DGT: Brain tumours. Br J Hosp Med 29: 148-158, 1983 4. Bignami A, Dahl D: Differentiation of astrocytes in the cerebellar cortex and the pyramidal tracts of the newborn rat. An immunofluorescence study with antibodies to a protein specific to astrocytes.

Although medulloblastomas ex vivo may express GFAP (5-7), it could not be detected in treated and untreated TE671 cells. The control U-251 MG glioma line known to express GFAP (47) was positive. GFAP has been induced in C-6 rat glioma cells by db-cAMP (23). Neuron specific enolase (NSE) was chosen as a marker for neuronal maturation as it has been demonstrated in neuronal-derived normal (48, 49) and malignant cell lines (28, 29, 50). NSE expression has been induced in vitro by many differentiation agents: db-cAMP (50) sodium butyrate (25), nerve growth factor (28) and phorbol esters (17).

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