Gliosarcoma

Exposure of 9L gliosarcoma cells to hydrogen peroxide stimulated PPP, which could be attenuated when the neurons were preincubated with the iron chelator desferrioxamine. 

Chadduck WM, Gollin SM, Gray BA, et al. 1987. Gliosarcoma with chromosome abnormalities in a neonate exposed to heptachlor. Neurosurgery 21.557-559. 

Wargotz ES, Sidawy MK, Jannotta FS. 1988. Thorotrast associated gliosarcoma including comments on Thorotrast use and review of sequelae with particular reference to lesions of the central nervous system. Cancer 62 58-60. 

A. Franko, C. Koch, D. Boisvert, Distribution of misonidazole adducts in gliosarcoma tumors and spheroids Implications for oxygen distribution. Cancer Res. 52 (1992) 3831-3837. 

J. R. James, Y. Gao, V. C. Soon, S. M. Topper, A. Babsky and N. Bansal, Controlled radiofrequency hyperthermia using an MR scanner and simultaneous monitoring of temperature and therapy response by H, Na and P magnetic resonance spectroscopy in subcutaneously implanted 9L-gliosarcoma. Int.. Hyperthermia, 2010, 26, 79-90. 

Gadolinium(III) was complexed to the DTPA component of ATN-10 for possible use in neutron capture therapy [113]. An additional benefit of the incorporation of gadolinium(III) into ATN-10 is the increase in the relaxivity of the agent [113]. Injection of Gd-ATN-10 into rats with 9L gliosarcomas demonstrated an increase in the signal intensity of the tumor. The agent potentially has toxicity problems, though, as it was demonstrated that the metal ions may dissociate from the complex. 

Fig. 13.1. This figure demonstrates confinement of the LCM to 9L gliosarcoma tumors in the Fischer rat (top left) and to C6 gliomas in the Sprague-Dawley rat (top right) with Oil Red-O lipid staining. Bottom left panel is the 9L tumor (in Fischer 344 rat) immediately after intravenous injection with diO-labeled LCM. Bottom right panel shows this same tumor. Here nine successive 0.8 pm tomographic sections in the Z axis from the confocal laser microscope illustrates the presence of the intracellular LCM. The scale bar is 10 pm. (Taken from ref. 531.)...

The distribution of LCM in the brain parenchyma was further analyzed using fluorescently labeled LCM and confocal laser scanning microscopy. As in the case of unlabeled LCM, rats bearing 9L gliosarcoma tumors were injected intravenously (i.e., via tail vein) with diO-LCM and sacrificed 2 min later. The brains were processed as described elsewhere (ref. 531). In this case,... 

There is an increased blood flow in brain tumors (ref. 589), and the blood-brain barrier is leaky in and around 9L tumors because the blood vessels associated with these (ref. 568), and other (ref. 565-567), tumors are fenestrated. This well-known leakiness of tumor capillaries, which in the case of brain tumors includes breaches in the blood-brain barrier (ref. 566,568 cf. Section 12.2), would allow extravasation of small particulate matter (cf. ref. 590-594) or LCM. Once in the tumor area, LCM remain there because of an affinity for tumor cell surface components (cf. ref. 531 see also Chapter 14). At least 4 different types of experimental tumors in rats (C6 glioma, 9L gliosarcoma, Novikoff hepatoma, and Walker-256 carcinosarcoma), as well as several spontaneous tumors in dogs (ref. 570), do interact with LCM in a preferential manner (cf. Chapters 12 and 13), suggesting that LCM affinity may be for tumor cells in general (ref. 531). 

Fig. 13.10 This photomicrograph demonstrates the tumor morphology of Fischer 344 rats bearing 9L gliosarcomas treated with cremophor-LCM (A) and paclitaxel-LCM (B,C). Experimental animals received one i.v. injection of 240 pg/kg paclitaxel-LCM each day for 5 consecutive days starting 10 days after the tumor inoculation. Control animals received cremophor-LCM. Tumors from animals treated with paclitaxel-LCM show extensive cell death (B) and hemorrhage (C). (Taken from ref. 532.)...

R.D. Fross, P.C. Wamke and D.R. Groothuis, Blood flow and blood-to-tissue transport in 9L gliosarcomas the role of the brain tumor model in drug delivery research, J. Neuro-Oncol. 11 (1991) 185-197. 

Rat F98 glioma cells were from R. Goodman, Ohio State University (Columbus, OH). The 9L gliosarcoma line was obtained from the Brain Tumor Research Center, University of California, San Francisco. Cells were maintained in 10% fetal calf serum in DMEM supplemented with penicillin/streptomycin and tested by the Gen-Probe Rapid Detection System (Fisher Scientific) to rule out mycoplasma contamination. Cells were harvested with 0.25% trypsin, counted, and resuspended in DMEM solution before intracranial implantation. 

Gliosarcoma Glioblastoma plus fibrosarcoma intermixed GFAP (S) fibronectin type IV collagen (S) laminin vimentin (S) Cerebrum... 

Glioblastoma/ gliosarcoma with epithelial metaplasia Structures of glioblastoma/gliosarcoma (Table 20.5) plus epithelial regions GFAP (S) S-100 (S) cytokeratin (S) EMA (S) Cerebrum CNS... 

Glioblastoma and Gliosarcoma with Epithelial Metaplasia (WHO Grade IV)... 

Rarely, gliosarcomas and glioblastomas produce adenoid formations or epithelial foci with squamous differentiation and keratin pearls.These regions stain immunohistochemically for CK and EMA (see Table... 

Lack of GFAP-positive neoplastic glia distinguishes fibrosarcoma from glioblastoma invading the meninges and from gliosarcoma. For specific features that differentiate individual sarcomas, see Chapter 4. 

McKeever PE, Zhang K, Nelson JS, et al. Type IV collagen messenger RNA localizes within cells of abnormal vascular proliferations of glioblastoma and sarcomatous regions of gliosarcoma. J Histochem Cytochem. 1993 41 1124. 

Horiguchi H, Hirose T, Kannuki S, et al. Gliosarcoma An immunohistochemical, ultrasttuctutal and fluotescence in situ hybridization study. Pathol Int. 1998 48 595-602. 

Boerman RH, Anderl K, Hetath J, et al. The glial and mesenchymal elements of gliosarcomas shate similat genetic altetations. J Neuropathol Exp Neurol. 1996 55 973-981. 

The unsubstituted AlClPc formulated in Cremophor oil emulsion (10% in saline) was shown to be preferentially retained by a gliosarcoma and was able to induce tumor necrosis in this model [39]. The same formulation induced complete EMT-6 tumor control at 0.25 jumol kg in Balb/c mice, which renders it more photoactive than the mono- and disulfonated AlClPc [25]. 

There are experimental data which show a synergistic or a potentiating effect of chemotherapeutic agents on PDT [80]. The combination of ACNU and HPD-mediated PDT results in significantly increased cytotoxicity in the 9L gliosarcoma [81]. This effect could further be increased by adding hyperthermia as a third treatment modality. The RIF-1 tumor proved to be insensitive to PDT and to doxorubicin but sensitive to cisplatin with no increased cytotoxic effect when both modalities were combined. In the EMT-6 tumor model all three modalities showed a mild effect when used independently, doxorubicin enhanced significantly the effect of PDT, whereas cisplatin did not [82]. Mitomycin C potentiates the effect of PDT in adenocarcinoma [83]. There are no reported clinical data on the interaction of PDT and chemotherapy. 

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