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PubMed1994

Unusual evolution and computerized tomographic appearance of a gliosarcoma.

A patient with a remote infarct, seizures, mild hemiparesis, and dysphasia became obtunded over four months and died. Computerized tomography (CT) over 5 years showed a consistent, large, wedge-shaped left hemisphere hypodensity with a central calcification, but without signs of mass effect. This was interpreted as an infarct of the left middle cerebral artery territory. Post-mortem examination of the brain revealed the entire area appearing as infarct on CT was a gliosarcoma. We suspect that the unusual CT appearance of the lesion was likely caused by multiple pathologies: a low grade glioma transforming into a gliosarcoma that was able to spread throughout the area of infarct encephalomalacia without revealing a typical CT appearance of mass effect. The patient's brief period of deterioration probably coincided with transformation of the tumor into a gliosarcoma. The variable CT characteristics of gliosarcomas are reviewed.

Brain Neoplasms↗
PubMedDate not supplied

Gliosarcoma: MR features.

PURPOSE: Our goal was to characterize the MR features of pathologically documented gliosarcoma and to determine if these features help differentiate gliosarcoma from other intracranial neoplasms. METHOD: MR studies of six patients with pathologically documented gliosarcoma were retrospectively analyzed. RESULTS: The tumors tended to be well defined lesions demonstrating either an inhomogeneous or cystic appearance with surrounding vasogenic edema. All tumors were characterized as primarily intraaxial but abutting a dural surface. On T2-weighted images, all tumors were of intermediate signal intensity with surrounding edema. The signal intensity of the tumor was similar to gray matter but was hypointense relative to other glial neoplasms. Postcontrast T1-weighted images showed intense tumor enhancement, often with a ring-like appearance. The isointense component on the T2-weighted images corresponded to this area of intense enhancement. CONCLUSION: Gliosarcoma exhibits some characteristic MR features. It should be included in the differential diagnosis of any tumor that appears to be intraaxial but abuts a dural surface and is much less hypointense on T2-weighted images than other glial neoplasms.

Adult↗
PubMed2005

Molecular characterization of PDGFR-alpha/PDGF-A and c-KIT/SCF in gliosarcomas.

Gliosarcomas are rare and poorly characterized malignant brain tumors that exhibit a biphasic tissue pattern with areas of gliomatous and sarcomatous differentiation. These tumors are histological variants of glioblastoma, displaying a similar genetic profile and dismal prognosis. Up-regulation of PDGFR subfamily of tyrosine kinase members, PDGFR-alpha and c-Kit, and their intracellular effectors RAS/RAF/MAPK has a crucial role in the cancer development. In addition, signal transduction mediated by activating mutations of c-Kit and PDGFR can be effectively blocked by specific tyrosine kinase inhibitors, such as Imatinib mesylate. The aim of this study was to characterize the molecular alterations of PDGFR signaling in gliosarcomas. Six cases were analyzed by immunohistochemistry for the expression of PDGFR-alpha, c-Kit and their ligands PDGF-A and SCF, respectively. The cases were further evaluated for the presence of activating mutations of PDGFR-alpha (exons 12 and 18) and c-kit (exons 9, 11, 13, and 17), as well as B-RAF (exons 11 and 15). Expression of PDGF-A was found in all cases and co-expression of PDGFR-alpha was observed in three cases. Four cases showed expression of SCF, and c-Kit was observed only in one case that also expressed SCF. Generally, immunoreaction predominates in the glial component. The mutational analysis of PDGFR-alpha showed the presence of an IVS17-50insT intronic insertion in two cases, one of them also with a 2472C > T silent mutation; this silent mutation was also found in another case. Glioma cell line analysis of IVS17-50insT insertion showed no influence on PDGFR-alpha gene splicing. No mutations were detected in c-kit and B-RAF oncogenes. Our results indicate that activating mutations of PDGFR-alpha, c-kit and B-RAF are absent in gliosarcomas. Nevertheless, the presence of a PDGFR-a/PDGFA and c-Kit/SCF autocrine/paracrine stimulation loop in a proportion of cases, supports the potential role of specific tyrosine kinase inhibitors in the treatment of gliosarcomas.

Base Sequence↗
PubMed2000

Gliosarcoma associated with a huge cyst--case report.

A 55-year-old female presented with a unique case of gliosarcoma with a huge cystic component manifesting as loss of consciousness, left-sided hemiparesis, and anisocoria. Computed tomography demonstrated a large cyst in the right frontal lobe, and enhancement of the mural nodule after administration of contrast medium. Emergent operation was performed. Xanthochromic fluid was aspirated, and the tumor was resected. The histological diagnosis was gliosarcoma based on the presence of gliomatous and sarcomatous components. She underwent a second operation because of tumor regrowth 3 weeks after the first operation. The postoperative course was satisfactory during radiation therapy with 60 Gy and chemotherapy. The diagnosis of gliosarcoma was difficult to make preoperatively because of the neuroradiological findings similar to low-grade gliomas. Gliosarcoma should be included in the differential diagnosis of huge cystic tumors.

Brain Diseases↗
PubMed2006

Gliosarcoma with features of osteoblastic osteosarcoma: a review.

CONTEXT: Gliosarcoma is a rare tumor of the central nervous system characterized by a biphasic histologic pattern, consisting of a gliomatous and a sarcomatous component, respectively. In most instances the sarcomatous component is represented by a fibrosarcoma, but other stromal malignancies have also been described. Osteosarcomatous differentiation in gliosarcoma has been rarely reported. OBJECTIVE: To review characteristic radiologic and histopathologic features of this rare neoplasm, to debate about possible differential diagnoses that should be taken into consideration, and to provide an overview of the potential histopathogenesis of gliosarcomas. DATA SOURCES: Relevant articles indexed in PubMed (National Library of Medicine) and reference medical texts. CONCLUSIONS: Recent molecular studies suggest that sarcomatous and gliomatous components of gliosarcoma might be derived from a single precursor cell clone, progressing in 2 subclones with distinct morphologic features during tumor evolution. Nonetheless, events determining splitting of the original clone into 2 histologic populations remain to be investigated.

Central Nervous System Neoplasms↗
PubMed2002

Granulocyte macrophage-colony stimulating factor gene transfer to induce a protective anti-tumoral immune response against the 9L rat gliosarcoma model.

The injection of irradiated tumor cells genetically engineered to express the granolocyte macrophage-colony stimulating factor (GM-CSF) is reported as stimulating antitumoral immunity in several animal models. We used the 9L gliosarcoma rat model to investigate the potency of this strategy in relation to the central nervous system. After in vitro transduction experiments to generate 9L murine cells producing GM-CSF (9LmGM-CSF cells), we found that with the exception of one rat subcutaneously (s.c.) grafted with 108 9LmGM-CSF cells, syngenic rats s.c. injected (dorsal route) with 106-108 viable 9LmGM-CSF cells did not develop s.c. 9L gliosarcomas, while rats s.c. grafted with the same number of naive 9L cells died between 25 and 45 days postgraft. Intracerebral stereotactic injections of 4.104 naive 9L (without s.c. 9LmGM-CSF treatment) killed all the rats within 18-24 days, while s.c. grafting with 108 9LmGM-CSF cells wholly prevented the development of 9L brain gliosarcomas. These results outline the feasibility of the GM-CSF gene transfer approach in glioma (or at least gliosarcoma) gene therapy and could therefore serve as a basis for the development of an adjuvant treatment of glioblastomas using GM-CSF-producing tumor cell vaccines.

Animals↗
PubMedDate not supplied

Gliosarcoma with liposarcomatous component, bone infiltration and extracranial growth.

Gliosarcoma is a highly malignant brain tumor consisting of both a glioblastoma and a mesenchymal component. The latter typically resembles fibrosarcoma, but differentiation patterns resembling osteosarcoma, chondrosarcoma, angiosarcoma and rhabdomyosarcoma have also been described. Molecular-genetic studies have shown that both glioblastoma and the mesenchymal component share identical cytogenetic abnormalities or mutations, suggesting a monoclonal origin from glial cells. We report an unusual case of gliosarcoma that presented as a large intracerebral tumor with infiltration of the temporal bone and the soft tissues in the infratemporal fossa. Microscopically, the tumor consisted of alternating areas of glioblastoma and fibrosarcoma. Focally, areas ofosteosarcomatous and liposarcomatous differentiation were found. Although gliosarcoma with transcranial penetration is very rare, it should be suspected in case of intracranial tumor with glioblastoma-imaging features, infiltration of bone and extracranial growth. Our case of liposarcomatous differentiation in gliosarcoma--together with another very recently reported similar case--expands the morphologic heterogeneity of this peculiar brain tumor.

Bone Neoplasms↗
PubMed1990

Boron neutron capture therapy of intracerebral rat gliosarcomas.

The efficacy of boron neutron capture therapy (BNCT) for the treatment of intracerebrally implanted rat gliosarcomas was tested. Preferential accumulation of 10B in tumors was achieved by continuous infusion of the sulfhydryl borane dimer, Na4(10)B24H22S2, at a rate of 45-50 micrograms of 10B per g of body weight per day from day 11 to day 14 after tumor initiation (day 0). This infusion schedule resulted in average blood 10B concentrations of 35 micrograms/ml in a group of 12 gliosarcoma-bearing rats and 45 micrograms/ml in a group of 10 similar gliosarcoma-bearing rats treated by BNCT. Estimated tumor 10B levels in these two groups were 26 and 34 micrograms/g, respectively. On day 14, boron-treated and non-boron-treated rats were exposed to 5.0 or 7.5 MW.min of radiation from the Brookhaven Medical Research Reactor that yielded thermal neutron fluences of approximately 2.0 x 10(12) or approximately 3.0 x 10(12) n/cm2, respectively, in the tumors. Untreated rats had a median postinitiation survival time of 21 days. Reactor radiation alone increased median postinitiation survival time to 26 (5.0 MW.min) or 28 (7.5 MW.min) days. The 12 rats that received 5 MW.min of BNCT had a median postinitiation survival time of 60 days. Two of these animals survived greater than 15 months. In the 7.5 MW.min group, the median survival time is not calculable since 6 of the 10 animals remain alive greater than 10 months after BNCT. The estimated radiation doses to tumors in the two BNCT groups were 14.2 and 25.6 Gy equivalents, respectively. Similar gliosarcoma-bearing rats treated with 15.0 or 22.5 Gy of 250-kilovolt peak x-rays had median survival times of only 26 or 31 days, respectively, after tumor initiation.

Animals↗
PubMed1989

[Therapeutic efficacy of intracarotid infusion of 20% mannitol with ACNU in Fischer rats with intracerebrally implanted 9L gliosarcoma].

The purpose of this study was to investigate the therapeutic effect of intracarotid infusion of 20% mannitol with ACNU chemotherapy in Fischer 344 rats with intracerebrally implanted 9L gliosarcoma, compared with giving them only ACNU intraperitoneally. Thirty 9L gliosarcoma bearing Fischer 344 rats were evaluated in the following 3 groups. Group I: control (no treatment); group II: treated by ACNU 20 mg/kg intraperitoneally on the 7th day after implantation of 9L gliosarcoma cells; group III: treated by intracarotid infusion of 20% mannitol 3.1 ml/min. and with the same dose of ACNU as in group II. Mean survival time after the inoculation of tumor cells into the brain was 15.1 days (group I), 21.8 days (group II) and 27.9 days (group III). In group II all tumor-bearing Fischer rats died within 24 days after inoculation of tumor cells, whereas in group III 5 out of 6 rats survived more than 25 days after them. Group III evidenced necrosis and degenerative findings with vacuole and microcyst without vascular proliferation in tumor tissues more than group II on the 7th day after ACNU treatment for the experimental brain tumor. On the 7th day after ACNU treatment of each group, BrdU labeling index was calculated in order to evaluate tumor proliferation. The Mean BrdU labeling index in tumor cells of group III demonstrated 7.5%, against 14.5% (about one half) in group II. From our experimental study of survival time and BrdU labeling index, it is suggested that osmotic blood brain barrier disruption chemotherapy by intracarotid infusion of 20% mannitol and ACNU was more effective than simple treatment by intraperitoneal injection of ACNU in the Fischer rats with intracerebrally implanted 9L gliosarcoma.

Animals↗
PubMed1986

Development of experimental models for meningeal neoplasia using intrathecal injection of 9L gliosarcoma and Walker 256 carcinosarcoma in the rat.

Two models for meningeal neoplasia have been developed in rats using intrathecal injection of 9L gliosarcoma and Walker 256 carcinosarcoma cells. Tumor cells were injected in unanesthetized animals through an indwelling catheter inserted at the cisterna magna to the level of the lumbar enlargement of the spinal cord. Survival of rats was dependent on the number of tumor cells injected. Spread of tumor was quantified by histology using a grading scale, and functional and behavioral changes were measured. Rats injected with 10(6) 9L gliosarcoma cells showed progressive weight loss, flaccid paralysis, and neurogenic bladder dysfunction and had a median survival of 11 days. The tumor frequently grew as a mass compressing the spinal cord. The 9L gliosarcoma tumor cells markedly invaded the Virchow-Robin spaces but exhibited only minimal invasion of the central nervous system parenchyma. The tumor reached the brain by day 10. Rats injected with 2 X 10(5) Walker 256 carcinosarcoma cells showed progressive weight loss and weakness and had a median survival of 6 days. The tumor grew within the leptomeninges in a discontinuous multifocal fashion and reached the brain by day 4. There was extensive invasion of the central nervous system parenchyma by Walker 256 tumor cells along the Virchow-Robin spaces resulting in hemorrhage and necrosis of grey and white matter. Hot plate and tail flick response times were significantly delayed only in the days immediately preceding death of animals with either 9L or Walker 256 tumor and were not good indicators of tumor progression. Loss of motor coordination and failure of the stepping and placing reflex on the other hand showed good correlation with spread of tumor measured histologically. Control animals injected with 0.9% NaCl or with lethally irradiated tumor cells showed no significant weight loss or functional or behavioral changes. The intrathecal 9L gliosarcoma and Walker 256 carcinosarcoma models show different characteristics of human meningeal carcinomatosis and will be used for studies of experimental chemotherapy with intrathecally administered antitumor drugs.

Animals↗
PubMed1994

Effects of nimodipine and dexamethasone on low-level CO2 laser-induced release of 51chromium from canine 2C5 gliosarcoma cells.

Low-energy penumbral irradiation of surgical lasers may produce undesirable effects on surrounding tissues. This study used a 51Cr cell labeling technique to determine if gliosarcoma cells could be therapeutically protected prior to their exposure to low-power laser irradiation. Canine 2C5 gliosarcoma cells with intracellular 51Cr were treated with nimodipine and/or dexamethasone and then exposed to low-power levels of CO2 laser. The 51Cr was released from the cells in a dose-dependent fashion following exposure to laser energy. Correlative analysis of the data indicated that a strong direct relationship between laser fluence and 51Cr release did exist for controls and drug-treated groups with coefficients of correlation r > or = +0.90 and coefficients of determination r2 > or = 0.82. However, comparison of the data from the drug-treated and control groups found that there was no significant difference between them (P > .05). Therefore, no protective or detrimental effects were observed with the use of nimodipine and/or dexamethasone on the gliosarcoma cells as tested in this system. Further investigation is necessary in order to define the mechanisms by which low-power level lasers affect these cells. These effects do not appear to be mediated through localization of mechanisms to the cell membranes or their constituent Ca2+ channels.

Animals↗
PubMed1996

Cerebral gliosarcoma: prognostic factors.

The authors report their results in a retrospective study of 6 cases of gliosarcoma. In 3 cases gliosarcoma presented features similar to those of glioblastoma, both at CT scan and macroscopically; in the other 3 cases they resembled meningioma. Average survival varied considerably and was correlatable to the CT features of the lesion (14 months for glioblastoma, 7 for meningioma). It seems likely that patients who have gliosarcoma with CT features suggestive of meningioma may have prolonged survival.

Aged↗
PubMed2000

Gliosarcoma with thallium-201 SPECT.

Thallium-201 (201Tl) chloride scintigraphy is the imaging method use for the detection of various tumors including glioblastoma, but only limited information on 201Tl uptake in gliosarcoma is available. We investigated a patient with gliosarcoma by means of 201Tl single-photon emission computed tomography (SPECT) and MRI. SPECT imaging revealed high 201Tl uptake in the tumor, which was closely correlated with contrast-enhancement on MRI. These results suggest that SPECT with 201Tl may be useful for detecting gliosarcoma and provide physiological information on this tumor.

Adult↗
PubMed2000

Histologically repeatedly confirmed gliosarcoma with long survival: review of the literature and report of a case.

OBJECTIVE AND IMPORTANCE: A rare case of gliosarcoma in a 61-year-old woman is presented with a stable situation over 22 years with an excellent quality of life. CLINICAL PRESENTATION: The patient was initially symptomatic and was operated on in 1975 for a deep-seated left parietal gliosarcoma. During the following 20 years, she was clinically asymptomatic until she complained of increasing headache in 1995. Neuroradiological imaging showed a sharply demarcated lesion on MRI at the former operative site, which was operated on again. Four months later, the residual tumour did grow again. INTERVENTION: As radiation therapy could not stop tumour progression and the neurological status worsened, the patient was operated on again for a massive tumour mass in the left parieto-occipital region, filling out nearly all of the previous resection cavity. Despite radio-immunotherapy, the patient finally died 22 years after the first discovery of the tumour. CONCLUSION: The present case shows that, in rare instances, gliosarcomas may show prolonged survival, although the underlying pathogenetic mechanisms for this clinical behaviour are not understood.

Brain Neoplasms↗
PubMed2005

Evaluation of in vitro and in vivo antitumor activity of BCNU-loaded PLGA wafer against 9L gliosarcoma.

The purpose of the present study was to develop implantable BCNU-loaded poly(D,L-lactide-co-glycolide) (PLGA) wafer for the controlled release of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and to evaluate its in vitro and in vivo antitumor activity. The release rate of BCNU from PLGA wafer increased with the increase of BCNU amount loaded and the release was continued until 7 days. In vitro and in vivo antitumor activity of BCNU-loaded PLGA wafer was investigated using in vitro cytotoxicity against 9L gliosarcoma cells and a subcutaneous (s.c.) solid tumor model of 9L gliosarcoma, respectively. The wafers containing BCNU showed more effective cytotoxicity than BCNU powder due to its short half-life and inhibited the proliferation of 9L gliosarcoma cells. BCNU-loaded PLGA wafer delayed the growth of the tumors significantly and increasing the dose of BCNU in the wafer resulted in a substantial regression of the tumor. These results of antitumor activity of BCNU-loaded PLGA wafer demonstrate the feasibility of the wafers for clinical application.

Animals↗
PubMed2004

Gliosarcoma arising from an anaplastic ependymoma: a case report of a rare entity.

We report the first case of a gliosarcoma arising from an anaplastic ependymoma and the second case of gliosarcoma arising from any type of ependymal neoplasm. The patient was a 48-year-old woman with a solid and cystic, peripherally enhancing, 7-cm right frontal mass lesion. Histologically, the lesion displayed characteristics of anaplastic ependymoma (grade III, World Health Organization scale). The tumor recurred despite multiple cycles of postoperative radiation and chemotherapy. After the fourth recurrence, the tumor displayed a biphasic pattern of differentiation. The first pattern was similar to the original anaplastic ependymoma, whereas there was a second new sarcomatous pattern resembling fibrosarcoma that was admixed with and overrunning the ependymal component. The spectrum of gliosarcoma is therefore expanded to include not only astrocytic and oligodendroglial components but ependymal components as well.

Brain Neoplasms↗
PubMed1995

Identical mutations of the p53 tumor suppressor gene in the gliomatous and the sarcomatous components of gliosarcomas suggest a common origin from glial cells.

Gliosarcomas are morphologically heterogeneous tumors of the central nervous system composed of gliomatous and sarcomatous components. The histogenesis of the latter is still a matter of debate. As mutations of the p53 tumor suppressor gene represent an early event in the development of gliomas, we attempted to determine whether both components of gliosarcomas share identical alterations of the p53 gene. Using single-strand conformation analysis (SSCA) and direct DNA sequencing of the p53 gene, we analyzed dissected gliomatous and sarcomatous parts of 12 formalin-fixed, paraffin-embedded gliosarcomas. The two tumors that contained a p53 alteration were found to carry the identical mutation (exon 5; codon 151, CCC-->TCC; codon 173, GTG-->GTA) in the gliomatous and the sarcomatous components. These findings suggest a common origin of the two cellular components from neoplastic glial cells.

Adult↗
PubMed1996

Efficacy of intralesionally administered cisplatin-impregnated biodegradable polymer for the treatment of 9L gliosarcoma in the rat.

OBJECTIVE: Use of biodegradable polymers for the local delivery of chemotherapy is a promising new strategy in the treatment of high-grade gliomas. We examine the benefit of local delivery of cisplatin, via biodegradable polymer, in the treatment of intracranial glioma in rats. This treatment is compared against intralesionally administered free cisplatin and systemic cisplatin. METHODS: The Fischer 344 9L gliosarcoma rat model was used with a cannula placed in the right frontal lobe. On Day 0, 5 x 10(3) 9L gliosarcoma cells were infused. Treatment was initiated on Day 7. In Experiment 1, polymer alone was infused intralesionally to rule out any inherent toxic or tumoricidal properties. In Experiment 2, polymer impregnated with 0.5, 5.0, and 25 mg/m2 cisplatin was infused intralesionally. In Experiment 3, the most effective dose of drug containing polymer was compared against a similar dose of intralesionally administered free cisplatin and the systemic administration of cisplatin. RESULTS: In Experiment 1, polymer alone demonstrated no inherent toxic or tumoricidal properties. In Experiment 2, polymer impregnated with 0.5 mg/m2 was 100% effective in eradicating intracranial tumor with minimal histological evidence of toxicity. At the 5.0 and 25 mg/m2 doses, local brain toxicity was significant. In Experiment 3, at Day 60, 8 of 12 animals treated with polymer containing 0.5 mg/m2 cisplatin were alive and tumor free. This compared with 3 of 13 tumor-free survivors for the group treated with intralesionally administered free cisplatin, and 0 of 13 and 0 of 11 survivors for the 50 and 100 mg/m2 intraperitoneally administered doses, respectively. CONCLUSION: The local instillation of cisplatin-impregnated biodegradable polymer, allowing the sustained release of high-dose chemotherapy locally, seems to be effective treatment for intracranial 9L gliosarcoma in the rat. Treatment was superior to intralesionally administered free or systemic cisplatin.

Animals↗