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At least 19 recordsLinked to original sources
PubMed1984

Cerebral gliosarcoma, pulmonary adenoid-cystic carcinoma, and pulmonary metastatic gliosarcoma: report of an untreated case.

An elderly woman had a cerebral gliosarcoma with a single pulmonary metastasis, together with a separate pulmonary adenoid-cystic carcinoma. Spontaneous extraneural metastases of primary intracranial neoplasms are exceedingly unusual; so far, only 8 proven cases are recorded in the English language medical literature. The association of cerebral gliosarcoma and a pulmonary adenoid-cystic carcinoma is presumably coincidental.

Aged↗
PubMed1991

Spindle-cell glioblastoma or gliosarcoma?

'Gliosarcomas' have long been considered to be mixed gliomas and sarcomas. The present study failed to define criteria which clearly delineate 'gliosarcomas' from glioblastoma multiforme and suggests that 'gliosarcomas' should be considered as spindle cell glioblastomas. A total of six cases originally diagnosed as 'gliosarcomas' were compared with four cases of glioblastoma multiforme. No clinical or prognostic features were defined which would clearly separate 'gliosarcomas' from glioblastoma multiforme. Macroscopically, biopsies from 'gliosarcomas' ranged from firm, apparently well-circumscribed tumours to poorly circumscribed lesions with a soft consistency resembling glioblastoma multiforme. Histology revealed a continuous spectrum in which 'gliosarcomas' with large reticulin-rich areas of spindle cells merged with typical glioblastomas containing only small islands of spindle cells and reticulin staining. Immunocytochemistry for glial fibrillary acidic protein (GFAP); S100 protein and alpha-smooth muscle actin (ASMA) showed that the majority of cells in reticulin-poor areas of 'gliosarcoma' and glioblastomas expressed S100 protein and GFAP; many expressed ASMA and some expressed both GFAP and ASMA. Spindle cells in reticulin-rich areas of 'gliosarcomas' and glioblastomas most frequently expressed ASMA but many cells also expressed S100 protein and GFAP; some cells expressed both GFAP and ASMA. The results of this study and a review of the literature suggests that there is a clinical, radiological and pathological continuum with glioblastoma and 'gliosarcoma' at different ends of the spectrum. It is suggested, therefore, that most, if not all, 'gliosarcomas' be redesignated as spindle cell glioblastomas and not be considered as a mixture of glioma and sarcoma.

Actins↗
PubMed1995

Clinicopathologic features of primary and postirradiation cerebral gliosarcoma.

BACKGROUND: Gliosarcoma is an uncommon malignant brain tumor with mixed glial and mesenchymal elements. Experience is limited to case series, and pathologic data are disparate, leading to uncertainty about clinical features, management, and histogenesis. METHODS: A clinicopathologic review of 32 patients with survival analysis and immunohistochemical studies was performed including glial fibrillary acidic protein analysis, alpha-1-antitrypsin (alpha-1-AT) analysis, and smooth muscle actin (SMA) analysis. RESULTS: Twenty-five patients had primary gliosarcoma, whereas 7 developed gliosarcoma after irradiation for glioblastoma multiforme (GBM). Clinical features were similar to those of GBM. Most tumors were intraaxial and diffusely infiltrating by radiologic studies and at surgery. Median survival for primary gliosarcoma was 25 weeks overall, with patients who received irradiation surviving longer (46 vs. 13 weeks, P < 0.025). Gliosarcoma occurring after irradiation appeared hyperdense by computed tomography in five of seven cases, and median survival was 53 weeks. Primary gliosarcoma was a dimorphic tumor with malignant glial elements and features of malignant fibrous histiocytoma (MFH) or fibrosarcoma and one osteosarcoma. Smooth muscle actin labeled tumor vessels heavily, but in 15/25 primary cases, it extended to the surrounding spindle cells. The remaining cases appeared morphologically like MFH and tended to be positive for alpha-1-AT. Postirradiation gliosarcoma was fibrosarcomatous with positive SMA in 75% of the cases examined. CONCLUSIONS: Gliosarcoma behaves clinically like GBM, and survival may be improved by cranial irradiation of selected patients. Smooth muscle actin reactivity in sarcomatous areas suggests histogenesis in some tumors from the smooth muscle within GBM, whereas others may arise via different mechanisms including differentiation from a pluripotential precursor. Transformation of the smooth muscle within GBM may have therapeutic implications for antiangiogenesis agents.

Actins↗
PubMed1998

Clinical outcome of gliosarcoma compared with glioblastoma multiforme: North Central Cancer Treatment Group results.

OBJECT: Gliosarcoma, a rare malignancy of the central nervous system, consists of gliomatous and sarcomatous elements. There are conflicting reports regarding its aggressiveness and cell line of origin compared with those of glioblastoma multiforme (GBM). The goal of this study was to compare clinicopathological features such as disease-free survival time and actual survival time in patients with gliosarcoma with a matched group of patients with GBM as well as with the entire group of patients with GBM. METHODS: The authors report on 18 cases of gliosarcoma derived from a series of 748 Grade 4 astrocytoma cases that were part of four consecutive randomized Phase III trials conducted between 1979 and 1996. In this series the gliosarcoma group represented only 2.4% of all GBMs and included 11 men and seven women with a median age of 61.5 years (range 31-81 years). The median tumor size was 5 cm (range 2-8 cm). The locations, all supratentorial, included temporal in 44%, parietal in 28%, frontal in 17%, and occipital in 11%. The 18 patients with gliosarcomas, all Grade 4 (World Health Organization classification), were compared with the entire group of 730 patients with GBM and a control group of 18 patients with GBM matched for known prognostic factors including patient age, randomization date, performance status, extent of resection, and protocol number. Patients in all treatment groups received radiation and nitrosourea-based chemotherapy. The median time to progression and the median survival times for the patients with gliosarcoma were 28.0 and 35.1 weeks as compared with 24.7 and 41.6 weeks for the entire group of patients with GBM (log rank test, p = 0.94 and 0.27, respectively) and 16.7 and 34.4 weeks in the control group (p = 0.20 and 0.84, respectively). In previous molecular cytogenetic analyses of gliosarcoma these authors have shown similar genetic changes in the gliomatous and sarcomatous components. CONCLUSIONS: The data obtained in this study support the conclusion that gliosarcoma shares significant clinical and genetic similarities with GBM and that the same principles should be applied for patient enrollment in research protocols and treatment for these two kinds of tumor.

Adult↗
PubMed1992

Epithelial and melanoma antigens in gliosarcoma. An immunohistochemical study.

Gliosarcomas are mixed tumors with malignant glial and mesenchymal elements. The number of GFAP-positive tumor cells decreases with the increase of sarcomatous components, until whole areas may be GFAP negative. These distinct differentiations may, however, lead to false interpretations in small tissue samples. In this connection, it is of interest that, according to other reports, glial tumors may be positive for different anti-keratin antibodies and this prompted us to undertake a systematic investigation of the immunoreactivity of gliosarcomas using a panel of well-characterized monoclonal antibodies against cytokeratins (KL1, AE 1/3, Lu-5, CK-19, CK MNF 116 and Ma-903). These cases were further studied with the anti-epithelial non-cytokeratin antibodies EMA, HEA 125, Ber-EP4, CEA as well as the melanoma-antibody HMB-45, Leu-M1, GFAP and vimentin. As screening study we examined 20 cerebral metastatic carcinomas, 21 malignant gliomas (including 6 gliosarcomas) and 3 metastatic melanomas with the monoclonal antibodies KL1 and HMB-45. All cerebral metastatic carcinomas and 4/6 gliosarcomas were positive for KL1, whereas all melanomas, 2 metastatic carcinomas and 3 gliosarcomas showed an immunostaining with HMB-45. All gliosarcomas were positive with at least one of the tested anti-cytokeratin antibodies. The gliosarcomas did not show an immunoreaction in any of the cases when CEA, HEA 125, Ber-EP4, EMA or Leu M1 were applied. In our opinion, the monoclonal antibodies HEA 125 and Ber-EP4 could obviously be helpful in differentiating gliosarcomas from metastatic carcinomas.

Antibodies, Monoclonal↗
PubMed2000

Genetic profile of gliosarcomas.

There are distinct genetic pathways leading to the glioblastoma, the most malignant astrocytic brain tumor. Primary (de novo) glioblastomas develop in older patients and are characterized by epidermal growth factor (EGF) receptor amplification/overexpression, p16 deletion, and PTEN mutations, whereas secondary glioblastomas that progressed from low-grade or anaplastic astrocytoma develop in younger patients and frequently contain p53 mutations. In this study, we assessed the genetic profile of gliosarcoma, a rare glioblastoma variant characterized by a biphasic tissue pattern with alternating areas displaying glial and mesenchymal differentiation. Single-strand conformation polymorphism followed by direct DNA sequencing revealed p53 mutations in five of 19 gliosarcomas (26%) and PTEN mutations in seven cases (37%). Homozygous p16 deletion was detected by differential polymerase chain reaction in seven (37%) gliosarcomas. The overall incidence of alterations in the Rb pathway (p16 deletion, CDK4 amplification, or loss of pRb immunoreactivity) was 53%, and these changes were mutually exclusive. Coamplification of CDK4 and MDM2 was detected in one gliosarcoma. None of the gliosarcomas showed amplification or overexpression of the EGF receptor. Thus gliosarcomas exhibit a genetic profile similar to that of primary (de novo) glioblastomas, except for the absence of EGFR amplification/overexpression. Identical PTEN mutations in the gliomatous and sarcomatous tumor components were found in two cases. Other biopsies contained p16 deletions, an identical p53 mutation, or coamplification of MDM2 and CDK4 in both tumor areas. This strongly supports the concept of a monoclonal origin of gliosarcomas and an evolution of the sarcomatous component due to aberrant mesenchymal differentiation in a highly malignant astrocytic neoplasm.

Adult↗
PubMed1997

Gliosarcoma. A study of 13 tumors, including p53 and CD34 immunohistochemistry.

OBJECTIVE: Gliosarcoma is a biphasic neoplasm composed of a glioblastoma multiforme admixed with a sarcomatous component that is presumed to arise from a malignant transformation of the hyperplastic vasculature elements. We studied 13 cases of gliosarcoma to describe the clinical and pathologic features of this tumor. In addition, immunohistochemical analysis using p53 and CD34 was performed in an attempt to examine the histogenesis of gliosarcomas. DESIGN AND SETTING: A retrospective study of 13 patients with gliosarcoma from a tertiary care center. RESULTS: The 13 patients (7 women, 6 men) had a median age of 62 years (range, 33 to 79 years). All patients were initially treated with surgical excision followed by adjuvant radiation therapy, and two received adjuvant chemotherapy. Nine patients died of disease (median, 9 months; range, 1 to 17 months). Three patients were alive with evidence of residual tumor at most recent follow-up (median, 18 months; range, 6 to 41 months). A single patient was lost to follow-up. Histologically, all neoplasms consisted of an admixture of glioblastoma multiforme and sarcomatous elements. The sarcomatous component resembled fibrosarcoma in 12 cases and a malignant fibrous histiocytoma in one case. The sarcoma appeared to arise from hyperplastic vasculature in five tumors. CD34 staining in all five of these cases was negative. Immunostaining for p53 was observed in eight tumors (61.5%). p53 positivity was definitely present in both glial and sarcomatous components in all but three positive cases. The degree of staining was comparable between the two elements in five cases, present in only the glial component in two cases, and not able to be reliably assigned to one or the other component in one case. CONCLUSION: Gliosarcoma is an aggressive-behaving neoplasm, as previously reported. The presence of p53-positive immunostaining, similar to glioblastoma multiforme, may be indicative of a role for the p53 gene in these neoplasms. A lack of CD34 staining does not support an endothelial cell origin for gliosarcoma.

Adult↗
PubMed1996

The glial and mesenchymal elements of gliosarcomas share similar genetic alterations.

The cellular origin of the sarcomatous component of gliosarcomas is controversial. It is not clear if the sarcoma arises in transition from the glial cells that comprise the gliomatous component or independently arises from non-neoplastic mesenchymal cells of the tumor stroma. Using comparative genomic hybridization (CGH) along with cytogenetic analysis, fluorescence in situ hybridization (FISH) analysis, and polymerase chain reaction (PCR) analysis of microsatellite allelic imbalance, we have evaluated the genetic alterations in the gliomatous and sarcomatous components of five gliosarcomas. The glial element was grade 4 fibrillary astrocytoma (glioblastoma multiforme) in all five tumors. The sarcoma elements were fibroblastic without osseous, chondroid, or angiosarcomatous differentiation. Gain of chromosome 7, loss of chromosome 10, deletions of the chromosome 9 p-arm, and alterations of chromosome 3 were frequently observed, demonstrating that gliosarcomas can be genetically classified as belonging to the spectrum of glioblastomas. Furthermore, the sarcomatous and gliomatous portions of each gliosarcoma investigated were similar with respect to both the presence and absence of specific genetic alterations. This observation supports the hypothesis that the sarcomatous component of a gliosarcoma either arises from the same common precursor cell as the gliomatous portion, or it arises from the gliomatous portion itself.

Adult↗
PubMed1994

Interphase cytogenetics of glioblastoma and gliosarcoma.

Interphase cytogenetics, i.e., in situ hybridization using probes to chromosome-specific DNA, enables histological identification of cells bearing numerical chromosome aberrations and cytogenetic analysis of composite tumors. We studied routinely processed tissues from seven glioblastomas and three gliosarcomas using biotinylated probes to pericentromeric alpha-satellite sequences on chromosomes 10, 17 and X. By applying various pretreatment protocols, an evaluable compromise between morphology and signal intensity was obtained in most cases. Compared to vascular cells with normal chromosomal counts, a significant subpopulation of glioblastoma cells showed monosomy 10 (four of five cases), monosomy 17 (one of seven cases) and loss of one X chromosome (one of seven cases). All monosomy 10 cases comprised additional areas where two copies of chromosome 10 were retained. Among the gliosarcomas, both the glioma and the sarcoma portion showed monosomy 10 in one case and monosomy 17 in another case. In contrast, in the third case of gliosarcoma, monosomy 10 was found only in the glioma portion, whereas a gain of chromosome X was observed in the sarcoma portion. We conclude that: (1) numerical chromosome aberrations can be detected in routinely processed brain tumor biopsy specimens using interphase cytogenetics, making retrospective studies feasible; (2) glioblastomas show intratumoral cytogenetic heterogeneity with formation of monoclonal cell clusters; and (3) sarcoma and glioma elements in gliosarcomas may exhibit the same or different numerical chromosome aberrations, suggesting various histogenetic pathways of the sarcoma-like portion.

Adult↗
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↗
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

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↗
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↗