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Influence of an anti-angiogenic treatment on 9L gliosarcoma: oxygenation and response to cytotoxic therapy.

Tissue oxygen tensions were measured in subcutaneously growing rat 9L gliosarcoma under normal air and carbogen breathing conditions prior to and after i.v. administration of a perflubron emulsion. When these animals were treated with the anti-angiogenic agents TNP-470 and minocycline for 5 days prior to oxygen measurement, tumor hypoxia was decreased compared with untreated tumors. Hypoxia, defined as the percent of pO2 readings < or = 5 mm Hg, was decreased from 71% in untreated air-breathing controls to 34% in animals treated with the anti-angiogenic agents, the perflubron emulsion and carbogen breathing. These effects were manifest in the increased response of the tumor to single-dose (10, 20 and 30 Gy) radiation therapy. Twenty-four hours after treatment with BCNU oxygenation of the tumors was not altered; however, 24 hr after administration of adriamycin oxygenation of the tumors was increased such that hypoxia in adriamycin-treated tumors in animals receiving the perflubron emulsion and carbogen was reduced to 21%. Tumor growth delay in the s.c. tumors was increased by the addition of treatment with the anti-angiogenic agents from day 4 through day 18 post-tumor cell implantation along with BCNU or adriamycin on days 7-11. Administration of the perflubron emulsion and carbogen breathing resulted in increased tumor growth delay with the chemotherapeutic agents alone and in combination with the anti-angiogenic agents. Life span in animals bearing intracranially implanted 9L gliosarcoma progressively increased with administration of the anti-angiogenic agents and then the anti-angiogenic agents and perflubron emulsion/carbogen compared to treatment with BCNU or adriamycin.

Animals↗

Low-level CO2 laser-induced release of 51chromium from canine 2C5 gliosarcoma cells.

Recently, interest has grown in the area of low-power laser effects upon tissues. We used a 51Cr cell labeling technique with glioma tissue to better understand these effects. Canine 2C5 gliosarcoma cells with intracellular 51Cr were exposed to CO2 laser in the range of 0.2 to 3.0 J/cm2. Correlative analysis of the data indicated that there is a strong direct relationship between laser fluence and the percent of total intracellular 51Cr released from the glioma cells with a coefficient of correlation (r) of +0.93. The calculated standard error of the correlation coefficient was +/- 0.06 and the coefficient of determination (r2) was 0.86. These results indicate that the 51Cr cell labeling technique is a useful method for quantifying the low-power laser effects on the integrity of the cell membrane of gliosarcoma cells in vitro. However, further investigation is needed to clarify the specific mechanisms by which the CO2 laser induces changes upon these cells.

Animals↗

Congenital gliosarcoma; so-called sarcoglioma.

A mixed glioma and sarcoma in a 3-month-old infant is presented as a rare case of gliosarcoma with a good response to treatment. This congenital case is quite different from those in adults: the tumor cells were mainly composed of sarcomatous elements; glial components were not anaplastic without obvious endothelial hyperplasia, but presented as reticulin-free islands, mimicking a reactive glioma in a sarcoma. It may be termed "sarcoglioma" to distinguish from a classic gliosarcoma. The origin of the rare mixed tumor may be related to a dysgenesis of both mesenchymal and glial elements.

Basal Ganglia↗

Childhood's gliosarcomas: pathological and therapeutical considerations on three cases and critical review of the literature.

BACKGROUND: Gliosarcoma is a rare cerebral tumor that has only recently been classified as a separate clinico-pathological entity, even though it remains closely related to glioblastoma in terms of both its clinical and therapeutic characteristics. The onset of this tumor during childhood is particularly unusual. DISCUSSION: The authors describe three cases of gliosarcoma in three patients of 13, 15, and 16 years old, in an attempt to identify any distinctive aspects of the "juvenile" variety. On the basis of their personal experience and in the light of the available literature, the authors review the salient features of this pathological condition in young patients to identify any distinctive aspects as well as to define the significance of the extent of the sarcomatous component and of a "meningioma-like" appearance of the lesion, in terms of survival. CONCLUSION: In particular, they emphasize how modern diagnostic-therapeutic protocols make it possible to achieve a massive cytoreduction of the lesion in absolute safety in many cases, while avoiding further deficits in others, thus ensuring not only significant survival times but also a good quality of life.

Adolescent↗

Synergistic cytotoxicity of the ribonucleotide reductase inhibitor didox (3,4-dihydroxy-benzohydroxamic acid) and the alkylating agent carmustine (BCNU) in 9L rat gliosarcoma cells and DAOY human medulloblastoma cells.

PURPOSE: Ribonucleotide reductase (RR) is the rate-limiting enzyme of de novo DNA synthesis and has been shown to be upregulated linked with proliferation and malignant transformation. It was therefore identified as an excellent target for antitumor therapy. In the present study we investigated the biochemical and cytotoxic effects of didox, an inhibitor of RR, as a single agent and in combination with BCNU, an alkylating anticancer drug, in 9L rat gliosarcoma cells and DAOY human medulloblastoma cells. METHODS: The effect of didox on the intracellular concentrations of deoxynucleosidetriphosphates (dNTPs) was studied in 9L cells. Pool sizes were determined by HPLC. In addition, the cytotoxic effects of didox and BCNU as single drugs and in equimolar combination were tested in 9L and in DAOY cells. Combination effects were determined according to the equation of Chou and Talalay. The expression of DNA repair-related genes was determined after exposure of 9L cells to BCNU, didox and a combination of the two compounds, using a cDNA array. RESULTS: Incubation of 9L cells with 30 microM didox for 24 h significantly decreased the intracellular concentrations of the DNA precursors dCTP (61% of control) and dGTP (17% of control), and significantly increased the concentration of dATP (155% of control). This dNTP imbalance compromised DNA synthesis and repair and might therefore have been, at least in part, responsible for the highly synergistic cytotoxic effects seen when BCNU was used simultaneously with didox in 9L and in DAOY cells. With almost all combinations tested, highly synergistic effects were seen, as indicated by combination indices of <1 according to the equation of Chou and Talalay. In 9L cells, BCNU upregulated the expression of DNA repair-associated genes, whereas coincubation of the cells with didox reduced overexpression of some of these repair-related genes. CONCLUSION: A combination of BCNU and didox was proven to act in a synergistic manner in two cell lines, 9L rat gliosarcoma and DAOY human medulloblastoma cells. Further in vivo tests using these two compounds systemically and/or locally at the tumor site might be warranted.

Animals↗

Infantile gliosarcoma: a case and a review of the literature.

INTRODUCTION: Gliosarcoma in infant is a very rare entity. CASE REPORT: The authors present a case of gliosarcoma in a 23-month-old boy. The patient was admitted to our hospital with persistent headache and frequent vomiting. MR imaging demonstrated a large frontal well-circumscribed lesion with a heterogeneous gadolinium enhancement. Although macroscopically the tumor was totally extirpated, the boy died of rapid tumor regrowth 2 months after surgery. The surgical specimens obtained from the tumor showed an admixture of two distinctive neoplastic tissues. One was a malignant mesenchymal feature. Its fibrosarcomatous nature was characterized by spindle-shaped cells with fine fibers that were deeply stained in silver preparations for reticulin. The other was gliomatous tissue forming islands surrounded by the sarcomatous tissues. Its glioblastomatous nature was obvious, as it was characterized by endothelial proliferation and perinecrotic pseudopalisading. Both tissues were histologically malignant, as evidenced by mitotic figure, high cellularity, atypical features, and variability. DISCUSSION: The literature concerning gliosarcomatous tumors is reviewed, and pathological and clinical features of the tumor are briefly discussed.

Brain Neoplasms↗

Gliosarcoma occurring 8 years after treatment for a medulloblastoma.

CASE REPORT: We present a rare case of a gliosarcoma occurring 8 years following treatment for a medulloblastoma. The patient was diagnosed with a medulloblastoma at the age of 13 years. We considered the possibility of a radiation-induced tumour and present evidence supporting this view. The second cerebral tumour was excised and confirmed to be a gliosarcoma. The tumour bed was re-irradiated with three-dimensional conformal radiotherapy (3DCRT). She remained well for 6 months, after which there was clinicoradiological progression. CONCLUSIONS: During long-term follow-up of patients with medulloblastomas, the possibility of radiation-induced neoplasms must be borne in mind.

Adolescent↗

Neutron capture therapy of the 9L rat gliosarcoma using the p-boronophenylalanine-fructose complex.

PURPOSE: Intraperitoneal (IP) injection of the solubilized fructose complex of L-p-boronophenylalanine (BPA-F) produced higher boron concentrations in a rat brain tumor model than was possible using intragastric (IG) administration of L-p-boronophenylalanine (BPA). The effectiveness of IP BPA-F was compared to IG BPA in boron neutron capture therapy irradiations of the 9L rat brain tumor model. METHODS AND MATERIALS: The time course of boron accumulation in tumor and normal tissues was determined in male F344 rats bearing either SC or intracerebral 9L gliosarcomas following a single IP injection of BPA-F. On day 14 after inoculation of intracranial tumors, rats were irradiated with single doses of either: 250 kVp X rays; the thermal neutron beam of the Brookhaven Medical Research Reactor following IG administration of BPA; or thermal neutrons following IP injection of BPA-F. Magnetic resonance imaging was used to visualize the tumor scars and to assess damage to the normal brain in long-term survivors. RESULTS: 4 h after IP injection of 1200 mg/kg of BPA-F the boron concentrations in tumor, blood, and normal brain were 89.6 +/- 7.6, 27.7 +/- 2.8 and 17.5 +/- 1.5 micrograms 10B/g, respectively. Two IG doses of BPA (750 mg/kg each, 3 h apart) produced 39 +/- 5, 12 +/- 1 and 10 +/- 1 micrograms 10B/g in tumor, blood and brain, respectively at 5 h after the second dose. Three groups of rats were treated with thermal neutrons: one following IG BPA and two groups following IP BPA-F. The total physical absorbed doses to the tumor in the three BNCT groups were 15.5 Gy (IG BPA, n = 12), 17.0 Gy (IP BPA-F, n = 8), and 31.5 Gy (IP BPA-F, n = 8), respectively. The median survival of the untreated controls was 22 days. The median survival of the rats treated with 22.5 Gy of 250 kVp X rays (n = 23) was 35 days with 20% long-term survivors. Fifty percent of the rats in the IG BPA + thermal neutrons group survived over 1 year. All rats in both groups that received IP BPA-F + thermal neutrons have survived over 8 months. Magnetic resonance imaging of the brains of the long-term boron neutron capture therapy survivors showed a scar at the site of tumor implantation in all animals. In the IP BPA-F high-dose group one rat showed evidence of edema and one rat showed a fluid-filled cyst replacing the tumor. CONCLUSION: The use of IP BPA-F has significantly improved long-term survival compared to IG BPA. The high percentage of long-term tumor control (100%, n = 16) in the intracerebral rat 9L gliosarcoma brain tumor model, together with little or no damage to the surrounding normal brain in the majority of surviving animals, demonstrate the substantial therapeutic gain produced by boron neutron capture therapy.

Animals↗

[Gliosarcomas. A case report].

Gliosarcomas account for 2% of glioblastomas. We report a case of gliosarcoma in a 65-year-old man, which presented as meningioma, and discuss diagnostic, therapeutic and prognostic aspects of this particular entity.

Aged↗

Gliosarcoma with epithelial differentiation: immunohistochemical and molecular characterization. A case report and review of the literature.

Few reported cases of gliosarcomas or glioblastomas with epithelial-like areas exist. Most cases were originally diagnosed as metastatic carcinoma. Focal expression of glial fibrillary acidic protein has helped characterize these tumors as having a glial origin. We report a case of gliosarcoma with multifocal, extensive areas of well-differentiated carcinoma; demonstrating squamous and glandular differentiation. The expression of glial fibrillary acidic protein and epithelial phenotype were mutually exclusive. We performed extensive immunohistochemical analyses and comparative genotypic analysis using microdissection to secure representative glial and epithelial components. Loss of heterozygosity was analyzed with a panel of 12 polymorphic microsatellite markers designed to indicate allelic loss and situated in proximity to known tumor suppressor genes located on chromosomes 1p, 9p, 10q, 17p and 19q. We found comparable patterns of acquired allelic loss between the glial and carcinomatous components, strongly supporting the monoclonal origin of this neoplasm. This case represents an extreme form of phenotypic divergence in a malignant glioma, and constitutes a difficult diagnostic challenge. This heterogeneity reflects the potential for a range of phenotypic expression in malignant gliomas that needs to be recognized. We suggest microdissection genotyping as a molecular technique to better characterize these tumors.

Aged↗

Early effects of PRS-irradiation for 9L gliosarcoma: characterization of interphase cell death.

We characterized the interphase cell death of 9L gliosarcoma after high-dose-rate, low-energy photon irradiation using the Photon Radiosurgery System (PRS), a novel device for interstitial radiotherapy. Within 24 hours after irradiation with a dose of 18 Gray, 22.0% of cells underwent metabolic cell death, whereas dead cells in controls stayed less than 5.0% (p<0.005). In the majority of sensitive cells, loss of membrane integrity preceded the lethal morphological changes. The response was dose-dependent over the range of 9-18 Gray, but saturation was obtained over 18 Gray. On the other hand, a significant (p < 0.01) increase in the number of TUNEL-positive cells with apoptotic morphology was detected 6-24 hours after irradiation, but the fraction remained 1.9-2.1% of the population and was independent of the doses between 9 and 25 Gray. Apoptotic cells were rarely observed in the control cells (0.3-0.6%). Our data indicate that single high-dose irradiation induces both necrotic and apoptotic interphase cell death in 9L gliosarcoma, but rapid cell death mostly occurs through the non-apoptotic pathway.

Apoptosis↗

Gliosarcoma cell death after radiosurgery in a rat model.

Therapeutic radiation and subsequent detection of tumor cell death has been performed mainly in vitro systems, making it difficult to accurately characterize the mechanisms of tumor cell death after radiosurgery. To better characterize what occurs to glioma cells after radiation therapy, we developed a rat model using the 9L gliosarcoma cell line implanted reproducibly to the caudate nucleus in rats. After 1 Gy radiation, 9L tumors in vivo induced mainly necrosis (determined by trypan blue exclusion) of 10 - 74 % at 6 - 72 hours post-radiation. This is in contrast to a previous in vitro study which demonstrated that 18 Gy of radiation induces considerably less cell death as determined by trypan blue exclusion (approximately 20 - 25 % at 6 - 72 hours post-radiation). However, significant amounts of apoptosis were detected as early as 6 hours after radiation. Apoptosis determination was by annexin V (marker of early apoptosis) and propidium iodide (marker of membrane stability) staining followed by flow cytometry detection. When caspase 3 and caspase 8 enzymatic activities (mediators of apoptosis) were measured from freshly explanted tumor cells, peak activity was found 6 hours after 1 Gy radiation (p < 0.01). Taken together, these data indicate the presence of apoptosis early after radiation therapy (1 Gy) which progressed to necrosis in a unique in vivo model of gliosarcoma that may prove useful in determining new therapeutic approaches to radiation therapy and tumor cell biology.

Animals↗

Primary cerebral gliosarcoma: report of 17 cases.

A retrospective study of 17 cases of primary cerebral gliosarcoma is presented. These uncommon highly aggressive intracranial neoplasms were seen at the Royal Preston Hospital, between 1973 and 1992. The patients' ages ranged from 21 to 73 years (mean 52), nine were males and eight were females. They presented with signs and symptoms of a rapidly expanding brain tumour. The diagnosis was suspected on radiological findings and confirmed by histological examination. Treatment involved surgical excision in 15 cases and biopsy in two followed by radiotherapy. Chemotherapy was given in three cases. Despite active management, median survival was only 9 months. The clinical, radiological and pathological features of these lesions are highlighted with emphasis on combined histochemistry and immunohistochemistry. The features of gliosarcoma and glioblastoma are compared and contrasted.

Adult↗

Response of rat intracranial 9L gliosarcoma to microbeam radiation therapy.

Radiotherapeutic doses for malignant gliomas are generally palliative because greater, supposedly curative doses would impart clinically unacceptable damage to nearby vital CNS tissues. To improve radiation treatment for human gliomas, we evaluated microbeam radiation therapy, which utilizes an array of parallel, microscopically thin (<100 microm) planar beams (microbeams) of synchrotron-generated X rays. Rats with i.c. 9L gliosarcoma tumors were exposed laterally to a single microbeam, 27 pm wide and 3.8 mm high, stepwise, to produce irradiation arrays with 50, 75, or 100 microm of on-center beam spacings and 150, 250, 300, or 500 Gy of in-slice, skin-entrance, single-exposure doses. The resulting array size was 9 mm wide and 10.4 mm high (using three 3.8-mm vertical tiers); the beam's median energy was -70 keV. When all data were collated, the median survival was 70 days; no depletion of nerve cells was observed. However, when data from the highest skin-entrance dose and/or the smallest microbeam spacings were excluded, the median survival time of the subset of rats was 170 days, and no white matter necrosis was observed. Others have reported unilateral single-exposure broad-beam irradiation of i.c. 9L gliosarcomas at 22.5 Gy with a median survival of only -34 days and with severe depletion of neurons. These results suggest that the therapeutic index of unidirectional microbeams is larger than that of the broad beams and that an application for microbeam radiation therapy in treating certain malignant brain tumors may be found in the future.

Animals↗

Photodynamic therapy of 9L gliosarcoma with liposome-delivered photofrin.

The effect of Photofrin encapsulated in a liposome delivery vehicle for photodynamic therapy (PDT) of the 9L gliosarcoma and normal rat brain was tested. We hypothesized that the liposome vehicle enhances therapeutic efficacy, possibly by increasing tumor tissue concentration of Photofrin. Male Fisher rats bearing a 9L gliosarcoma were treated 16 days after intracerebral tumor implantation with either Photofrin in dextrose (n = 5) or Photofrin in liposome (n = 6). Nontumor-bearing animals were treated with Photofrin delivered either in dextrose (n = 4) or liposome (n = 4) vehicle. Tissue concentrations of Photofrin delivered either in dextrose (n = 4) or liposome (n = 4) vehicle were measured in tumor, brain adjacent to tumor and in normal brain tissue. Photofrin was administered (intraperitoneally) at a dose of 12.5 mg/kg and PDT (17 J/cm2 of 632 nm light at 100 mW/cm2) was performed 24 h after Photofrin administration. Brains were removed 24 h after PDT and stained with hematoxylin and eosin for analysis of cellular damage. The PDT using Photofrin in the liposome vehicle caused significantly more damage to the tumor (P < 0.001) than did PDT with Photofrin in dextrose. The PDT of tumor with Photofrin delivered in liposomes caused a 22% volume of cellular necrosis, while PDT of tumor with Photofrin delivered in dextrose caused only scattered cellular damage. Photofrin concentration in tumors was significantly higher (P = 0.021) using liposome (33.8 +/- 18.9 micrograms/g) compared to dextrose delivery (5.5 +/- 1.5 micrograms/g). Normal brain was affected similarly in both groups, with only scattered cellular necrosis. Our data suggest that the liposome vehicle enhances the therapeutic efficacy of PDT treatment of 9L tumors.

Animals↗

A case of gliosarcoma appearing as ischaemic stroke.

OBJECTIVES: Ischaemic stroke attributable to malignant brain tumour is a rarely reported phenomenon and even various imaging techniques including angiography do not necessarily lead to an accurate diagnosis. CASE DESCRIPTION: A 46-year-old, previously healthy man developed apoplectic symptoms with slight right sided hemiparesis and global aphasia. The computed tomography (CT) scan showed lesions of the left temporal lobe and the paraventricular white matter suggestive of left middle cerebral artery (MCA) infarction. Carotid angiography demonstrated compression of the M1 segment of the MCA and occlusion of temporal MCA. The patient initially refused magnetic resonance imaging (MRI) because of claustrophobia. Because of fluctuating symptoms and successive worsening of the condition over weeks an MRI scan was conducted under general anaesthesia. Beneath temporal, opercular, and subcortical infarctions it revealed a left temporal tumour. A tumour biopsy disclosed a gliosarcoma (WHO grade IV). Microscopical examination of the surgical specimen demonstrated invasion of tumour cells into the wall of a greater pre-existing blood vessel. CONCLUSIONS: Malignant brain tumours may cause ischaemic infarction. This is a rare but important differential diagnosis for the origin of strokes. The authors describe the first case with infiltration of intracranial blood vessels by tumour cells of a gliosarcoma.

Brain Ischemia↗

Synergistic effect between intraneoplastic methotrexate and radiation on experimental intracerebral rat gliosarcoma.

Methotrexate (MTX) alone has a limited effect against malignant brain tumors, but we previously demonstrated a beneficial synergism between MTX and radiation therapy (XRT) against RT-9 gliosarcoma. Because the beneficial effects of that study were limited by systemic toxicity and poor brain penetration of MTX, we have continued our studies using direct intracerebral MTX therapy. Male CD-Fisher rats with intracerebrally implanted RT-9 gliosarcoma and indwelling brain tumor catheters were treated with intracerebral injections of MTX, whole-brain XRT, or a combination of both. MTX was given either as one of two "high-dose" treatments, on the basis of whole-body doses, or two "low-doses," on the basis of average brain weight. MTX alone at lower doses and XRT alone each prolonged survival moderately. High-dose MTX was highly toxic, but low-dose MTX was well tolerated. Combined MTX and XRT caused a significant prolongation of survival in all animals that survived treatment long enough to die from tumor growth.

Animals↗

Regional differences in apoptosis in murine gliosarcoma (T9) induced by mild hyperthermia.

There are several reports of apoptosis induced by mild hyperthermia both in vitro and in vivo. However, in tumour nodules, regional differences in apoptosis induced by hyperthermia have not been studied morphologically or quantified. In this study, apoptosis was identified on the basis of its characteristic morphology, and was quantified in different tumour regions (margin and centre) by light and electron microscopy and discussed the correlation with necrosis. Apoptosis was induced in solid nodules of gliosarcoma (T9) in vivo by heating for 30 min in a water bath at 43 degrees C. The gliosarcoma cells showed a rapid increase in the number of apoptotic cells following mild hyperthermia. There was a regional difference in the rate of apoptosis immediately after hyperthermia. Necrosis was markedly enhanced only in the centre of the tumour 3 and 6 h after hyperthermia. These combined responses of apoptosis and necrosis seem to be caused by the microenvironmental change in the intratumour location.

Animals↗