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PubMed2003

Prognostic significance of annexin VII expression in glioblastomas multiforme in humans.

OBJECT: Glioblastoma multiforme (GBM) is the most common and lethal primary brain tumor in adults. It is nearly uniformly fatal, with a median survival time of approximately 1 year, despite modem treatment modalities. Nevertheless, a range of survival times exists around this median. Efforts to understand why some patients live longer or shorter than the average may provide insight into the biology of these neoplasms. The annexin VII (ANX7) gene is located on the human chromosome 10q21, a site long hypothesized to harbor tumor suppressor genes associated with prostate and other cancers. To test whether ANX7 expression might be a predictor for GBMs, we examined ANX7 expression, p53 accumulation, and the MIB-1 labeling index in a retrospective series of 99 GBMs. METHODS: In all 99 cases, the patient's age, Karnofsky Performance Scale (KPS) score before surgery, extent of surgery, tumor location, and immunohistochemical features were analyzed using univariate and multivariate analyses to identify whether any significance exists among ANX7 expression, p53 accumulation, the MIB-1 labeling index, and survival time. Kaplan-Meier analyses demonstrated that a higher KPS score before surgery (< 0.0001), total tumor excision (p = 0.0072), young patient age (p = 0.03), and ANX7 expression (p = 0.0006) correlated with longer survival. Multivariate Cox regression analyses demonstrated that ANX7 expression was the strongest predictor of outcome (p < 0.0001), independent of all other variables. In addition, ANX7 expression correlated with higher MIB-1 immunostaining, but did not correlate with p53 accumulation. Moreover, a significant positive correlation was observed between p53 and MIB-1 staining. CONCLUSIONS: These findings indicate that a higher KPS score before surgery, total tumor excision, young patient age, and ANX7 expression correlate with longer survival in patients with GBMs. Multivariate Cox regression analyses demonstrated that ANX7 expression was the strongest predictor of outcome (p < 0.0001) and was independent of all other variables.

Adult↗

PubMedDate not supplied

Extensive local and systemic therapy in extraneural metastasized glioblastoma multiforme.

Cases of extracranial metastases of glioblastoma multiforme to sites such as bones, spleen, lung, liver and kidneys have been reported but available information about treatment of organ and bone metastases is extremely scarce. In this report a case of glioblastoma multiforme (GBM) of the temporal lobe with subsequent liver and bone metastases is described and the success of different chemotherapy regimens is discussed. Liver and bone metastases were effectively treated with temozolomide and later with carboplatin and docetaxel. Two years after first diagnosis symptomatic local recurrence occurred. Therefore a stereotactic fractionated radiotherapy was performed. As a result of relapse of liver metastases the patient received chemotherapy with adriamycin, cyclophosphamide and etoposide. Visceral metastases were stable, but nevertheless the patient died from local progression 3 years after first diagnosis. In conclusion, liver metastases of GBM can be effectively treated by chemotherapy. This case report suggests suitable substances which can be chosen according to clinical circumstances.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed2000

Analysis of tissue chimerism in nude mouse brain and abdominal xenograft models of human glioblastoma multiforme: what does it tell us about the models and about glioblastoma biology and therapy?

In situ hybridization coupled to immunohistochemistry for antigens of interest allows unequivocal identification of tumor cells from reactive stroma cells and normal adjacent structures in human glioblastoma multiforme grafts transplanted into nude mice. With this methodology, we have explored the development of glioblastoma multiforme solid grafts transplanted into nude mouse brains or flanks. The brain transplants closely resembled the human situation, particularly in relation to differentiation and growth patterns. The morphological features of peritumoral reactive gliosis were similar to those observed in humans. A mouse glial stroma within the main tumor masses was also demonstrated. Kinetic studies showed that the compartment of isolated tumor cells that infiltrated host brains and the reactive gliosis constituted two cycling cell populations. Despite VEGF protein expression by tumor cells and some reactive astrocytes, the abnormally permeable microvascular beds were not hyperplastic. The observation of a non-infiltrative pattern of growth when grafts were established in host flanks demonstrated that the organ-specific environment plays a determining role in the growth and invasive properties of glioblastoma. The phylogenetic distance between man and mouse and the recipient immunoincompetence should not impose serious limitations on the use of this model for studying malignant glioma biology and therapy in vivo.

Abdominal Neoplasms↗

PubMed1978

Spinal subarachnoid metastasis from primary intracranial glioblastoma multiforme.

Twenty-five patients with glioblastoma multiforme were autopsied at our institution in 7 years. Spinal cords were examined in 20 and 5 were found to have spinal leptomeningeal metastases. Clinical and neuropathological findings of these 5 patients are presented and factors possibility influencing such spread are analyzed. Review of previous studies of intracranial glioblastomas discloses only 14 reported cases with spinal leptomeningeal metastases confirmed at autopsy since 1931. We conclude that spinal leptomeningeal metastases in glioblastoma multiforme are a common occurrence. These findings are of little significance at present with our poor success at control of the primary lesion. Frequency of involvement of the spinal subarachnoid space will be significant, when we are able to better treat the primary tumor. Knowledge of the significant possibility of this phenomenon will allow earlier and more frequent clinical diagnosis.

Adolescent↗

PubMed2000

Long-term survival of glioblastoma multiforme: importance of histopathological reevaluation.

The overall prognosis for patients with glioblastoma multiforme is extremely poor. However, a small proportion of patients enjoy prolonged survival. This study investigated retrospectively the extent to which erroneous histopathological classification may contribute to long-term survival of patients initially diagnosed with "glioblastoma multiforme." We compared two age- and gender-matched patient groups with different postoperative time to tumor progression (TTP), defined as "short-term" for TTP of less than 6 months (n = 54), and "long-term" for TTP of more than 12 months (n = 52). Histological specimens of the corresponding tumors, all primarily diagnosed as glioblastoma multiforme, were reevaluated according to the current World Health Organization (WHO) classification of central nervous system tumors, with the investigators being blinded to clinical outcome. Among the tumors from short-term TTP patients, one tumor (2%) was reclassified as anaplastic oligoastrocytoma (WHO grade III) while the remaining 53 were confirmed as glioblastoma multiforme. In contrast, 13 tumors (25%) from the long-term TTP patients were reclassified, mostly as anaplastic oligodendroglioma (WHO grade III; n = 7) or anaplastic oligoastrocytoma (WHO grade III, n = 2), respectively. In addition, three were reclassified as anaplastic astrocytoma (WHO grade III), and one was identified as anaplastic pilocytic astrocytoma (WHO grade III). Our data indicate that a sizable proportion of glioblastoma patients with long-term survival actually carry malignant gliomas with oligodendroglial features. The correct histopathological recognition of these tumors has not only prognostic but also therapeutic implications, since oligodendroglial tumors are more likely to respond favorably to chemotherapy.

Adult↗

PubMed1990

Spinal cord glioblastoma multiforme with intracranial dissemination--case report.

A case of spinal cord glioblastoma multiforme with intracranial dissemination is reported. A 23-year-old female was admitted to a local hospital complaining of lumbago. Myelography revealed an intramedullary thoracic tumor. The tumor was partially removed through a laminectomy at Th11-L1. The histological diagnosis was glioblastoma multiforme, and focal irradiation (total 50 Gy) was given. Eight months after the operation, symptoms of increased intracranial pressure appeared. Computed tomographic (CT) scans showed marked hydrocephalus, and multiple tumors at anterior horns of bilateral lateral ventricles. A ventriculoperitoneal shunt and an Ommaya reservoir into the left lateral ventricle were emplaced. Three months later, she was transferred to our hospital. CT scans showed enhanced lesions in the fourth ventricle, anterior horn of the left lateral ventricle, septum pellucidum, and pituitary gland. Suboccipital craniectomy was performed, and the mass around the fourth ventricle was partially removed. Histological examination of the tumor specimens showed glioblastoma multiforme. Postoperatively, she received whole brain irradiation (total 50 Gy), and intrathecal injection of beta-interferon via the Ommaya reservoir. However, she died of respiratory insufficiency. It is considered that the spinal cord glioblastoma multiforme disseminated into the intracranial space.

Adult↗

PubMed2001

Multicenter phase II trial of temozolomide in patients with glioblastoma multiforme at first relapse.

BACKGROUND: Recurrent glioblastoma multiforme (GBM) is resistant to most therapeutic endeavors, with low response rates and survival rarely exceeding six months. There are no clearly established chemotherapeutic regimens and the aim of treatment is palliation with improvement in the quality of life. PATIENTS AND METHODS: We report an open-label, uncontrolled, multicenter phase II trial of temozolomide in 138 patients (intent-to-treat [ITT] population) with glioblastoma multiforme at first relapse and a Karnofsky performance status (KPS) > or = 70. One hundred twenty-eight patients were histologically confirmed with GBM or gliosarcoma (GS) by independent central review. Chemotherapy-naïve patients were treated with temozolomide 200 mg/m2/day orally for the first five days of a 28-day cycle. Patients previously treated with nitrosourea-containing adjuvant chemotherapy received 150 mg/m2/day for the first five days of a 28-day cycle. In the absence of grade 3 or 4 toxicity, patients on the 150 mg/m2 dose schedule were eligible for a 200 mg/m2 dose on the next cycle. RESULTS: The primary endpoint was six-month progression-free survival assessed with strict radiological and clinical criteria. Secondary endpoints included radiological response and Health-related Quality of Life (HQL). Progression-free survival at six months was 18% (95% confidence interval (CI): 11%-26%) for the eligible-histology population. Median progression-free survival and median overall survival were 2.1 months and 5.4 months, respectively. The six-month survival rate was 46%. The objective response rate (complete response and partial response) determined by independent central review of gadolinium-enhanced magnetic resonance imaging (MRI) scans was 8% for both the ITT and eligible-histology populations, with an additional 43% and 45% of patients, respectively, having stable disease (SD). Objectively assessed response and maintenance of a progression-free status were both associated with HQL benefits (characterized by improvements over baseline in HQL domains). Temozolomide had an acceptable safety profile, with only 9% of therapy cycles requiring a dose reduction due to thrombocytopenia. There was no evidence of cumulative hematologic toxicity. CONCLUSIONS: Temozolomide demonstrated modest clinical efficacy, with an acceptable safety profile and measurable improvement in quality of life in patients with recurrent GBM. The use of this drug should be explored further in an adjuvant setting and in combination with other agents.

Adult↗

PubMed2002

Alzheimer pathology in elderly patients with glioblastoma multiforme.

CONTEXT: Alzheimer disease (AD) and glioblastoma multiforme (GBM) have similar peak, age-specific incidence rates; however, to my knowledge, only 1 case of GBM associated with AD has been reported to date. The frequency of AD pathology, including neuritic plaques, diffuse plaques, neurofibrillary tangles, and cerebral amyloid angiopathy in patients with GBM is unknown. Studies of cancer occurrence in patients with AD are contradictory, with frequencies reported as equal to and as less than that in the general population. The GBM/AD nonconcordance may reflect underreporting of AD pathology or other factors. OBJECTIVE: To compare the frequency and extent of neocortical AD pathology in autopsy cases involving patients aged 60 to 82 years, both with and without GBM. Design.-Case-control study. Setting.-Pathology department of a university hospital. PATIENTS: Thirty-six autopsy cases of GBM patients aged 60 to 82 years; 54 cases of patients in the same age group without GBM or other primary brain tumors. METHODS: Examination of tumor sections for GBM and of neocortical sections for AD pathology according to Consortium to Establish a Registry for Alzheimer Disease (CERAD) guidelines. RESULTS: Glioblastoma multiforme was confirmed in all tumor cases. Alzheimer disease pathology was present in 42% of cases with GBM and in 48% of cases without GBM; 28% of GBM cases had CERAD age-related plaque scores indicative or suggestive of AD; 43% of cases without GBM had CERAD age-related plaque scores indicative or suggestive of AD. CONCLUSIONS: Alzheimer disease pathology was underreported in both GBM and non-GBM patients. The influence of neurodegenerative processes on GBM symptoms and therapy in elderly patients requires further study.

Aged↗

PubMed2006

Recurrent glioblastoma multiforme: advances in treatment and promising drug candidates.

Recurrent glioblastoma multiforme is a lethal disease with currently available treatment options having a limited impact on outcome. In this article, current and novel therapeutic approaches in the treatment of recurrent glioblastoma multiforme, including chemotherapy, targeted molecular agents, virotherapy/gene therapy and immunotherapy and challenges in developing novel therapeutic agents for glioblastoma multiforme will be discussed.

Angiogenesis Inhibitors↗

PubMed2005

Positive and negative associations of human leukocyte antigen variants with the onset and prognosis of adult glioblastoma multiforme.

Associations of genetic factors with malignant gliomas have been modest. We examined the relationships of human leukocyte antigen (HLA) and related polymorphisms to glioblastoma multiforme in adult Caucasians (non-Hispanic Whites) from the San Francisco Bay area. For 155 glioblastoma multiforme patients and 157 control subjects closely matched by ethnicity, age, and gender, PCR-based techniques resolved alleles at HLA-A, -B, -C, and -DRB1 loci along with short tandem repeat polymorphisms of MICA exon 5 and TNFb. By multivariable logistic regression, B*13 and the B*07-Cw*07 haplotype were positively associated with glioblastoma multiforme (P=0.01 and <0.001, respectively), whereas Cw*01 was the only variant showing a negative association (P=0.05). Among glioblastoma multiforme patients, progression to death after diagnosis was slower in those with A*32 (relative hazard, 0.45; P<0.01) and faster in those with B*55 (relative hazard, 2.27; P<0.01). Thus, both the occurrence and the prognosis of glioblastoma multiforme could be associated with specific but different HLA genotypes. B*07 and the B*07-Cw*07 haplotype are much more common in Caucasians than other ethnic groups in the U.S., which may partially explain the higher incidence of glioblastoma multiforme in Caucasians.

Adult↗

PubMedDate not supplied

Irradiation fields and doses in glioblastoma multiforme: are current standards adequate?

AIMS AND BACKGROUND: The optimum conventional radiotherapy in glioblastoma multiforme patients has not been clearly defined by prospective trials. To better characterize a standard radiotherapy in glioblastoma multiforme, the impact on survival of different fields and doses was analyzed in a retrospective single center series. METHODS: One hundred and forty-seven patients with glioblastoma multiforme, submitted to biopsy only (n = 15), subtotal (n = 48) or total resection (n = 82) and who completed the planned postsurgical radiotherapy, were considered. The median age was 57 years, the male/female ratio 1.5/1, and the performance status > or =70 in 76%. Whole brain irradiation, followed by a boost to partial brain, was used in 75 cases with a whole brain dose of 44-50 Gy (median, 46) and a partial brain dose of 56-70 Gy (median, 60 Gy). Partial brain irradiation alone was used in 72 patients with a dose of 56-70 Gy (median, 61 Gy). Ninety-eight patients received 56-60 Gy (median, 59 Gy) to partial brain whereas 49 patients received 61-70 Gy (median, 63 Gy). RESULTS: There was an almost significantly longer survival in patients irradiated to the partial brain alone with respect to those also receiving whole brain radiotherapy (P = 0.056). Doses >60 Gy significantly prolonged survival (P = 0.006). Multivariate analysis confirmed that the impact on survival of radiation dose was independent of age, performance status, extent of surgery, field of irradiation and the use of chemotherapy. The extent of irradiation field was not independently related to improved survival. CONCLUSIONS: Our retrospective findings suggest that we reflect on the adequacy of the current standard irradiation parameters. Well-designed prospective trials are necessary to standardize the radiotherapy control group in patients with glioblastoma multiforme to be compared in phase III trials with innovative therapeutic approaches.

Adult↗

PubMed2003

Specific patterns of DNA copy number gains and losses in eight new glioblastoma multiforme cell lines.

Eight cell lines newly established from glioblastoma multiforme were examined by comparative genomic hybridization for their patterns of genomic imbalance. The total number of DNA copy number alterations (CNAs) found in the eight cell lines varied between 15 and 24. This characterized the examined cell lines (or the tumors they were derived from) as distinctly progressed in karyotypic evolution. The most frequent CNAs were gains of the entire chromosome 6 or, at least, parts of it, and of 7p22, which were found in all eight cell lines. Other changes present in seven of the eight cell lines were gains of 3q26qter and the entire chromosome 7 and losses of segments on chromosome 4q (e.g., 4q34q35) and of the short arm of chromosome 10. Enh(3q21q25), dim(4q22q33) and dim(4qter), dim(13q22), enh(15q14), and enh(18q22q23) were found in six of the eight cell lines. Several other CNAs [e.g., dim(9p21)] were found in common in five or less of the eight lines. Using a hierarchical cluster analysis, the specific patterns of genomic imbalance allowed various groupings of the examined cell lines. Although a close relation could be confirmed among all examined lines on the basis of shared CNAs, two main groups could be roughly differentiated. Among those there were also more or less closely related subgroups. However, also alterations which were restricted to one single cell line each were found, e.g., dim(1q41qter), dim(2q22qter), enh(4p), dim(5p), dim(4p13pter), dim(8q21qter), enh(9p), dim(9q), dim(11p14pter), enh(12q15q23), enh(13q21), dim(14q21qter), dim(15q21qter), dim(19q), and enh(22q). The comparison of the obtained data on gains and losses of DNA copy numbers in specific chromosomal segments with the data on localization of genes possibly associated with the biology of glioblastoma multiforme additionally shows high conformity but also disparity of the examined cell lines among each other, as well as compared to primary glioblastoma multiforme. Eventually, each of the cell lines could be characterized by its specific pattern of genomic imbalance.

Aged↗

PubMed1990

Brain stem and spinal metastases of supratentorial glioblastoma multiforme: a clinical series.

Although the spread of supratentorial glioblastoma multiforme to the brain stem and spine has been extensively described in published autopsy series, information on the diagnosis, treatment, and subsequent clinical course of patients manifesting symptoms of glioblastomatous dissemination ante mortem remains scant. We report a series of 11 patients having the signs and symptoms of neuraxis dissemination of supratentorial glioblastoma multiforme. All patients had radiographic documentation of metastases by either contrast-enhanced myelograms or enhanced magnetic resonance imaging scans. Ten presented with spinal involvement, whereas one presented with lower cranial neuropathies secondary to diffuse involvement of the basal cisterns. The mean age of the patients was 38.5 years, and the mean time interval between diagnosis of intracranial disease and diagnosis of metastases was 14.1 months. After diagnosis of tumor spread, subsequent mean survival time was 2.8 months. All patients received additional radiotherapy to the areas of metastasis, but the clinical response to radiotherapy was quite poor. This study confirms previous reports in the literature suggesting that metastases occur in younger patients and in patients with extended survival. The findings suggest that the relatively infrequent clinical incidence of the symptomatic spread of glioblastoma multiforme, as compared with the frequent incidental discovery of such spread at autopsy, may be the result of the limited survival of the affected patients, and not due to the biology of the tumor.

Adolescent↗

PubMed2001

MIB-I as a proliferative activity marker of the multiform glioblastomas.

MIB-I is a proliferative activity marker of multiform glioblastomas which are the most frequent tumors of the central nervous system. They are characterizad by differential rate and prognosis. The aim of the study was to determine the proliferative activity of multiform glioblastomas and estimation of the correlation between tumors' proliferative activity and tumors' localization, size, patients' age and sex. 24 patients (18 females and 6 males) with multiform glioblastomas were analyzed. The mean patients' age was 52.1. The proliferative activity was calculated as a proliferation index: IP for MIB-I. Cells with positive reaction were determined by MIB-I which was compared to all neoplastic cells. The most frequent localization of the tumors were frontal and temporal lobes of the brain. The size of the tumors ranged from 2.5 to 5.3 cm (mean 3.9). Mean IP was 43.2 (SD+/-17.4). We found no correlation between IP MIB-I and localization of the tumor, patients' age and sex. There was a marginal statistically significant correlation between IP MIB-I and size of the tumor (p=0.005).

Antigens, Nuclear↗

PubMed1999

Glioblastoma multiforme with epithelial appearance: a case report.

A case of glioblastoma multiforme with epithelial appearance, which was difficult to diagnose at first operation, is described. Microscopy revealed small, darkly staining anaplastic cells which were densely packed. In some areas, these cells were arranged in a tubular, gland-like pattern mimicking a poorly differentiated epithelial neoplasm. Immunostaining of glial fibrirally acidic protein (GFAP) was negative in the densely compact anaplastic areas and within the epithelial patterns, except for a small number of cells in one area. Further pathological study at the second and third operations indicated that the tumor consisted of neoplastic astrocytes and had characteristic features of glioblastoma multiforme, including necrosis, pseudopalisading, and endothelial proliferation. Many of the tumor cells were GFAP-positive. This rare case of glioblastoma multiforme was compared with cases reported in the literature.

Adult↗

PubMed1990

Cell proliferation patterns in the diagnosis of astrocytomas, anaplastic astrocytomas and glioblastoma multiforme: a Ki-67 study.

Although astrocytomas, anaplastic astrocytomas and glioblastoma multiforme differ in their clinical courses, histological distinction between these three tumours and between astrocytomas and anaplastic astrocytomas in particular may be unclear on histology alone especially in small biopsies. In the present study, a more objective way of distinguishing between the three types of tumour is sought. Frozen sections from 26 astrocytomas, 26 anaplastic astrocytomas and 38 glioblastomas were stained by an indirect immunoperoxidase technique using the monoclonal antibody Ki-67 which binds to nuclear proteins in the G1, S, G2 and M phases of the cell cycle. The Ki-67 staining was assessed quantitatively through direct observation of the stained sections by the use of a drawing tube attached to a microscope. A minimum of 1000 cells was counted in each case and labelled cells were expressed as a percentage of the total number of cells. These results, when correlated in each case with the histology of the tumour in paraffin sections, showed Ki-67 labelling indices ranging from 0 to 1.9% (mean 0.5% SD +/- 0.54) in astrocytomas, 0.6 to 10.9% (mean 4.1% SD +/- 2.8) in anaplastic astrocytomas and 0.9 to 16.2% (mean 6.4% SD +/- 3.34) in glioblastoma multiforme. The differences in the three types of tumour were statistically significant. The results suggest that Ki-67 staining is a useful addition to the panel of techniques for distinguishing between astrocytomas, anaplastic astrocytomas and glioblastoma multiforme.

Antibodies, Monoclonal↗

PubMed1994

Quantitative immunohistological analysis of the microvasculature in untreated human glioblastoma multiforme. Computer-assisted image analysis of whole-tumor sections.

Because histologically prominent microvascular proliferation is frequently present in glioblastoma multiforme, it has been hypothesized that this neoplasm is particularly dependent on neovascularization for its continued growth and that antiangiogenic therapy might be especially useful. To quantify the histological aspects of microvascular proliferation in glioma, a feasible and reproducible method was developed for computer-assisted image analysis of the visualized microvasculature in glial tissue. This method was used to compare several vascular parameters in histological whole-tumor sections of untreated human glioblastoma multiforme with those in histologically normal cerebral cortex and white matter. There was a significant increase in mean number, area, and perimeter of blood vessels per microscopic field in glioblastoma multiforme compared to normal cerebral white matter. In a substantial number of tumor fields, however, the vascular density was in the same range as that of normal cerebral white matter. The striking heterogeneity of the microvasculature within glioblastoma multiforme was illustrated by the significantly higher standard deviation for the vascular parameters in tumor tissue. The results of this study suggest that many regions of glioblastomas multiforme are not overtly angiogenesis dependent and may be difficult to treat by antiangiogenic therapy alone.

Adult↗

PubMed1989

Patterns of failure following treatment for glioblastoma multiforme and anaplastic astrocytoma.

Recurrence patterns of glioblastoma multiforme (25) and anaplastic astrocytoma (9) were studied using CT scans of 34 patients who received all or a portion of their surgical treatment at Memorial Sloan-Kettering Cancer Center from January 1983 through February 1987. Thirty-two patients presented with unifocal tumors and two with multifocal tumors. All patients received radiation therapy following initial surgery. Eighteen patients who underwent re-operation following CT evidence of recurrence had histologic verification of recurrent tumor; sixteen patients had radiographic evidence of recurrence only. Seventy-eight percent (25/32) of unifocal tumors recurred within 2.0 cm of the pre-surgical, initial tumor margin, defined as the enhancing edge of the tumor on CT scan. Fifty-six percent (18/32) of tumors recurred within 1.0 cm of the initial tumor margin. Tumors for which a gross total resection was accomplished tended to recur closer to the initial tumor margin than did subtotally resected tumors (p greater than 0.1). Extensive pre-operative edema was associated with a decreased distance between initial and recurrent tumor margins. Large tumors were generally not more likely to recur further from the initial tumor margin than were smaller tumors. No unifocal tumor recurred as a multifocal tumor. Only one tumor (initially near the midline) recurred in the contralateral hemisphere. The findings support the use of partial brain irradiation for post-operative treatment of glioblastoma multiforme and anaplastic astrocytomas, and may help to determine the most appropriate treatment volume for interstitial irradiation.

Adult↗