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PubMed2003

Antiangiogenic effects of dexamethasone in 9L gliosarcoma assessed by MRI cerebral blood volume maps.

Depending on dose, dexamethasone has been shown to inhibit or stimulate growth of rat 9L gliosarcoma and decrease the expression of vascular endothelial growth factor (VEGF), an important mediator of tumor-associated angiogenesis. We demonstrate, by constructing relative cerebral blood volume (rCBV) maps with MRI, that dexamethasone also decreases total blood volume while increasing microvascular blood volume in Fischer rats bearing intracranial 9L gliosarcoma. Animals were inoculated with 1 x 10(5) 9L gliosarcoma tumor cells. On days 10-14 after tumor cell inoculation, animals were intra-peritoneally injected with dexamethasone (3 mg/kg) over 5 days. MRI-derived gradient echo (GE) and spin-echo (SE) rCBV maps were created to demonstrate total vasculature (GE) and microvasculature (SE). After MRI studies were performed, the rat's vasculature was perfused with a latex compound. Total vessel volume and diameters were assessed by microscopy. Dexamethasone decreased the tumor-enhancing area of postcontrast T1-weighted images (P < 0.0001) and total tumor volume(P = 0.0085). In addition, there was a greater than 50% decrease in GE rCBV (total vasculature) (P = 0.007) as well as a significant decrease in total fractional blood volume, as validated by histology (P = 0.0007). Conversely, there was an increase in SE rCBV signal (microvasculature) in animals treated with dexamethasone (P = 0.05), which was consistent with microscopy (P < 0.0001). These data demonstrate that (1) dexamethasone selectively treats tumor vasculature, suggesting a vessel-size selective effect and (2) MRI-derived rCBV is a noninvasive technique that can be used to evaluate changes in blood volume and vascular morphology.

Angiogenesis Inhibitors↗

PubMed1999

Gliosarcoma: a case with unusual epithelial feature.

Astrocytic tumors, particularly gliosarcoma, may contain epithelial features in the form of trabecular, adenoid, papillary arrangement, and squamous metaplasia. A case of gliosarcoma with unusual epithelial feature is described. The patient was a 60-year-old male with frequent seizures. The mass was 4 cm and in the left frontal lobe. Trabecular or rarely adenoid arrangement of neoplastic astrocytes was present in the mucinous stroma, and there was a distinctive transition between the trabecular area and typical anaplastic astrocytoma. The tumor cells in the trabecular area showed positive immunostain for glial fibrillary acidic protein, but did not react with various kinds of cytokeratin. The sarcomatous area was undifferentiated and was not labeled by factor-VIII, desmin, and anti-smooth muscle actin. Occurrence and histogenesis of epithelial features in gliosarcoma are reviewed. The importance to recognize the existence of epithelial feature in malignant astrocytic tumor is emphasized.

Brain Neoplasms↗

PubMed2006

Gliosarcoma with liposarcomatous differentiation: the new member of the lipid-containing brain tumors family.

Gliosarcoma is a rare malignant, biphasic brain tumor composed of glioblastoma multiforme and sarcomatous components. Various types of sarcomatous differentiation are described in this tumor: fibrosarcomatous, malignant fibrous histiocytoma-like, chondrosarcomatous and osteosarcomatous types. We report an extremely unusual variant of liposarcomatous differentiation in gliosarcoma in 72-year-old woman. Fat cells were presented by atypical multivacuolar and monovacuolar lipoblasts, stained positive for S100. p53 that was positive in both glial and mesenchymal cells of the tumor were negative in the lipoblasts. To the best of our knowledge, this is the first report in the literature of liposarcomatous differentiation in gliosarcoma.

Aged↗

PubMed1994

Gliosarcomas: pathological spectrum.

Pathological spectrum as seen in sixteen cases of gliosarcomas out of 81 cases of glioblastomas is described. Temporal lobe involvement (37.5%) and fibrosarcomatous pattern (62.5%) were found to be most frequent. Osteochondromatous element was found in recurrence of one gliosarcoma. Minimal criteria for diagnosis, pitfalls in diagnosis, differential diagnosis and histogenesis of gliosarcoma are discussed.

Adolescent↗

PubMed1997

A clinico-pathological study of 29 cases of gliosarcoma with special reference to two unique variants.

In the present series, the clinical and pathological features of 29 patients of gliosarcoma diagnosed over a 12 yr period (1984-1995) are reviewed. Gliosarcomas constituted 0.48 per cent of all intracranial tumours and 4.9 per cent of all cases of glioblastoma multiforme. Most patients (68.6%) with these tumours were above 40 yr of age. However, an interesting observation in the present series was that 10.3 per cent of patients (3/29) were below 14 yr of age, the youngest being 9 months. A male preponderance was noted and the temporal lobe was involved in 55 per cent patients. Histologically, in 25 of the 29 tumours, the sarcomatous component had the appearance of fibrosarcoma. Tumours from 4 patients were unique in that one showed rhabdomyoblastic differentiation in the mesenchymal areas as confirmed by immunohistochemical stains and electron microscopy (gliomyosarcoma). In three others, the neoplastic spindle cell component was closely associated with discrete areas of osteogenic sarcoma. Follow up in 12 patients (including the 4 patients with unique variants) revealed poor outcome similar to glioblastomas. All of them died within 1 month to 1.5 yr following surgery and postoperative radiotherapy. This study possibly represents the most comprehensive and largest series of gliosarcomas being reported from India.

Adolescent↗

PubMed1990

Gliosarcoma of the posterior fossa with features of a malignant fibrous histiocytoma.

A rare case of gliosarcoma occurring in the posterior fossa of a 62-year-old man is reported. Histologically, the tumor closely resembled that of a typical case of malignant fibrous histiocytoma (MFH). Such features have not been reported previously in gliosarcoma. The importance of using an immunoperoxidase preparation against the glial fibrillary acidic protein (GFAP) in diagnosing gliosarcoma is emphasized. Our case also lends support to the contention that MFH-like histologic features may occur in poorly differentiated neoplasms of diverse origins.

Brain Neoplasms↗

PubMed1993

Gliosarcoma with features of chondroblastic osteosarcoma.

BACKGROUND: The occurrence of osteoid-chondral elements in gliosarcoma is extremely rare and has been reported in only two cases. A new, rare case of gliosarcoma with osteosarcomatous differentiation in a 55-year-old man and histogenesis of osteoid-chondral tissue in gliosarcoma is discussed. METHODS: Surgically removed tumor tissues were examined immunohistochemically and electron microscopically, and a histologic examination was performed. RESULTS: Immunohistochemical and electron microscopic studies confirmed the presence of glial, fibroblastic, and osteoid-chondral elements. A major part of the sarcomatous tissue was undifferentiated and stained only by vimentin. Some areas of osteoid-chondral tissue were positive for glial fibrillary acidic protein (GFAP). CONCLUSIONS: These data suggest that osteoid-chondral elements came from the sarcomatous portion and GFAP positivity is not restricted to astrocytes and has been seen particularly in chondroid areas of non-glial tumors.

Brain Neoplasms↗

PubMed1987

Growth of 9-L and RT-9 gliosarcoma in female rats.

Published studies of 9-L and RT-9 gliosarcoma have been done only in male rats and it is widely assumed that these tumors do not grow in female rats. In this study 9-L and RT-9 gliosarcoma was inoculated into the brains of male and female Fisher CD rats. The tumors grew with essentially the same incidence and survival time in both sexes, confirming that female rats can be used as well as male rats in experiments using RT-9 and 9-L gliosarcomas.

Animals↗

PubMed1989

Gliosarcoma: an immunohistochemical study.

Gliosarcomas contain both neuro-ectodermal and mesenchymal elements. Its histogenesis has been much debated and endothelial and adventitial fibroblast origins have been suggested, as has a "histiocytic" origin following the demonstration of antiprotease activity. Eight gliosarcomas have been examined with a panel of ten monoclonal and polyclonal antibodies to investigate the origin of the sarcomatous element. Glial fibrillary acid protein expression showed a sharp distinction between gliomatous and sarcomatous tumour components. Contrary to some previous reports factor 8-related antigen and Ulex europeus agglutinin stained vascular luminal endothelium but no tumour cells. Vimentin and fibronectin expression was extensive and confined largely to sarcomatous areas. Desmin and neurofilament protein could not be demonstrated in any of the cases. Numerous cells, particularly in the sarcoma areas, expressed alpha-1-antitrypsin and -chymotrypsin. A proportion of these stained for the monocyte/macrophage marker MAC 387. Four cases focally exhibited a true storiform pattern and this and the immunohistochemical results suggest analogies with the fibrous histiocytomas. These tumours contain reactive histiocytes but are now thought to be derived from fibroblasts or from pluripotent mesenchymal cells in perivascular adventitia. This resembles the pattern exhibited in the sarcomatous component of gliosarcomas.

Adult↗

PubMed1984

GFAP, F VIII/RAg, laminin, and fibronectin in gliosarcomas: an immunohistochemical study.

GFAP, Factor VIII/RAg, laminin, and fibronectin were immunohistochemically investigated in 15 glioblastomas and 15 gliosarcomas . GFAP was found variably positive in the glial areas. F VIII/RAg characterizes the endothelial cells and in gliosarcomas suggests the origin of the sarcomatous component from the endothelial proliferations. Laminin separates the two components and characterizes the inner and the outer basement membranes in the vessels. It is multiplied and thickened in endothelial proliferations, while it is often fragmented in the larger vessel wall proliferations. Our observations confirm that gliosarcoma represents the last stage of a process which starts with the endothelial hyperplasia of glioblastoma.

Antigens↗

PubMedDate not supplied

Gamma interferon transduced 9L gliosarcoma. Cytokine gene therapy and its relevance to cellular therapy with alloreactive cytotoxic T lymphocytes.

In earlier studies, we demonstrated that intratumoral infusions of alloreactive cytotoxic T lymphocytes (aCTL), sensitized to the major histocompatibility complex (MHC) antigens of the host, effectively retarded the intracranial growth of Fischer 9L gliosarcoma. We further demonstrated that continuous in vitro exposure to gamma-interferon (gammaIFN) upregulates MHC on 9L gliosarcoma cells and that they were better targets of anti-Fischer aCTL. We hypothesized that the efficacy of cellular therapy with aCTL could be further improved by in situ transduction of the tumor with retroviral vectors coding for gammaIFN, which would generate continuous secretion of the cytokine and maintain upregulated MHC expression by the tumor cells. 9L gliosarcoma and Herpes simplex virus thymidine kinase (tk) transductants of those cells were transduced with a retrovirus carrying the murine gammaIFN gene. By limiting dilution, clones of these cells, designated 9Lgamma 7, 9Lgamma tk8, and 9Lgamma tk10, which produced similar levels of gammaIFN (383-411 ng gammaIFN/10(6) cells/24 h) were isolated. The production of gammaIFN by one clone, 9Lgamma 7, was stable when monitored over 6 weeks in vitro. The clones also demonstrated upregulated MHC class I expression, and the tk-transduced clones maintained their sensitivity to ganciclovir. Compared to the wildtype cells, 9Lgamma 7 had approximate 6- and 1.5-fold increases in the relative antigen densities of MHC I and II, respectively. Addition of exogenous gammaIFN to 9Lgamma 7 cultures did not significantly increase the MHC expression. In cytotoxicity assays, 9Lgamma 7 cells, or 9Lgamma 7 incubated with exogenous gammaIFN, were better targets of aCTL than the parental 9L cells. The growth rate of 9Lgamma-transduced cells was decreased compared to the wildtype cells both in vitro and in vivo. Proliferation studies with transwell plated 9L, 9Lgamma 7, and 9Lgamma tk10 cells in various combinations revealed that the secreted cytokine itself caused a decrease in proliferation. However, the transduced cells exhibited a much reduced growth rate, which likely was a consequence of redirected metabolic activity of the cells. In vivo growth of the 9L and 9Lgamma 7 tumors in rat brains given identical inoculums similarly demonstrated significantly reduced 9Lgamma 7 tumor volumes at various timepoints, indicative of slower growth of the gammaIFN-producing tumors.

Animals↗

PubMed1992

Smooth muscle can comprise the sarcomatous component of gliosarcomas.

The sarcomatous component of gliosarcomas is thought by many to originate from the vascular proliferation seen in glioblastoma multiforme and has, therefore, been assumed to be endothelial. Immunohistochemical staining of four gliosarcomas has led us to an alternate theory. Pathologically all four tumors were composed of at least two cell types; the first had a stellate, glial appearance and the second was either spindled or polygonal in shape. Polygonal cells were associated with glomeruloid vascular structures in some areas. Both components of each neoplasm were cytologically malignant. Glial fibrillary acidic protein and S-100 antibodies stained most of the glial-appearing cells and some of the spindled cells, but not the polygonal cells. Muscle specific alpha-actin and smooth muscle specific alpha-actin antibodies stained only the malignant spindled and polygonal cells and normal vascular smooth muscle. Ulex europaeus agglutinin I and anti-factor VIII/related antigen antibody stained only cells lining vascular lumina. The staining results suggest that the malignant mesenchymal component of these tumors is of smooth muscle origin. Having demonstrated elsewhere that glomeruloid vascular structures of glioblastoma multiforme contain smooth muscle cells, we propose here that gliosarcomas can represent one end of the spectrum of glioma-induced vascular smooth muscle proliferation.

Actins↗

PubMed1991

[Two autopsied cases of radiation-induced gliosarcoma].

Two autopsied cases of radiation induced gliosarcoma are presented in detail with a review of the literatures. Case 1 was that of a 36-year-old female who was found to have a metastatic choriocarcinoma in the right occipital lobe and received radiation therapy of 45 Gy. Four years later CT scan showed a new enhanced tumor in the cerebellum within the previously irradiated field. Total removal was performed and histological diagnosis of the tumor was a gliosarcoma. She died 12 months after the operation. Case 2 was that of a 63-year-old male who had a protoplasmic astrocytoma in the left temporal lobe and received radiation therapy of 60 Gy after surgery. The tumor recurred in the left temporal base after 9 years. Histological finding of the surgical specimens showed gliosarcoma. The patient died 2 months after he was operated on. The tumors had obviously two defined neoplastic components. One was gliomatous features with anaplastic glial cells which stained for glial fibrillary acidic protein. The other was malignant mesenchymal features with spindle shaped fibrosarcoma cells which contained numerous reticulin fibers. Postmortem examination revealed these similar features. Criteria for identifying a tumor as a radiation induced neoplasm have been proposed by Fajado. The main criterion is that the induced tumor should occur in the previously irradiated field. Secondly, it should appear after a latent period. Thirdly, the pathology should be different from the initial neoplasm. Our cases fulfil these criteria.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMedDate not supplied

Computed tomography of gliosarcoma.

Five cases of rare gliosarcoma are described with pathologic correlation. Because of its sarcomatous component, gliosarcoma tends to present as a sharply defined, round or lobulated, hyperdense solid mass with relatively homogeneous contrast enhancement and peritumoral edema. Sharp demarcation of the tumor from surrounding tissue may lead to complete removal and prolonged survival despite high malignancy. However, aggressive tumor regrowth occurs often after incomplete resection. The genesis of gliosarcoma is also discussed.

Adolescent↗

PubMed1983

Immunogenetic and immunologic aspects of gliosarcoma growth in rats.

Growth of the chemically induced, transplantable rat brain tumor gliosarcoma 9L (GS-9L) is under immunogenetic control. Both susceptible and resistant rats produce an immune response to the tumor, but the response is qualitatively different in the two groups. The intraperitoneal administration of gliosarcoma-9L cells in resistant KGH rats causes the production of cytotoxic lymphocytes and macrophages, and in susceptible F344 rats suppressor lymphocytes are produced. After gliosarcoma-9L cells were administered to (KGH x F344)F1 and backcross rats, tumor susceptibility or resistance and the nature of the immune response correlated well with the histocompatibility type, indicating the parallel genetic control of both traits. However, a second gene or gene complex, not linked to the major histocompatibility complex, may participate in the regulation of tumor growth.

Animals↗

PubMed1993

[A case of gliosarcoma associated with large cyst].

A case of gliosarcoma with a large cyst is reported. A 22-year-old female was admitted to our hospital with complaints of blurred vision and headache. Plain skull x-ray films showed a radiolucent area in the right frontal area. Computed tomography (CT) revealed an iso-dense mass in the right frontal lobe with a large cyst. After administration of contrast medium, the solid part and cyst wall were well enhanced and the content of the cyst was slightly enhanced. CT number of the cyst fluid was increased from 64.2 to 83.5 Hounsfield units, after administration of the contrast medium. Axial T1-weighted magnetic resonance image (MRI) revealed an iso-intense mass with marked enhancement by Gd-DTPA in the same area. A large cyst was shown to be located in the dorsal part of the mass. A small round protrusion, 10 mm in diameter, was found on the anterior portion of the mass on this MRI. Right carotid angiogram showed a tumor stain fed by the frontopolar artery. Right frontal lobectomy including the tumor was carried out with a preoperative diagnosis of glioblastoma. The patient received radiation therapy of 60Gy (whole brain 40Gy; focal 20Gy) and chemotherapy postoperatively. Histologically, necrosis, hemorrhage and endothelial hyperplasia were revealed at the tumor lesion. The tumor was composed of proliferation of glial and mesenchymal elements. The glial element appeared as fibrillary astrocytoma and polar spongioblastoma. The mesenchymal element showed sarcoma. As mentioned above, this tumor was diagnosed as gliosarcoma. It was difficult to make a diagnosis of gliosarcoma preoperatively because of the complex findings similar to malignant gliomas in conventional neuroradiological imaging.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Interstitial chemotherapy of the 9L gliosarcoma: controlled release polymers for drug delivery in the brain.

The administration of drugs directly into the central nervous system using polymers as drug carriers may improve the treatment of malignant brain tumors. In this study, the effect of the interstitial, localized delivery of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) incorporated into controlled release polymers implanted adjacent to the 9L gliosarcoma was assessed in s.c. and intracranial (i.c.) models. In the s.c. experiment, the 9L gliosarcoma was implanted in the flank of rats and subsequently treated with BCNU either (a) delivered in controlled release polymers inserted adjacent to the tumor or (b) administered systemically by i.p. injections or by controlled release polymers inserted at a site distant from the tumor. The interstitial release of BCNU adjacent to the tumor in the flank resulted in a significant tumor growth delay of 16.3 days, as compared to a growth delay of 9.3 and 11.2 days obtained with the systemic administration of BCNU. In the i.c. experiment, the 9L gliosarcoma was implanted in the brain of Fischer 344 rats and treated either (a) with controlled release polymers containing BCNU inserted into the brain or (b) with the systemic i.p. administration of BCNU. The interstitial release of BCNU in the brain resulted in a significant 5.4- to 7.3-fold increased survival, compared with a 2.4-fold increased survival after the systemic administration of the same dose of BCNU. The two groups with i.c. tumors treated interstitially had 17 and 42% cures, but no long-term cures were obtained in the group treated with systemic therapy. The localized, controlled delivery of chemotherapeutic agents in the s.c. tissues and in the brain via polymeric carriers may be more effective than standard systemic chemotherapy. This approach could be used to deliver a wide variety of agents into the central nervous system to treat diverse neuropathological conditions which remain refractory to systemic therapy.

Animals↗

PubMed2001

TmDOTP(5-) as a (23)Na shift reagent for the subcutaneously implanted 9L gliosarcoma in rats.

The use of TmDOTP(5-) as an in vivo (23)Na NMR shift reagent (SR) for subcutaneously implanted 9L gliosarcoma was evaluated. TmDOTP(5-) produced a single sharp extracellular peak after about 50-60 min of infusion, and did not cause any changes in the (31)P resonance areas or chemical shifts, suggesting that the SR is homogeneously distributed in the extracellular space and does not alter tumor bioenergetic status. TmDOTP(5-) and CoEDTA(-) as extracellular space markers gave identical results for relative extracellular space (0.25 +/- 0.03 and 0.25 +/- 0.04, respectively) and intracellular Na(+) concentration (19.3 +/- 4.0 mM and 18.6 +/- 3.9 mM, respectively), indicating that the biodistribution of the SR is the same as the well-accepted extracellular space marker. The in vivo T(1) and T(2) relaxation times of intra- and extracellular Na(+) were also measured. Our results indicate that TmDOTP(5-) promises to be an effective shift reagent and extracellular space marker in the 9L gliosarcoma and perhaps other tumors. Magn Reson Med 45:436-442, 2001.

Animals↗