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Results for “GLIOBLASTOMA MULTIFORME”

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PubMed1988

The antineoplastic effect of methylprednisolone pulse therapy in two patients with glucocorticoid receptor-positive glioblastoma multiforme.

Glucocorticoids in high concentrations inhibit in vitro the growth rate of glioblastoma multiforme. This presupposes the presence of glucocorticoid receptors in the cytoplasma. Glucocorticoid receptor positive patients with histological glioblastoma multiforme were postoperatively treated with high dose methylprednisolone pulse therapy during which CT-scanning initially demonstrated tumor regression. One patient's tumor size was unchanged after 24 weeks, whereas in the other patient, the tumor size after decreasing for 1 month began increasing again. The survival rate, at the present 15 and 10 months, without irradiation therapy and the decreasing glucocorticoid receptor concentrations at reoperations indicate an antineoplastic effect by continuous high-dose glucocorticoid pulse therapy.

Adult↗

PubMed2006

Adding chloroquine to conventional treatment for glioblastoma multiforme: a randomized, double-blind, placebo-controlled trial.

BACKGROUND: Malignant cell clones resistant to chemotherapy and radiotherapy frequently lead to treatment failure in patients with glioblastoma multiforme. Preliminary studies suggest that adding chloroquine to conventional therapy may improve treatment outcomes. OBJECTIVE: To examine the effect of adding chloroquine to conventional therapy for glioblastoma multiforme. DESIGN: Randomized, double-blind, placebo-controlled trial. SETTING: National Institute of Neurology and Neurosurgery of Mexico. PATIENTS: 30 patients with surgically confirmed glioblastoma confined to 1 cerebral hemisphere, with a Karnofsky performance score greater than 70, no comorbid disease, and age younger than 60 years. INTERVENTIONS: Oral chloroquine at 150 mg/d for 12 months beginning on postoperative day 5 or placebo. All patients received conventional chemotherapy and radiotherapy. MEASUREMENTS: Primary outcome was survival after surgery; surviving patients were followed up to October 2005. Periodic evaluation using the Karnofsky scale and imaging studies, as well as hematologic tests and ophthalmologic examinations, was done in all patients. RESULTS: Median survival after surgery was 24 months for chloroquine-treated patients and 11 months for controls. At the end of the observation period, 6 patients treated with chloroquine had survived 59, 45, 30, 27, 27, and 20 months, respectively; 3 patients from the control group had survived 32, 25, and 22 months, respectively. Although not statistically significantly different, the rate of death with time was approximately half as large in patients receiving chloroquine as in patients receiving placebo (hazard ratio, 0.52 [95% CI, 0.21 to 1.26]; P = 0.139). LIMITATIONS: The observed advantage of chloroquine may be due to chance; differences in pretreatment characteristics and conventional treatment regimens could not be adjusted for because of the small sample size. CONCLUSIONS: Chloroquine may improve mid-term survival when given in addition to conventional therapy for glioblastoma multiforme. These results suggest that larger, more definitive studies of chloroquine as adjuvant therapy for glioblastoma are warranted.

Adult↗

PubMed2000

Hypofractionation in glioblastoma multiforme.

PURPOSE: To compare conventional fractionation with hypofractionation in patients with a glioblastoma multiforme. Endpoints of the analysis are overall survival and palliative effect. MATERIALS AND METHODS: From 1988 to 1998, 155 patients with pathologically confirmed glioblastoma multiforme were prospectively analysed. Patients without irradiation and patients receiving an interstitial boost were excluded from this analysis. Three different radiation schemes were used in subsequent periods; 33x2, 8x5 and 4x7 Gy. In the last 5 years a scheme of 4x7 Gy conformal irradiation was given to poor prognosis patients. The more favourable group received the conventionally fractionated scheme up to 66 Gy. RESULTS: Median survival was 7, 5.6 and 6.6 months for the 33x2, 8x5 and 4x7 Gy, respectively. In general, patients in the hypofractionation group had far worse prognostic factors compared with patients treated with the conventional scheme. The period of neurological improvement or stabilisation was similar between the 4x7 and 33x2 Gy group. CONCLUSION: An extreme hypofractionation scheme of 4x7 Gy conformal irradiation in poor prognostic glioblastoma patients is well tolerated, convenient for the patient and provides equal palliation without negative effects on survival compared with conventional fractionation.

Adult↗

PubMed1989

Communicating hydrocephalus occurring in the postoperative course of glioblastoma multiforme.

We experienced a case of glioblastoma multiforme which exhibited dementia, gait disturbance, headache, and urinary incontinence six months after subtotal removal of the tumor. These symptoms were not due to tumor recurrence, but to communicating hydrocephalus. Communicating hydrocephalus in cases of malignant brain tumors has not often been reported. We discuss the development of this abnormality.

Brain Neoplasms↗

PubMed1984

Extracranial metastasis of cerebral glioblastoma multiforme: case report.

A patient with glioblastoma multiforme of the right cerebral hemisphere that was treated by surgical removal followed by cobalt therapy is presented. The patient's only neurological deficit at the initial presentation had been a left homonymous hemianopsia, which remained unchanged after operation. He had maintained a good functional state for about 18 months. Then, because of low backache, he was restudied thoroughly, and a bony destructive lesion was found in the body of the 4th lumbar vertebra. A computed tomographic scan-guided biopsy of this lesion revealed a histopathological picture similar to that of the primary cerebral glioma. This metastatic glioma of the spine was treated with cobalt therapy with good clinical (i.e., pain relief) response. The case represents extracranial metastasis of cerebral glioblastoma, which is rarely seen. A brief review of the literature and of the theories concerning dissemination is presented.

Brain Neoplasms↗

PubMed2007

Therapeutic advances for glioblastoma multiforme: current status and future prospects.

Glioblastoma multiforme (GBM) is the most common central nervous system malignancy. It is rapidly progressive with rare opportunity for cure. After three decades of laboratory and clinical research, a newly evolved chemoradiotherapy approach using the alkylating agent temozolomide during and after radiotherapy has resulted in the first significant impact on this disease. Here we discuss the basis for this positive interaction as well as potential mechanisms of resistance to it. Additionally, in the context of current and planned research, we explore approaches to take advantage of this combination and the use of targeted therapies to exploit cell signaling alterations found in GBM. We anticipate that a multimodality approach directed at tumor-specific biology will result in more meaningful advancements in the treatment of this fatal disease.

Antineoplastic Agents↗

PubMed1976

Fast neutron beam radiotherapy of glioblastoma multiforme.

Twenty-one patients with glioblastoma multiforme were treated with fast neutron beam irradiation of the whole brain. Therapy was well tolerated up to calculated doses of 1.850 radn+y in 12-18 increments over 6 weeks. The survival rate 6 month after initiation of treatment was 62%, not significantly different from conventional photon therapy; average posttreatment survival appears to be shortened compared to photon therapy. No improvement or prolonged maintenance of existing neurologic function was observed. Autopsy findings in seven patients showed replacement of tumor by coagulative necrosis persisting at least 16 months posttreatment, paucity of tumor cells with infrequent mitosis, and suppression of macrophage response. These findings differ from those in conventionally irradiated patients. No treatment-related changes were documented by conventional gross and histologic studies of the irradiated brains distant from the tumors. Thus the deaths of patients in this study appear to be related to unexplained causes other than progressive growth of tumor.

Brain Neoplasms↗

PubMed2001

The analysis of peri-tumor necrosis following the subcutaneous implantation of autologous tumor cells transfected with an episome transcribing an antisense insulin-like growth factor 1 RNA in a glioblastoma multiforme subject.

A subject inflicted with glioblastoma multiforme who received partial tumor resection and radiotherapy was recruited for an ex vivo gene therapy protocol using irradiated autologous tumor cells that had been engineered to suppress the expression of insulin-like growth factor I as the tumor vaccine. After subcutaneous injection for 8 weeks, the subject developed peri-tumor necrosis with mass effect. The authors wondered whether this event could have resulted from the tumor vaccine. The tissue section bordering the necrotic tumor tissue to the viable normal tissue was examined for nature of any infiltrated cells and their activities. Lymphocytes, macrophages, and a small number of neutrophils diffused into the necrotic tumor tissue were found. The infiltrated lymphocytes consisted of both CD4+ and CD8+ T cells. The functional activity of these lymphocytes was demonstrated by the active production of interferon y and tumor necrosis factor alpha based on the respective immunofluorescent staining localized to these cells. This finding is compatible with the proposed mechanism underlying the tumor vaccination. However, the contribution of radiation treatment to this event cannot be clearly ruled out.

Brain Neoplasms↗

PubMed2006

Identification of tumor precursor cells in the brains of primates with radiation-induced de novo glioblastoma multiforme.

The pathogenesis of de novo glioblastoma multiforme (GBM) is poorly understood and precursor cells are not known. To gain insight into the pathogenesis of GBM we analyzed brains from primates that developed de novo tumors ten years after whole brain radiation. Four animals had clinical and radiological evidence of GBM, and two animals had no evidence of GBM at the time of euthanization. Tumor precursor cells were identified diffusely scattered in the grossly normal white matter of all animals including two monkeys without evidence of GBM by MR-imaging or on autopsy examination. Tumor precursors demonstrated cellular atypia and mitoses, and were negative for tumor-associated markers GFAP, EGFR and p53. The cells were positive for Ki67 and N-CoR, the nuclear corepressor of astroglial differentiation. These results suggest that radiation-induced nuclear damage to neural stem cells or early astrocytic precursor cells can prevent normal differentiation and lead to tumor development. The findings provide insight into the tumorigenesis of de novo GBMs and suggest a new strategy for treatment of these lethal tumors by targeting both inactivation of N-CoR and inhibition of EGFR.

Animals↗

PubMed1987

Comparison of cytologic composition with microfluorometric DNA analysis of the glioblastoma multiforme and anaplastic astrocytoma.

The DNA content of selected areas of 16 glioblastoma multiforme predominantly composed of small anaplastic cells was investigated. These findings were contrasted with those of five cases of anaplastic astrocytomas. The microfluorometric determination of DNA was performed on mechanically isolated single cells stained by the Feulgen method, obtained from selected areas of the neoplasms in paraffin blocks. Twelve of 16 cases of glioblastoma multiforme had a main population that was diploid-near diploid. Although four of the five anaplastic astrocytomas disclosed a diploid-near diploid main population there was a more complex DNA distribution than in the small cells in glioblastomas. These differences were evident using two numerical DNA indices obtained from the analysis of each tumor histogram which defined, respectively, the extent to which the main tumor cell population deviated from euploid values and the probabilities to have multiple stemlines with abnormal DNA content. The results suggest that small anaplastic cells which appear to represent the most aggressive population in glioblastomas have a DNA content diploid-near diploid, and in malignant gliomas the degree of aneuploidy of the main stemline is not related to the biologic behavior of the neoplasm.

Adult↗

PubMed2003

Quality-adjusted survival after tumor resection and/or radiation therapy for elderly patients with glioblastoma multiforme.

OBJECTIVE: Prognostic factors are poorly defined for the elderly subpopulation with glioblastoma multiforme and have been exclusively related to conventional survival analysis. In this study an additional quality adjusted survival analysis (QAS) was performed. The prognostic evaluation of both survival- and QAS data after standard treatment were checked for concordant/discordant findings. Their usefulness for estimation of treatment effects and treatment strategies was then evaluated. METHODS: 123 patients >or= 65 years of age with a supratentorial, de novo glioblastoma were included in the current retrospective report. Microsurgery plus radiation therapy (planned tumor dose: 60 Gy) was performed in 58 patients, and radiation therapy alone after stereotactic biopsy (planned tumor dose: 60 Gy) in 65 patients. The functional status of each patient was scored when joining the study and at every follow-up using 15 selected neurological signs and symptoms (NSSs). Gradation of severity of each NSS was performed with subjective weights. Survival time of each patient was adjusted according to any changes in these NSSs to become the Quality Time (Q-TIME). Time intervals spent with side effects of the treatment (TOX) were subtracted from Q-TIME to become the patient's QAS (QAS = Q-TIME-TOX). Prognostic factors for both survival and QAS were obtained from the Cox model. RESULTS: Overall survival and QAS were 24 weeks and 10.5 weeks, respectively. Perioperative morbidity and mortality were 5.2 % and 1.7 % in the surgery group and 1.5 % and 1.5 % in the biopsy group, respectively (p > 0.05). Tumor resection gained favorable prognostic importance for patients with midline shift in terms of both survival and QAS (p < 0.0001). Otherwise, radiation therapy alone was as effective as surgery plus radiation therapy (concordant finding). A pretreatment Karnofsky Score (KPS) < 70 was an unfavorable predictor for QAS (p < 0.002) but not for survival (discordant finding). Median QAS for patients with a pretreatment KPS < 70 was only 10 weeks. Age did not reach prognostic relevance. CONCLUSION: The dramatic decrease of QAS as compared with survival indicates extremely limited posttreatment improvement and/or rapid deterioration of the neurological score after standard treatment for the older subpopulation with glioblastoma multiforme. Supportive treatment should be considered for patients with a pretreatment KPS < 70.

Aged↗

PubMed2004

Discrepancy between lesion distributions on methionine PET and MR images in patients with glioblastoma multiforme: insight from a PET and MR fusion image study.

OBJECTIVE: To examine (11)C-methyl methionine (MET) accumulation on positron emission tomographic (PET) imaging of glioblastoma multiforme to determine the distribution of metabolic abnormality compared with magnetic resonance imaging (MRI). METHODS: Contemporaneous MRI was superimposed on corresponding MET-PET images in 10 patients with newly diagnosed glioblastoma multiforme before treatment. Differences between the extended area of MET accumulation on PET imaging (MET area), the gadolinium (Gd) enhanced area on T1 weighted images (Gd area), and the abnormal high signal intensity area on T2 weighted images (T2-high area) were assessed. RESULTS: The MET area was larger than the Gd area and included the entire Gd area. The discrepancy in volume between the MET and Gd areas became greater with increasing tumour diameter. On average, 58.6% of the MET area was located within the Gd area, 90.1% within 10 mm outside the Gd area, 98.1% within 20 mm, and 99.8% within 30 mm. A newly developed Gd area had emerged in five of the 10 cases up to the time of study. In three of the five cases this was in the MET area even after complete surgical resection of the Gd area on the initial MRI; in the remaining two it originated in the residual Gd area after surgery. In all cases, the T2-high area was larger than the MET area. The MET area extended partly beyond the T2-high area in nine cases, and was completely within it in one. CONCLUSIONS: Glioblastoma multiforme cells may extend over the Gd area and more widely with increasing tumour size on Gd-MRI. The T2-high area includes the greater part of the tumour but not its entire area. The methods reported may be useful in planning surgical resection, biopsy, or radiosurgery.

Adult↗

PubMed2000

Evaluation of pre-radiotherapy cyclophosphamide in patients with newly diagnosed glioblastoma multiforme. Writing Committee for The Brain Tumor Center at Duke.

Cyclophosphamide is an alkylating agent that has shown activity in the treatment of pediatric brain tumors, including high-grade gliomas. This study was designed to evaluate the response of patients with newly diagnosed glioblastoma multiforme to pre-radiotherapy cyclophosphamide. Fourteen patients with glioblastoma multiforme were treated with high-dose cyclophosphamide (2 g/m2/day for 2 doses every 28 days) followed by either sargramostim or filgrastin. Sargramostim was given 250 microg/m2 subcutaneously twice a day continuing through the leukocyte nadir until the absolute neutrophil count was more than 1000 cells/microl for 2 consecutive days. The filgrastin dose was 10 microg/kg given subcutaneously once daily until the post nadir absolute neutrophil count was > or = 10,000 cells/microl. A total of 46 courses was given. Four patients received a total of 3 courses, 7 patients completed 4 courses and 3 patients received 2 courses. Three patients demonstrated complete response; 3 stable disease; and 8 progressive disease. The most common toxicity was hematologic, requiring platelet and packed red blood cell transfusions, with 13 admissions for neutropenia with fever. There were no deaths related to infection or bleeding. These results suggest that high-dose cyclophosphamide has modest activity with acceptable toxicity against newly diagnosed glioblastoma multiforme.

Adolescent↗

PubMedDate not supplied

3'-Deoxy-3'-[F-18]fluorothymidine positron emission tomography in patients with recurrent glioblastoma multiforme: comparison with Gd-DTPA enhanced magnetic resonance imaging.

INTRODUCTION: The accumulation of 3'-deoxy-3'-[F-18]fluorothymidine (FLT) on positron emission tomography (PET) images in patients with glioblastoma multiforme was evaluated and correlated with gadopentetate dimeglumine (Gd-DTPA) enhancement in magnetic resonance images (MRIs). METHODS: FLT studies in 10 patients with recurrent glioblastoma multiforme were retrospectively investigated. Dynamic emission data were acquired for 60 minutes immediately after injection of FLT. The standardized uptake value (SUV) for tumor and reference tissue (contralateral hemisphere and ipsilateral cerebellum) was calculated. The volumes of the metabolically active part of the tumor (V (PET)) and that of the Gd-DTPA enhancing part of the tumor (V (MR)) were calculated. RESULTS: FLT uptake in tumors peaked before 5 minutes and sometimes as early as 0.5 minutes, and reached a constant level at approximately 10 minutes after injection. The reference tissue time-activity curves had an early peak and reached a constant low background level. All tumors had increased FLT uptake and showed Gd-DTPA enhancement. The SUV in tumor was significantly higher than that in the reference tissue (P<0.0001). A significant correlation between V (PET) and V (MR) was found (P<0.0001) although there was a difference in the areas of Gd-DTPA enhancement and FLT uptake. CONCLUSION: These preliminary results indicate that FLT-PET may be useful for the detection of recurrent glioblastoma multiforme. Our data in a relatively small patient population do not support a clear-cut relationship between FLT accumulation and Gd-DTPA enhancement. Further pathologic correlation will determine if it can be used for detecting recurrent tumoral disease.

Adult↗

PubMed2006

TRAIL-receptor expression is an independent prognostic factor for survival in patients with a primary glioblastoma multiforme.

PURPOSE: In order to improve the survival of patients with a glioblastoma multiforme tumor (GBM), new therapeutic strategies must be developed. The use of a death inducing ligand such as TRAIL (TNF Related Apoptosis Inducing Ligand) seems a promising innovative therapy. The aim of this study was to quantify the expression of the death regulating receptors TRAIL-R1, TRAIL-R2 and TRAIL on primary GBM specimens and to correlate this expression with survival. EXPERIMENTAL DESIGN: Expression of TRAIL and TRAIL-receptors was assessed by immunohistochemistry, both quantitatively (% of positive tumor cells) and semi-quantitatively (staining intensity) within both the perinecrotic and intermediate tumor zones of primary GBM specimens. RT-PCR of GBM tissue was performed to show expression of TRAIL receptor mRNA. RESULTS: Immunohistochemistry showed a slight diffuse intracytoplasmic and a stronger membranous staining for TRAIL and TRAIL receptors in tumor cells. Semi-quantitative expression of TRAIL showed a significantly higher expression of TRAIL in the perinecrotic zone than in the intermediate zone of the tumor (P=0.0001). TRAIL-R2 expression was significantly higher expressed than TRAIL-R1 (P=0.005). The antigenic load of TRAIL-R2 was positively correlated with survival (P=0.02). Multivariate analysis of TRAIL-R1 within the study group (n=62) showed that age, gender, staining intensity, antigenic load, % of TRAIL-R1 expression, were not statistically correlated with survival however radiotherapy was significantly correlated (multivariate analysis: age: P=0.15; gender: P=0.64; staining intensity: P=0.17; antigenic load: P=0.056; % of TRAIL-R1 expression: P=0.058; radiotherapy: P=0.0001). Subgroup analysis of patients who had received radiotherapy (n=47) showed a significant association of % of TRAIL-R1 expression and the antigenic load of TRAIL-R1 with survival (multivariate analysis: P=0.036, respectively, P=0.023). Multivariate analysis of TRAIL-R2 staining intensity and antigenic load, within the study group (P=0.004, respectively, P=0.03) and the subgroup (P=0.002, respectively, P=0.004), showed a significant association with survival. RT-PCR analysis detected a negative relation between the amount of TRAIL-R1 mRNA and the WHO grade of astrocytic tumors (P=0.03). CONCLUSIONS: TRAIL-R1 and TRAIL-R2 expression on tumor cells are independent prognostic factors for survival in patients with a glioblastoma multiforme. Both receptors could be targets for TRAIL therapy. As TRAIL-R2 is more expressed, in comparison with TRAIL-R1, on GBM tumor cells, TRAIL-R2 seems to be of more importance as a target for future TRAIL therapy than TRAIL-R1.

Apoptosis↗

PubMed1993

Influence of location and extent of surgical resection on survival of patients with glioblastoma multiforme: results of three consecutive Radiation Therapy Oncology Group (RTOG) clinical trials.

PURPOSE: The influence of tumor site, size, and extent of surgery on the survival of patients with glioblastoma multiforme treated on three consecutive prospectively randomized Radiation Therapy Oncology Group trials employing surgery and irradiation plus or minus chemotherapy was studied. METHODS AND MATERIALS: Six hundred forty-five patients with a diagnosis of glioblastoma multiforme on central pathological review were analyzed for survival with respect to known prognostic factors, that is, age and Karnofsky Performance Status, as well as extent of surgery, site, and size. Surgical treatment consisted of biopsy only in 17%, partial resection in 64%, and total resection in 19%. Tumors were located in frontal lobe in 43%, temporal lobe in 28%, and parietal lobe in 25%. Maximum tumor diameter as determined on computed tomography or magnetic resonance imaging scans was less than 5 cm for 38%, between 5-10 cm for 56% and greater than 10 cm for 6% of patients. The extent of surgical therapy was the same for tumors greater than 5 or greater than 10 cm, whereas total resection was more often performed for tumors less than 5 cm. The extent of surgery did not appear to vary with age or site. RESULTS: Patients undergoing total resection had a median survival of 11.3 months compared to 6.6 months for patients with a biopsy only. A significant difference in median survival was also found for partial resection versus biopsy only treatment (10.4 vs. 6.6 months). There was no difference in survival for the different tumor sizes. Patients with frontal lobe tumors survived longer than those with temporal or parietal lobe lesions (11.4 months, 9.1 months, and 9.6 months, respectively) (p = 0.01). A Cox multivariate model confirmed a significant correlation of age, Karnofsky Performance Status, extent of surgery, and primary site with survival. The best survival rates occurred in patients who had at least three of the following features: < 40 years of age, high Karnofsky Performance Status, frontal tumors, and total resection (17 months median). CONCLUSION: We conclude that biopsy only yields inferior survival to more extensive surgery for patients with glioblastoma multiforme treated with surgery and radiation therapy.

Adult↗

PubMed1985

The glioblastoma multiforme in Georgia, 1977-1981.

To characterize the incidence and mortality of the glioblastoma multiforme as it is seen at the primary care level, a retrospective study was done through the Georgia Tumor Registry on 299 patients with histologically confirmed supratentorial glioblastoma multiforme. Specifically, the age incidence distribution, sex ratio, and the postoperative survivals were studied. The Registry also provided the opportunity to define the relative racial frequencies of this neoplasm in a large biracial population. The mean age of the patients at the time of surgery was 58.6 years and the age group having the highest incidence was 60 to 74 years. The overall ratio of affected males to females was 1.04 to 1. The postoperative survival periods were considerably shorter than those reported from large cooperative clinical trials. The overall postoperative survivals at 12 and 24 months were only 22% and 4%, respectively. Advancing age had a strong negative relationship with the length of survival such that the 50% survival for patients less than 30 years of age was 17 months, for those age 30 to 44 years it was 10.2 months, for those age 45 to 59 it was 5.8 months, and for those older than 60 it was only 2.2 months. The study confirmed previous suggestions that the incidence of the neoplasm is considerably higher in whites. There were 2.3 glioblastomas in whites for every one in blacks. No difference was noted in the length of survival between whites and blacks.

Adolescent↗

PubMedDate not supplied

[Glioblastoma multiforme in a patient with a second complete remission of Hodgkin's disease].

INTRODUCTION: Treatment of Hodgkin's disease contributes to the appearance of second malignant neoplasias such as glioblastoma multiforme. Amongst the known etiological hypotheses is alteration of the immune system secondary to chemotherapy. We seek new hypotheses relating this rare association. With better understanding of the causes provoking the appearance of these tumors new strategies could be designed for treatment. CLINICAL CASE: A 26 year old man who was in a second complete remission of a nodular sclerosis type of Hodgkin's disease complained of headache and evening fever. Magnetic resonance showed a right frontal 6 x 5 x 4 cm cystic lesion with a vascular solid zone, with irregular margins and surrounded by vasogenic oedema. On investigation there were reduced levels of immunoglobulins G (522 mg/dl)) and M (38 mg/dl). The lesion was removed surgically and histological studies confirmed the diagnosis of glioblastoma multiforme. CONCLUSIONS: Although immunosuppression may contribute to the appearance of secondary neoplasia, it is not the only hypothesis in the case of glioblastoma multiforme occurring in a patient with Hodgkin's disease. In the literature similar cases, both isolated and familial, have been reported and may have been affected by genetic or environmental factors which are as yet unknown.

Adult↗