Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-three patients were treated at the Methodist Hospital, Baylor College of Medicine (Houston) between 1983 and 1987, for high-grade gliomas which had recurred after conventional external-beam radiation therapy. The mean dose to the tumor volume from the external-beam therapy was 5800 cGy. Thirteen patients had recurrent astrocytoma Grade 4 (glioblastoma), whereas 20 had recurrent astrocytoma Grade 3 (anaplastic astrocytoma). All patients were treated for their recurrence by the combination of reexcision of as much of the tumor mass as was technically feasible and intraoperative radiogold (198Au) seed implantation of the residual tumor and/or tumor bed. The mean dose to the tumor volume from the implant was 4000 cGy. For the 13 patients treated for recurrent glioblastoma the 1-year, 2-year, and 3-year survival rates were 46%, 15%, and 8%, respectively. For the 20 patients treated for recurrent anaplastic astrocytoma the 1-year, 2-year, and 3-year survival rates were 75%, 50%, and 15%, respectively. Survival was measured from the time of implant. The median survival for patients with glioblastoma was 9 months. The median survival for patients with anaplastic astrocytoma was 17 months. One patient died in the immediate postoperative period from a gastrointestinal bleed. No patient required reoperation for radiation necrosis. The authors believe that this technique is an effective treatment for patients with high-grade gliomas recurring after external-beam radiation therapy, and are now including interstitial irradiation in the initial management of selected patients with high-grade gliomas.
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PMID:Interstitial radiogold implantation for the treatment of recurrent high-grade gliomas. 216 43

Morphologic features of the autopsied specimen of 22 cases with supratentorial gliomas treated by surgery, radiation and/or chemotherapy were analysed, and the characteristics of recurrence of gliomas were searched for. The cases consisted of anaplastic 12 astrocytoma and 10 glioblastoma. The results were as follows: 1) Characteristic CT findings before death were regrowth of the tumor mass or the occurrence of a new enhanced lesion in 21 out of 22 cases. The enhanced lesion showing regrowth of the tumor located in the same site as the previous tumor mass in 21 cases. The new enhanced lesion resulting from a trans-or subependymal tumor spread, was seen in the ventricular wall, and these findings were a characteristic feature of the recurrence of gliomas. 2) Modes of extension of the tumor were subdivided into 3 types. One was the expansive or infiltrative type caused by regrowth of the residual tumor. In the second pattern, a spread of tumor cells occurred along the myelinated fiber tracts to the brain stem (60%), or to the contralateral cerebral hemisphere through the corpus callosum (50%). The third mode of tumor propagation was cerebrospinal fluid seeding with intraventricular or subarachnoid tumor regrowth (45%). 3) Characteristic histological findings shown in the original tumor bed were those of increased cellularity with endothelial proliferation, widespread necrosis with occlusion of the blood vessels, occurrence of the gemistocytic astrocytes and large bizarre cells. Thickening of wall of the blood vessels due to effect by radiation was followed by occlusion of the blood vessels. Large necrosis in the tumor tissue was caused by those process and others. Necrotic area was mainly circumscribed and corresponded to the territory of the vessels. One of the specific findings in the morphological changes of the tumor cells was giant cell formation which were monstrous cell, giant cell (12 cases out of 22), and gemistocytic cell (in all cases). These specific cells were supposed to the degenerative changes of the tumor cells exposed while withstanding such adverse conditions as hypoxia, radiation and chemotherapy. 4) Infiltration distant from the primary lesion which were defined only by microscopical examination was demonstrated as both through myelinated fiber tracts in 8 cases and through perivascular spaces in 2 cases. Reinvasion of the tumor cells from the subarachnoid spaces to the brain parenchyma was along the Virchow-Robins spaces of the penetrating blood vessels in the latter cases.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Morphologic findings and biologic behavior in the high grade glioma--a postmortem study of 22 cases]. 247 32

Twenty-four adults with glioblastoma multiforme (astrocytoma, grade 4) underwent postoperative large dose fraction radiotherapy (LDFR; 5 Gy twice weekly) with Linac X-rays. The outcome in this group was compared with that of 26 patients who received conventional fractionated radiotherapy (CFR; 2 Gy 5 times weekly). The time, dose, and fractionation (TDF) factor was about 100 in both groups. The survival rates following LDFR and CFR were, respectively, 63% vs 65% at 1 year; 36% vs 8% at 2 years; 17% vs 4% at 3 years; and 4% vs 0% at 5 years. Although the survival curve for LDFR was superior to that for CFR, the difference was not statistically significant. Autopsies of nine LDFR and 13 CFR patients showed no residual tumor in one case and no cases, respectively; small residual tumor in three cases in each group; extensive coagulation necrosis of the tumor and surrounding brain tissue in one LDFR and four CFR patients; tumor proliferation in three LDFR and four CFR cases; and mixed glioblastoma and fibrosarcoma in one LDFR and two CFR patients. These results suggest that maximum tumor removal followed by LDFR may offer a better prognosis for patients with glioblastoma than that offered by surgery plus CFR.
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PMID:Large dose fraction radiotherapy in the treatment of glioblastoma. 255 May 92

The histological changes in various tissues irradiated with lasers are well known. Our own previous observations with the optical microscope confirm those already reported in the laser literature. If tissue is treated with various laser sources, the results are similar, with the characteristic three layers from the outside toward the inside of carbonization, coagulative necrosis, and edema. Otherwise, only the shapes and sizes of the lesions differ, with craters of different depths. In this paper, we report an ultrastructural study of the changes occurring in the periphery of the laser lesions in both normal human brain and neoplastic tissues (gliomas and meningiomas). Continuous-wave CO2 and Nd:YAG lasers were used at different exposure times and powers and the effects of high-peak pulsed CO2 laser radiation has also been investigated. The study, performed during neurosurgical procedures was mostly focused on microcirculation at 1.5-3 mm outside the area of coagulative necrosis, at the level of the edema zone. Only lesions of the blood brain barrier are produced in normal brain by CO2 radiation (power ranging from 40 to 80 W; exposure time from 3 to 10 seconds). The same results were achieved by Nd:YAG radiation of short duration (3 seconds) regardless of the power used (40 and 80 W). Long-duration Nd:YAG radiation (10 sec; power: 40-80 W) produces endoluminal phenomena leading to the complete occlusion of the capillaries. In neoplastic brain tissues, microcirculation does not seem to be impaired by CO2 radiation. More marked lesions are produced in tumors even after Nd:YAG short-time radiation. Endoluminal obliteration is observed in meningiomas and perivascular hemorrhage occurs in highly vascularized gliomas. According to these results, the risk of delayed post-operative hemorrhages, noticed in some patients with glioblastoma operated on by Nd:YAG lasers, suggests that residual tumor in the cavity should be treated by CO2 laser because of its minimal damage of microcirculation.
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PMID:Effects at the periphery of the laser lesion in human brain and its tumors after CO2, Nd:YAG, and CO2 high-peak pulsed radiation. 309 Mar 89

The prognostic importance of tumor size was studied in 510 patients with malignant glioma (80% with glioblastoma multiforme) in the Valid Study Group of Study 80-01 of the Brain Tumor Study Group (now the Brain Tumor Cooperative Group [BTCG]). The endpoint was length of survival from randomization, which occurred within 3 weeks of definitive surgery. Following randomization, patients were scheduled to receive radiotherapy (RT) (6,020 cGy) during a 7-week period, along with continuing courses of chemotherapy. Computed tomographic (CT) scan information was available for 124 patients preoperatively, 300 patients postoperatively (preradiation), and 218 patients 9 weeks post-RT (+/- 3 weeks). Tumor size was determined as area (length x width) on the contrast-enhanced scan and survival was compared by log rank statistics. Preoperative tumor area was unrelated to survival (P = .48), but postoperative area was significantly prognostic (P less than .0001); the smaller the residual tumor, the longer the patient lived. Patients with a 75% or greater resection, as determined by measuring the difference between the preoperative and the postoperative scans, tended to have better survival, but the difference was not significant (P = .16). The post-RT area was strongly related to survival (P less than .00001). The percent change in area between the pre- and post-RT scans was also prognostic. Tumor size was of prognostic importance independent of the other known prognostic variables: age, Karnofsky performance score, and whether the tumor was glioblastoma or anaplastic astrocytoma. We conclude that the amount of tumor remaining after surgery is an important baseline variable at the start of RT, and that the tumor size 9 weeks following RT is also prognostic. Surgical resection is most important when it leaves the least amount of residual tumor.
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PMID:The prognostic importance of tumor size in malignant gliomas: a computed tomographic scan study by the Brain Tumor Cooperative Group. 333 97

The histological classification, pathophysiology, and treatment modalities of malignant gliomas (glioblastoma, malignant astrocytoma) were reviewed with reference to the WHO classification of primary brain tumors and the recent progress made in glioma biology. Patients with glioblastoma and malignant astrocytoma showed, respectively, 10.6% and 22.2 of the five-year survival rate according to the All Japan Brain Tumor Registry. In order to improve the prognosis of malignant glioma patients, many clinical trials have been conducted throughout the world. Malignant gliomas that grow in and invade the brain parenchyma cannot be cured by surgical resection. One should treat the residual tumor with irradiation, chemotherapy and immunotherapy. Radiation therapy alone and radiation therapy plus chemotherapy using nitrosoureas or procarbazine have been proved statistically to be more effective for malignant gliomas than supportive care and radiation therapy alone, respectively. Prospective clinical trials support the view that malignant gliomas should be treated vigorously using a multimodal approach that includes surgical resection, high-dose radiation therapy, and prolonged maintenance chemotherapy.
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PMID:[Treatment modalities for malignant gliomas with reference to their pathophysiology]. 394 92

For patients with nonresectable glioblastoma (GB) or recurrent GB, we have recently been using an interstitial chemotherapy with biodegradable polylactic acid pellets containing nimustine chloride (ACNU), in combination with superselective arterial ACNU injection, routine irradiation and chemotherapy. The ACNU pellets are prepared by mixing polylactic acid powder and ACNU, and then melting the mixture at low temperature and moulding it into a thin pellet. Pharmacological anticancer activity was experimentally demonstrated by the finding that a region of suppression was present surrounding an ACNU pellet placed in a B6 melanoma cell culture disc, but that no such suppression was present around a control pellet. In order to determine the spatial and temporal distribution of ACNU, a small pellet (ACNU: 0.6 mg) was implanted in the frontal lobe of rats. ACNU concentration determined by HPLC was 61.0 micrograms/g brain tissue on day 1. 22.5 on day 3, and 5.5 on day 7; small amounts of ACNU were in fact released for at least 4 weeks after implantation. This pellet was used for the clinical treatment of 11 GB patients. Four patients had several pieces of pellets implanted immediately after CT-guided stereotactic biopsy, and the other 7 had pellets placed in residual tumor after partial removal at craniotomy. No ACNU was detectable in serum. CT studies obtained at subsequent appropriate intervals disclosed gas formation around the pellets, a slight increase in edema, and necrosis or decrease in CT enhancement of tumor beginning around day 12 after implantation. Bone marrow suppression did not occur, since ACNU was administered interstitially and in the range of 50-200 mg (average: 126 mg) per patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interstitial chemotherapy with biodegradable ACNU pellet for glioblastoma. 762 27

In the vast majority of studies that address the role of surgery in the management of high-grade gliomas, the degree of tumor removal accomplished is solely based on the intraoperative perception of the neurosurgeon. Despite its fundamental importance for a comparison of different treatment modalities, little systematic effort has been made to evaluate the residual gross tumor by neuroimaging methods immediately after surgery. We report the results of a prospective study using contrast-enhanced computed tomography and magnetic resonance imaging (MRI) to monitor 60 patients after the resection of a high-grade glioma. In each case, the first scans were obtained between Days 1 and 5 after surgery, followed by serial imaging every 2 to 3 months, usually until the condition of the patient deteriorated severely or the patient died. Gadolinium-enhanced MRI proved to be extremely valuable for assessing gross residual tumor when performed during Days 1 to 3 after the resection of a preoperatively enhancing high-grade glioma. This timing avoided surgically induced contrast enhancement and minimized interpretative difficulties. In delineating residual tumor, MRI was vastly superior to computed tomography. About 80% of tumor "recurrences" emerged from definitely enhancing remnants, as revealed by early postoperative MRI. The neurosurgeon's estimation of gross tumor burden reduction could be shown to be much less accurate (by a factor of 3) than the postoperative assessment by modern neuroimaging. In our series, residual tumor enhancement was the most predictive prognostic factor of survival in patients with glioblastoma, followed by radiotherapy. Patients with a residual tumor postoperatively had a 6.595-times higher risk of death in comparison to patients without a residual tumor. Patients undergoing radiotherapy had a 0.258-times lower risk of death in comparison to patients who were not treated with radiation. Concerning survival, the prognostic significance of both variables surpassed age and performance.
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PMID:Early postoperative magnetic resonance imaging after resection of malignant glioma: objective evaluation of residual tumor and its influence on regrowth and prognosis. 808 2

In order to reassess the value of quantitative thallium-201 brain SPECT in the differentiation of miscellaneous brain tumors, we studied a total of 89 patients--35 pre-operative patients suspected of having a brain tumor and 54 post-operative patients with a brain tumor. We came to the conclusion that quantitative Tl-201 brain SPECT was very useful in discriminating cerebral radiation necrosis from recurrent tumor, estimating residual tumor burden, and detecting tumor regrowth earlier in postoperative patients. In preoperative patients, however, Tl-201 SPECT cannot be used effectively to differentiate glioma from other intracranial tumors, although intense uptake of Tl-201 may provide evidence of glioblastoma or a hypervascular lesion.
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PMID:Reassessment of quantitative thallium-201 brain SPECT for miscellaneous brain tumors. 829 52

A large number of oncogenes have been identified as aberrant in gliomas, but only the erbB oncogene (gene encoding the epidermal growth factor receptor [EGFR]) is amplified in an appreciable number. The loss or mutation of tumor-suppressor genes located on different autosomes may be associated with progression of malignant gliomas. The p53 tumor-suppressor gene (located on chromosome 17) is frequently associated with the loss of one allele in malignant gliomas, although a large number of malignant gliomas have no p53 mutations. Some of the latter tumors have an amplified murine double minute 2 (MDM2) gene, which suppresses p53 gene activity. Genetic material from chromosome 10 may also be lost, especially in glioblastoma multiforme. In addition to the aberrant expression of EGFR, another growth factor, platelet-derived growth factor, or PDGF (ligand and/or receptors) can be overexpressed, giving cells a selective growth advantage. The blood-brain barrier is substantially altered in malignant gliomas, resulting in cerebral edema. Therapy for malignant gliomas includes surgery, radiation therapy, and chemotherapy. Surgical resection that leaves little residual tumor produces longer survival than less vigorous surgery. Radiation therapy to a dose of at least 60 Gy is required to treat malignant gliomas. Increased survival beyond that produced by standard external radiotherapy requires much larger doses; interstitial radiotherapy permits such dosing. Radiosurgery is being tested. Chemotherapy with nitrosoureas is modestly useful but appears to benefit patients with anaplastic astrocytoma more so than those with glioblastoma.
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PMID:Biology and treatment of malignant glioma. 950 24


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