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PubMed2001

Spinal leptomeningeal metastasis from cerebral glioblastoma multiforme presenting with radicular pain: case report and literature review.

BACKGROUND: We present a case of spinal leptomeningeal metastasis from an intracranial glioblastoma multiforme that presented with radicular pain. CASE DESCRIPTION: A 55-year-old man with a previously treated supratentorial glioblastoma multiforme presented with a 12-month history of thoracic radicular pain. MRI of the thoracic spine demonstrated an intradural extramedullary metastatic tumor deposit at the levels of T8-T10. External beam radiotherapy to the thoracic spine provided a minimal decrease in the intensity of the radicular pain. The lack of appreciation of the metastatic potential of the primary intracranial tumor resulted in delayed diagnosis and treatment. CONCLUSION: Spinal leptomeningeal metastasis needs to be suspected in patients with a past history of intracranial glioblastoma multiforme, who present with the clinical features of radiculopathy or myelopathy. Awareness of this condition will facilitate appropriate intervention.

Diagnosis, Differential↗
PubMed2004

Preliminary study on pharmacokinetics of dacarbazine and fotemustine in glioblastoma multiforme patients does not indicate gender-specific differences.

Twelve patients (six female and six male) with histologically proven glioblastoma multiforme were investigated during the administration of the first cycle of dacarbazine (D; 200 mg/m) and fotemustine (F; 100 mg/m). In total, 18 blood samples were collected for pharmacokinetic analysis (maximum plasma concentration, area under the concentration-time curve and total clearance) of D and F at 14 time points during therapy. D, its metabolite 5-aminoimidazole-4-carboxamide and F were evaluated by reversed-phase HPLC. For statistical calculations, groups were compared by the non-parametric Wilcoxon test. p<0.05 was considered statistically significant. No significant gender-dependent differences were observed in the pharmacokinetics of D and F. An additional response re-evaluation of 100 patients (50 female and 50 male) with glioblastoma multiforme, treated at our institution with D and F, gave no hint of any gender-dependent different response rates. We conclude that there is no evidence, neither from pharmacokinetic nor from our clinical data, to consider different dosages of D and F in female and male patients with glioblastoma multiforme.

Adult↗
PubMedDate not supplied

Preradiation chemotherapy with VM-26 and CCNU in patients with glioblastoma multiforme.

AIMS AND BACKGROUND: The objective of the study was to evaluate the efficacy of combined chemoradiation in patients with newly diagnosed glioblastoma multiforme. The main end points were time to progression and overall survival. METHODS: Thirty-one patients with glioblastoma multiforme underwent surgery whenever possible and then received intravenous VM26 (120 mg/m2) and oral CCNU (120 mg/m2) for three cycles followed by radiotherapy (60 Gy). RESULTS: Surgery consisted of a complete resection in 39% of patients, partial resection in 35% and a biopsy in 26%. Sixteen patients had clinical or radiological evidence of progression during or after chemotherapy. Hematologic toxicity was mild. Forty-five percent of patients received the scheduled dose of radiation. The outcome was disappointing, with a median time to progression of 18 weeks and median survival of 37.17 weeks. CONCLUSIONS: The survival of patients with glioblastoma multiforme remains disappointing. Multimodal therapy does not seem to modify the evolution of the tumor. Stratification according to prognostic factors might detect a potential benefit of other therapeutic approaches.

Administration, Oral↗
PubMed1993

Subsets of glioblastoma multiforme defined by molecular genetic analysis.

Glioblastoma multiforme is a clinically and histologically heterogeneous lesion; however, to date, it has not been possible to subdivide glioblastomas on a clinical, histopathological or biological basis. Previous studies have demonstrated that loss of portions of chromosomes 10 and 17 and amplification of the epidermal growth factor receptor (EGFR) gene are the most frequent genetic alterations in glioblastoma. We therefore examined 74 glioblastomas from 67 patients for loss of heterozygosity on chromosomes 10 and 17, and for amplification of the epidermal growth factor receptor gene, to determine whether glioblastomas can be subtyped on a genetic basis. Using Southern blot analysis we were able to detect different patterns of genomic alterations. Eighteen of 67 informative patients were characterized by a loss of heterozygosity on the short arm of chromosome 17 in the tumor tissue. Forty-five of 64 informative patients showed a loss of heterozygosity on chromosome 10. Amplification of the epidermal growth factor receptor gene was noted in 25 of 67 patients and was restricted to those glioblastomas that had lost portions of chromosome 10. Epidermal growth factor receptor gene amplification occurred significantly more often in patients without chromosome 17p loss than in patients with chromosome 17p loss (p = 0.01). In addition, those glioblastomas with a loss of chromosome 17p occurred in patients significantly younger than those with glioblastomas characterized by EGFR gene amplification (p = 0.001). These data emphasize the genetic heterogeneity of glioblastoma and suggest the division of glioblastoma into genetic subsets.

Adolescent↗
PubMed1995

Therapy of glioblastoma multiforme: a cumulative experience of 10 years.

PURPOSE: Comparison of the effect of different therapeutic modalities on survival time of patients with glioblastoma multiforme operated on during the last decade (1980-1990). PATIENTS AND METHODS: The records of 157 consecutive patients with the histological diagnosis of glioblastoma multiforme were analysed for survival with respect to age of patients, extent of surgery, influence of re-operation and adjuvant postoperative treatment. The latter included fractionated radiotherapy, chemotherapy (BCNU. CCNU with Vincristine) and photodynamic therapy (PDT). RESULTS: Analysis of variance showed a significant effect for survival after macroscopically radical surgery (p = 0.005), postoperative radiotherapy (p < 0.001), chemotherapy (p < 0.01). Low age (p < 0.05) and a postoperative Karnofsky performance score (KPS) > or = 60 (p < 0.001) had a positive influence: the site of tumour and pre-operative presence of seizures had no significant influence (p > 0.1) on survival time. CONCLUSION: We conclude that the current adequate management of glioblastoma multiforme should include surgical resection followed by adjuvant treatment such as radiotherapy and chemotherapy.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1991

Effect of recombinant fibroblast interferon and recombinant immune interferon on growth and the antigenic phenotype of multidrug-resistant human glioblastoma multiforme cells.

To study the effect of drug resistance on the response of stage IV astrocytomas to interferon, a human glioblastoma multiforme cell line, GBM-18, was transfected with an expression-vector plasmid containing a human multidrug resistance (MDR) gene (pHaMDR1/A), and clones surviving in colchicine were isolated. GBM-18 multidrug-resistant subclones displayed cross-resistance to other chemotherapeutic agents, including vincristine, doxorubicin, and dactinomycin. The multidrug-resistant phenotype was reversible when GBM-18 multidrug-resistant cells were cultured in colchicine and the calcium-channel blocker verapamil. The level of the MDR1 gene (also known as PGY1) message was increased in GBM-18 multidrug-resistant cells selected for increased resistance to colchicine, and this effect was not correlated with an amplification of the MDR1 gene. In both parental GBM-18 and GBM-18 multidrug-resistant cells, growth was suppressed to a greater degree when cultures were treated with the combination of fibroblast interferon (IFN-beta) and immune interferon (IFN-gamma). Parental cells and multidrug-resistant subclones varied in their de novo and/or interferon-modulated expression of HLA class I and class II antigens, a high-molecular-weight melanoma-associated antigen, and intercellular adhesion molecule 1 (ICAM-1). Of the antigens tested, ICAM-1 and HLA class I antigens were the most sensitive to enhanced expression induced by IFN-beta and IFN-gamma when used alone or in combination. The results of the present study indicate that multidrug-resistant human glioblastoma multiforme cells retain their increased sensitivity to the antiproliferative activity of the combination of IFN-beta plus IFN-gamma, and differences in antigenic phenotype are apparent in independent multidrug-resistant glioblastoma multiforme clones.

Antibodies, Monoclonal↗
PubMed1985

[Spinal epidural metastasis of glioblastoma multiforme: a case report].

It is generally accepted that the metastases of intracranial glioma to extracranial location are rare. In such a case the minimal criteria proposed originally by Weiss should usually be satisfied if a report is to be considered as an acceptable case of metastasizing central nervous system glioma outside the central nervous system. We report a case of glioblastoma multiforme, fulfilling Weiss' criteria, metastasizing the spinal epidural space. The patient was a 32-year-old male, who underwent craniotomy and subtotal removal of a glioblastoma multiforme in the left parietooccipital area. He was additionally treated with irradiation and chemotherapeutic agents. Twelve months after the craniotomy, he was admitted again to our clinic because of sudden onset of severe lumbago, paraplegia and urinary disturbance. Diagnosis of a spinal epidural tumor was made and laminectomy (Th10-L1) was performed. At operation, an epidural mass was found, however no invasion to the spinal cord or dura was noted. Histological diagnosis of the tumor was glioblastoma multiforme. Although he was treated with radiation, pulmonary metastasis was manifested one month later, and the condition of the patient deteriorated. He died 21 months after the first operation and 8 months after the second operation. Even at the terminal stage, his consciousness was clear without any sign for recurrence of intracranial tumor. The general autopsy was done and multiple metastatic lesions of glioblastoma multiforme in paratracheal and paraaortic lymph node, left pleura, both lungs and spinal cord were observed. The present case suggests that the surgical intervention, irradiation, and chemotherapy may contribute to extracranial metastasis of a glioblastoma.

Adult↗
PubMed1993

Surgical resection and radiation therapy versus biopsy and radiation therapy in the treatment of glioblastoma multiforme.

There has been considerable controversy over the concept of treating glioblastoma multiforme with cytoreductive surgery. Therefore, a retrospective study of cases treated between 1986 and 1991 was conducted to analyze and compare the results of stereotactic biopsy followed by radiation therapy performed in 58 patients with those of surgical resection plus radiation therapy in 57 patients. In both groups, conventionally fractionated radiation (1.7 to 2.0 Gy/day) was delivered, with a total dose of 50 to 60 Gy. Biopsy was performed only in patients with tumors judged to be inoperable. These patients carried a higher surgical risk and were in worse neurological condition than the patients in the resection group. The median survival time for the resection group was 39.5 weeks, as compared with 32 weeks for the biopsy group. This difference was not significant. The most important prognostic factor was the patient's age. The treatment variable biopsy versus resection did not reach prognostic relevance. In patients with midline shift who underwent biopsy, the Karnofsky Performance Scale score decreased in more patients during radiation therapy. The clinical status 6 weeks after surgery, however, showed no significant differences between the two groups. The comparable survival times for the two groups place doubt on the concept of treating glioblastoma multiforme with cytoreductive surgery. Presently, radiation therapy is the most effective treatment for patients with glioblastoma. There is no question that decompressive surgery followed by radiation therapy should be performed whenever necessary for sever space-occupying lesions and when it will not cause new neurological deficits.

Aged↗
PubMed1998

Carboplatin chemotherapy before irradiation in newly diagnosed glioblastoma multiforme.

The authors evaluated the efficacy of neoadjuvant carboplatin chemotherapy before external-beam irradiation in patients who had histologically proven glioblastoma multiforme. Twenty-five patients were treated with carboplatin, 600 mg/m2, intravenously once every 4 weeks for a total of 4 planned cycles. External-beam irradiation (60 Gy involved field) was planned after carboplatin. Of 15 patients who had residual tumor assessable for response, seven had stable disease, six had partial responses, one had a complete response, and one had progressive disease. Two of the patients who had partial responses progressed before radiotherapy. Of 10 who had gross total resections, two progressed after 3 to 4 cycles. The median time to tumor progression was 8.4 months. Median survival was 19.2 months. Myelotoxicity and other side effects of treatment were modest. Carboplatin chemotherapy after biopsy or resection of glioblastoma multiforme before irradiation is feasible. These results warrant further clinical investigation of the role that carboplatin chemotherapy may have in the treatment of patients who have newly diagnosed glioblastoma multiforme.

Adult↗
PubMed2006

Early growth response gene-1 regulates hypoxia-induced expression of tissue factor in glioblastoma multiforme through hypoxia-inducible factor-1-independent mechanisms.

Hypoxia strongly up-regulates tissue factor and promotes plasma clotting by glioblastoma multiforme, but transcriptional mechanisms remain undefined. Here, we investigated the potential roles of early growth response gene-1 (Egr-1), Sp1, nuclear factor-kappaB (NF-kappaB), activator protein-1 (AP-1), and hypoxia-inducible factor-1 (HIF-1) in the hypoxic regulation of tissue factor by glioblastoma multiforme cells in vitro. Hypoxia (1% O2) strongly induced Egr-1 mRNA within 1 hour and led to nuclear localization of Egr-1 protein. Using luciferase reporter plasmids in glioma cells, we found that hypoxia dramatically increased luciferase activity in cells with constructs containing Egr-1-binding sites but not in cells with constructs containing AP-1- or NF-kappaB-binding sites. Electrophoretic mobility shift assays revealed hypoxia-induced Egr-1, but not Sp1, binding to oligonucleotides containing the Egr-1/Sp1 motif of tissue factor gene promoter. Using an expression vector containing the minimal tissue factor promoter (-111 to +14 bp) and small interfering RNA (siRNA) directed at Egr-1 and Sp1 mRNAs, we found that Egr-1 was required for maximal hypoxic induction of promoter activity. Forced overexpression of Egr-1 but not Sp1 by cDNA transfection caused up-regulation of tissue factor in glioma cells under normoxia (21% O2), whereas siRNA directed at Egr-1 strongly attenuated hypoxia-induced tissue factor expression. To examine the effects of HIF-1alpha on tissue factor expression, we used glioma cells stably transfected with a HIF-1alpha siRNA expression vector and found that HIF-1alpha mRNA silencing did not affect tissue factor expression under hypoxia. We conclude that hypoxic up-regulation of tissue factor in glioblastoma multiforme cells depends largely on Egr-1 and is independent of HIF-1.

Cell Hypoxia↗
PubMed2001

Phase II study of thalidomide in the treatment of recurrent glioblastoma multiforme.

Treatment options and prognosis remains poor for patients with recurrent glioblastoma multiforme. These tumors are highly vascularised and over express angiogenic factors such as vascular endothelial growth factor and may potentially be responsive to antiangiogenic therapies. We present the results of a phase II trial of Thalidomide, an antiangiogenic agent, in the treatment of recurrent glioblastoma multiforme. Patients were treated with 100 mg/day of Thalidomide, increased at weekly intervals by 100 mg to a maximum tolerated dose of 500 mg/d. Forty-two patients were enrolled, with 38 patients being assessable for response and 39 for toxicity. Two patients (5%) achieved a partial response and 16 (42%) had stable disease. The median survival was 31 weeks and the 1-year survival was 35%. Patients who had a partial response or stable disease had either a stabilisation or improvement in quality of life scores or performance status. Overall Thalidomide was well tolerated with no grade 4 toxicities and no treatment related deaths. The median maximum tolerated dose was 300 mg/day. The most common toxicity was fatigue to which patients developed tachyphylaxis. There was no correlation demonstrated with plasma vascular endothelial growth factor levels and response or survival. Thalidomide is a well-tolerated drug that may have some activity in the treatment of recurrent glioblastoma. Optimum dosing with antiangiogenic agents is currently under investigation. Chronic low dose therapy may be required to see conventional responses or improvements in time to progression. The dose required to achieve optimal biological impact may be better defined once we have established reliable surrogate endpoints.

Adult↗
PubMed1997

Carbogen and nicotinamide combined with unconventional radiotherapy in glioblastoma multiforme: a new modality treatment.

PURPOSE: A new radiotherapy schedule to treat glioblastoma multiforme after surgery, combining nicotinamide and carbogen. METHODS AND MATERIALS: We analyzed 36 patients with glioblastoma multiforme treated after surgery with radiotherapy, Nicotinamide and Carbogen as follows: 7 patients were treated with accelerated fractionation: two fractions/day, 1.5 cGy/fraction, 6 h interval, 5 days/week, total dose 60 Gy in 4 weeks; 8 patients were treated with the same irradiation scheduling plus Nicotinamide at the dose of 4 g and 2 g in capsules, respectively, 1 h before the first and the second irradiation fraction; 21 patients were treated with accelerated radiotherapy, Nicotinamide, and Carbogen (inhaled 10 min before radiotherapy and during the whole course of irradiation). On the basis of surgical removal our patients were subdivided in three groups: totally resected, with residual tumor <50%, or >50%. Radiotherapy with accelerated fractionation was completed in the scheduled time without side effects on the whole group of patients and Carbogen inhalation did not cause significant change of cardiopulmonar parameters. The toxicity observed was predominant in the gastrointestinal tract and was related to Nicotinamide. RESULTS: The median survival time (M.S.T.) was 10 months, as reported by others authors with conventional treatment, but in patients without surgical residual tumor and submitted to the complete treatment schedule, the survival at 35 months was around 25%. CONCLUSIONS: We conclude that this method is feasible with acceptable toxicity; analyzing the survival curves appears to be a trend towards an improvement in survival in the subgroup of patients with gross total removal treated with the combination of Carbogen, Nicotinamide, and accelerated fractionation.

Administration, Inhalation↗
PubMed2005

Extremely rare glioblastoma multiforme of the conus medullaris with holocord and brain stem metastases, leading to cranial nerve deficit and respiratory failure: a case report and review of the literature.

BACKGROUND: Spinal glioblastoma multiforme (GBM) is an uncommon entity and metastases are extremely rare. Glioblastoma multiforme of the conus medullaris is a rare and highly aggressive entity that can quickly progress to a dismal state. Proper diagnosis via histopathologic and immunochemical staining with close clinical and radiological follow-up is important for the management of this very aggressive tumor. CASE DESCRIPTION: The authors report the clinical features, histopathologic and immunochemical staining characteristics, as well as the radiographic evidence of a case of primary GBM of the conus medullaris with metastases to the whole spinal cord and brain in a 20-year-old man who presented with low back pain and bilateral lower extremity weakness and numbness. Review of the pathology slides using histopathologic and immunochemical staining showed GBM. Serial magnetic resonance scans, performed after the initial surgery, demonstrated enlargement of the primary GBM in the conus medullaris with metastases to the thoracic and cervical spinal cord as well as to the brain. CONCLUSIONS: Glioblastoma multiforme of the conus medullaris with such clinical findings is extremely rare. We analyze similar cases in the literature and discuss the importance of monitoring the progression of such an entity as well as the need for aggressive management of the different complications as they arise to maintain a good quality of life.

Adult↗
PubMed2004

Glioblastoma multiforme in three baboons (Papio spp).

Glioblastoma multiforme is the most malignant astrocytic neoplasm and the most common brain neoplasm of humans. Spontaneous neoplasms of the brain are rare in nonhuman primates. This report describes three glioblastomas in adult captive-reared baboons. The animals exhibited a range of clinical signs, including depression, weight loss, weakness, and blindness. All three neoplasms were located in the cerebrum, with extension into the pons in one case. Histologically, the tumors were similar and were characterized by cellular pleomorphism, multinucleated cells, areas of necrosis, microvascular proliferation (glomeruloid bodies), and palisading of neoplastic cells around blood vessels and areas of necrosis. Two baboons exhibited gemistocytic differentiation, and in one baboon, the neoplastic cells were predominantly spindle shaped with a fascicular growth pattern. Immunohistochemical staining for glial fibrillary acidic protein, vimentin, and S-100 protein was positive, whereas immunostaining for synaptophysin and chromogranin A was negative. Positive staining for the cell proliferation marker Ki67 ranged from 8.2% to 13.9%. Terminal deoxynucleotidyl transferase mediated dVTPnick end labeling (TUNEL) staining ranged from 1.8% to 5.7%. These baboon glioblastomas share many features with those of humans.

Animals↗
PubMed2003

Atypical presentation and progression of glioblastoma multiforme in a 6-year-old girl: multidisciplinary case report.

Glioblastoma multiforme is the most common adult malignant brain tumor but is notably less common in children. The authors describe the case of a child who presented for evaluation and treatment of neurologic signs caused by a brain stem glioma. Response to radiotherapy and chemotherapy with temozolomide was initially positive, but later extensive leptomeningeal metastasis developed. Biopsy proved the lesion to be glioblastoma multiforme. During salvage irradiation to the spine and unirradiated brain, the patient complained of hip and femur pain. Subsequent radiographs demonstrated multiple bony metastases. This pattern of spread is uncharacteristic and emphasizes the importance of adequate metastatic evaluation.

Bone Neoplasms↗
PubMed2004

Salvage chemotherapy with cyclophosphamide for recurrent, temozolomide-refractory glioblastoma multiforme.

BACKGROUND: The primary objective of the current prospective Phase II study of cyclophosphamide (CYC) in adult patients with recurrent, temozolomide-refractory glioblastoma multiforme was to evaluate 6-month progression-free survival (PFS). METHODS: Forty patients (28 men and 12 women) ages 28-67 years (median age, 51.5 years), with recurrent glioblastoma multiforme were treated. All patients had been treated previously with surgery and involved-field radiotherapy (median dose, 60 grays [Gy]; range, 59-61 Gy). In addition, all patients were treated adjuvantly with either nitrosourea-based chemotherapy (21 patients: procarbazine, lomustine, and vincristine in 13 patients; carmustine in 8 patients) or temozolomide (19 patients). Twenty-one patients who were treated previously with a nitrosourea were treated with temozolomide at the time of first recurrence. Twenty-one patients were treated with CYC at the time of second recurrence, and 19 patients were treated with CYC at the time of first recurrence. CYC was administered intravenously on 2 consecutive days (750 mg/m2 per day) every 4 weeks (operationally defined as a single cycle). Neurologic and neuroradiographic evaluations were performed every 8 weeks. RESULTS: All patients were evaluable. In total, 170 cycles of CYC (median, 2 cycles; range, 2-12 cycles) were administered. CYC-related toxicity included alopecia in all patients (100%), anemia in 6 patients (3.5%), thrombocytopenia in 7 patients (4.1%), and neutropenia in 9 patients (5.3%). Four patients required transfusions (two required red blood cell transfusion, and two required platelet transfusion). One patient developed neutropenic fever without bacteriologic confirmation. No treatment-related deaths occurred. Seven patients (17.5%; 95% confidence interval [95% CI], 8-33%) exhibited a neuroradiographic partial response, 11 patients (27.5%; 95% CI, 15-44%) had stable disease, and 22 patients (55%) had progressive disease after a single cycle of CYC. The time to tumor progression ranged from 2 months to 18 months (median, 2 months). Survival ranged from 3 months to 24 months (median, 4 months). In patients with either a neuroradiographic response or stable disease (n = 18 [45%]), the median time to tumor progression was 6 months (range, 4-18 months; 95% CI, 6-8 months), and the median survival was 10 months (range, 5-24 months; 95% CI, 8-10 months). The 6-month PFS rate was 20%. CONCLUSIONS: CYC exhibited modest efficacy with acceptable toxicity in the current cohort of adult patients with recurrent glioblastoma multiforme, all of whom had previously experienced treatment failure after temozolomide chemotherapy.

Adult↗