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Results for “Glioblastoma multiforme”

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At least 19 recordsLinked to original sources
PubMedDate not supplied

[Effect of serotonin on the viability of rats with transplanted glioblastoma multiforme].

Mongrel adult albino female rats with multiform glioblastoma transplanted to the right cerebellar hemisphere were given subcutaneous injections of 8 mg/kg of a serotonin-creatine sulphate solution beginning with the 3rd and to the 28th postoperative days. Rats with a tumor inoculated at the same periods and given injections of a physiological saline solution served as controls. The injection of serotonin leads to a significant increase in the survival of rats by 20% as compared to the survival of rats in the control group, but practically has no effect on the life span of sick animals. Consequently, serotonin either produces an antineoplastic effect in which case the animals do not contract the disease, or it has no effect on the tumor so that the animals die of the developing tumor. Study of the tryptophan content in the neoplasm and the 5-OIAA content in urine provides evidence of a disturbed serotonin synthesis and metabolism in these neoplasms.

Animals↗
PubMed1975

Multicentric and isolated multifocal glioblastoma multiforme simulating metastatic disease.

Single case reports of multicentric glioblastoma multiforme and multifocal glioblastoma multiforme tumours are presented. Multicentric glioblastoma multiforme tumours are those which have no macroscopic or microscopic connection. Multifocal gliomatous tumours, on the other hand, are those with either gross or microsopic continuity or evidence of cerebral spinal fluid spread and/or local metastases. The cerebral scintigram findings, cerebral angiogram studies and pathological description of these entities are presented. These lesions may be mistaken for metastases. In patients with multiple cerebral lesions multiple primary malignancies of brain should be considered when there is no clinical or radiographical evidence for extracranial primary neoplasms.

Aged↗
PubMedDate not supplied

[The effect of megavolt radiation therapy on glioblastoma multiforme].

The paper deals with morphological changes in glioblastoma multiforme following megavoltage radiotherapy (1.25 and 25 MeV). Both tumour cell death and glioblastoma multiforme tissue destruction resulted from 6,000-7,500 rads megavoltage irradiation. Depending upon the time following irradiation the histological study showed the prevalance of either acute aseptic inflammation, or coagulation necrosis, or degenerative changes leading to the formation of glial and connective tissue scars and dystrophic calcification. Glioblastoma multiforme, rich in cell elements with hyperchromatic nuclei and having a high mitotic activity, proved to be the most radiosensitive tumour. The highest radioresistance was noted in tumours with a tendency to haemorrhages and necroses.

Brain Neoplasms↗
PubMed1977

Extracranial metastases of glioblastoma multiforme confirmed by electron microscopy.

A case of glioblastoma multiforme which metastasized to the pleura and the lymph nodes of the neck is described. The metastases were detected during the life of the patient. The glial nature of the metastases was confirmed by electronmicriscopic demonstration of typical 90-100 angstrom wide glial fibrils occupying the tumor cell cytoplasm. Electronmicroscopy is recommended to prove the astrocytic nature of a metastatic glioblastoma multiforme. A review of the literature of histologically documented extracranial metastases of glioblastoma multiforme reveals an increase in frequency in recent years. Increased efforts at detection and documentation or an increase in occurrence caused by new methods of treatment are the two possible explanations for this trend.

Brain Neoplasms↗
PubMed1978

Glioblastoma multiforme: morphology and biology.

Glioblastoma multiforme, representing about 50% of all gliomas, encompasses a group of intrinsic tumours of the brain in later years (age peak around 50 years), the morphological hallmarks of which are an ensemble of variations in tumour cell and tissue structure featuring its biological malignancy. Glioblastoma, while sometimes appearing as a distinct "primary" tumour type, is usually accepted as an extreme manifestation of anaplasia and dedifferentiation of glia, mostly astrocytic. The astrocytic nature of most glioblastomas has been confirmed by ultrastructural studies and progressive differentiation of tumours maintained in organotypic tissue culture. Reproducible experimental models are particularly induced by oncogenic RNA (oncorna) viruses. The cell kinetic parameters are similar to those of other solid malignant tumours except for a comparatively low growth fraction of glioblastoma. The frequent occurrence of giant cells as well as of regressive changes with necrosis and vascular responses are indirect (secondary) indicators of malignancy which coincide with histochemical (enzymatic anisochronia) and biochemical data (lower level of glia specific S100 protein than in differentiated gliomas). Vascular proliferation, a characteristic feature of glioblastoma, may occasionally progress to sarcomatous transformation with development of gliosarcomas (mixed glial-mesenchymal tumours). While dissemination of glioblastoma through the cerebrospinal pathways is not uncommon, extraneural distant metastatic spread is rare, and usually observed after craniotomy. The results of modern neuro-oncology support the pathogenetic view that glioblastoma results from neoplastic transformation of glial elements with continuing dedifferentiation. This transformation can be experimentally induced by various factors including oncogenic DNA (oncorna) viruses by using a reverse transcriptase, while there is indirect evidence for an oncorna-virus information in human glioblastoma. The significance of immunological factors in the pathogenesis of brain tumours and in the course of neoplastic transformation of glia is not yet understood, but both morphological and immunological data are in favour of a cell mediated immunological reaction against tumour-specific antibodies. Since immunological factors and changes in cytokinetics are apparently active after the transformed tumour cells proliferate, all available therapeutic methods, including radiation, chemotherapy, and immunotherapy of glioblastoma only influence the final stages of neoplastic development with clinical manifestation of the tumour. In spite of modern combination and multimodality therapy schemes the prognosis of glioblastoma is still poor.

Adult↗
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↗
PubMed1976

Glioblastoma multiforme in children.

Of 488 children with central nervous system neoplasms, 43 (8.8%) had glioblastomas, 22 of which were in the cerebral hemispheres, 16 in the brain stem, two in the cerebellum, and three in the spinal cord. The male to female ratio was 3:2. Glioblastoma multiforme of the cerebral hemispheres occurred at a mean age of 12.7 years, and the frontal lobe was the most commonly involved. Main presenting symptoms included headache (85%), nausea or vomiting (65%), and seizures (35%). Papilledema (45%) was the most common physical finding. The longest survivals were achieved by a combination of operation and radiation (22 months). Brain stem glioblastomas occurred at a mean age of 6.7 years, with the pons as the most frequent site. Nausea or vomiting (50%) and headache (36%) were the main presenting symptoms; the major physical findings were ataxia (43%), cranial nerve palsies (28%), and paresis (28%). The length of survival was greatest with radiation alone (10.5 months). The period of survival of children with glioblastoma multiforme was significantly increased with steroid therapy. Glioblastoma multiforme behaves similarly in children and adults. Intracranial glioblastomas have a more rapidly fatal course than that of other similarly situated gliomas in childhood.

Adolescent↗
PubMed1979

Multiple pulmonary lesions in a patient treated with BCNU (1,3-bis(2-chloroethyl)-1-nitrosourea) for glioblastoma multiforme.

A patient with a glioblastoma multiforme who was treated with BCNU, developed rapidly progressive pulmonary disease. The pulmonary changes were studied pathologically and included atypical alveolar cell hyperplasia, hyaline membranes, and interstitial fibrosis. These lesions contributed to the patient's demise and may be related to the administration of BCNU.

Brain Neoplasms↗
PubMed1977

Soluble membrane antigens of brain tumors. I. Controlled testing for cell-mediated immune responses in a long surviving glioblastoma multiforme patient.

A patient with glioblastoma multiforme survived 18 years after diagnosis and underwent 20 operations for extracranial metastasis. An immunologic survey of the patient was made over a 1-year-period using in vitro tests of lymphocyte responsiveness and skin tests with control and tumor antigens isolated from autologous and allogenic brain cell membranes. Two tissue-associated soluble cell membrane antigens also present in normal white matter, and two tumor-associated antigens (TAA) produce cell-mediated immune responses in patients with brain tumors. One of these tumor-associated antigens predominates in meningioma cells. In addition some low molecular weight components appeared, which seemed to be unique for the glioblastoma cells from the long-surviving patient.

Antigens↗
PubMed1975

Treatment of glioblastoma multiforme. A review.

Experience in irradiating 114 patients with glioblastoma multiforme is reviewed. The split-course therapy utilized in this series, even to high doses (approximately 5 600 rad in 20 fractions over 45 to 50 days), was not associated with an improved survival and does not seem of benefit over conventional fractionation. Adding BCNU (or perhaps tri-iodothyronine) to medium field (less than 135 mc) and moderate dose irradiation (5 000 rad in 25 treatments in 33 days) may improve the outlook for patients with glioblastoma multiforme. An expanded controlled clinical trial to assess this promise of improved treatment results seems indicated.

Adolescent↗
PubMed1979

Prognostic significance of lesion size for glioblastoma multiforme.

From March 1974 to December 1976, 56 patients with glioblastoma multiforme had precraniotomy computed tomography (CT) scans from which the lesion size was determined by measuring the cross-sectional area. Thirty-two patients underwent surgery followed by irradiation, and 24 had surgery followed by irradiation and chemotherapy. There was no difference in survival between the 16 patients with small lesions and the 16 patients with large lesions in the surgery plus radiation alone group, nor in the 16 patients with small and 8 patients with large lesions in the surgery, radiation and chemotherapy group. Minimum follow-up was one year. Other possible prognostic factors including age, tumor grade, radiation dose, and performance status were comparable for each subgroup. Lesion size in glioblastoma multiforme appears unrelated to prognosis.

Adolescent↗
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↗
PubMed1979

Controlled study with BCNU vs. CCNU as adjuvant chemotherapy following surgery plus radiotherapy for glioblastoma multiforme.

From September, 1972 to December, 1976, 102 consecutive patients operated on for glioblastoma multiforme were randomized, after total or subtotal tumor resection, to receive irradiation alone, irradiation plus BCNU or irradiation plus CCNU. BCNU and CCNU adjuvant chemotherapy was repeated every 6--8 weeks as long as the patients remained in complete remission. Patients were comparable for median age, type of surgery, and histological grade III and IV. Radiotherapy was administered at the tumor dose of about 5000 rads in all three groups. The percent of optimal dose administered was 96% for BCNU and 93% for CCNU. In the group treated with radiotherapy alone (32 cases) the median survival was 10.5 months, while in the groups treated with BCNU (34 cases) and CCNU (36 cases) the median survival was 12 and 16 months, respectively. Both relapse-free (P = 0.05) and total survival (P = 0.03) were significantly improved only in patients who were treated with radiotherapy plus CCNU compared to patients receiving radiotherapy alone after surgery. Present results show that in resectable glioblastoma multiforme, a slightly improved survival rate can be achieved by the prolonged use of adjuvant CCNU following maximal surgical resection and radiotherapy. The cure rate was not improved.

Brain Neoplasms↗
PubMedDate not supplied

[ABO blood groups in glioblastoma multiforme].

The distribution of ABO blood groups was analysed statistically in 271 patients treated for glioblastoma multiforme. The control group included 500 patients treated for craniocerebral trauma. A statistically significant difference was observed in the distribution of ABO blood groups between these patient groups, with higher frequency of group A and lower of group O in the patients with glioblastoma multiforme.

ABO Blood-Group System↗
PubMed1978

An example of how patient selection can influence survival in glioblastoma multiforme.

Drawing on experience in evaluating postsurgical treatment of glioblastoma multiforme, it is concluded that results of clinical trials programs can be greatly affected by the status of patients who are selected for study. Investigations report results only on patients considered "evaluable," a portion of the total which may be less than 20%. Improvement in patient survival should not be conceived to be due to aggressive treatment unless patient selection has been accounted for.

Brain Neoplasms↗
PubMed1975

Atypical astrocytes and Rosenthal fibers in a case of amyotrophic lateral sclerosis associated with a cerebral glioblastoma multiforme.

A case of amyotrophic lateral sclerosis (ALS) and cerebral glioblastoma multiforme is presented in which bizarre astrocytes were found in the degenerating lateral corticospinal tracts, along with Rosenthal fibers, which were present in the corticospinal tracts of the lower medulla and spinal cord, and in anterior horns. These bizarre astrocytes did not result from direct infiltration of tumor from the cerebrum. "Malignant transformation" and/or an exceptionally intense glial response to the corticospinal tract degeneration are discussed as possibilities for the development of these bizarre astrocytes. Rosenthal fiber formation is described, to our knowledge, for the first time in ALS.

Adult↗
PubMed1976

Cerebellar glioblastoma multiforme in an adult.

One of the few well documented cases of cerebellar glioblastoma multiforme in an adult is reported. In addition, to our knowledge, it is the first reported case in which the angiographic, pneumoencephalographic, nuclear scan and CAT data have been correlated. In this case the CAT scan proved the most sensitive in the demonstration of tumor.

Age Factors↗