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)

We have developed a human brain tumor model in immunodeficient rats that gradually changes its phenotype by serial passages in vivo, from a highly infiltrative, non-angiogenic one with numerous stem cell markers [low-generation (LG) tumor] to a more typical glioblastoma one with extensive angiogenesis and necrosis [high-generation (HG) tumor]. In this study we determined the metabolic properties of these two phenotypes, using (1)H MRS. The LG tumors showed an intact blood-brain barrier and normal vascular morphology, as shown by MRI and Hoechst staining. In contrast, the HG tumors exhibited vascular leakage and necrosis. The animals with HG tumor had raised concentrations of choline and myo-inositol, and decreased concentrations of glutamate and N-acetylaspartate. In the LG tumor group, similar changes in metabolic concentrations were detected, although the alterations were more pronounced. The LG tumors also had higher concentrations of choline, taurine, and lactate. Subdividing the LG and HG tumors into large and small tumors revealed a significant increase in choline and decrease in glutamate as the LG tumors increased in size. Our results show that metabolic profiles produced by (1)H MRS can be used to distinguish between two distinct glioblastoma phenotypes. More pronounced anaerobic metabolism was present in the LG stem-cell-like tumors, suggesting a more malignant phenotype.
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PMID:Two distinct tumor phenotypes isolated from glioblastomas show different MRS characteristics. 1861 1

At least 10% of glioblastoma relapses occur at distant and even contralateral locations. This disseminated growth limits surgical intervention and contributes to neurological morbidity. Preclinical data pointed toward a role for temozolomide (TMZ) in reducing radiotherapy-induced glioma cell invasiveness. Our objective was to develop and validate a new analysis tool of MRI data to examine the clinical recurrence pattern of glioblastomas. MRIcro software was used to map the location and extent of initial preoperative and recurrent tumors on MRI of 63 patients in the European Organisation for Research and Treatment of Cancer (EORTC) 26981/22981/National Cancer Institute of Canada (NCIC) CE.3 study into the same stereotaxic space. This allowed us to examine changes of site and distance between the initial and the recurrent tumor on the group level. Thirty of the 63 patients were treated using radiotherapy, while the other patients completed a radiotherapy-plus-TMZ treatment. Baseline characteristics (median age, KPS) and outcome data (progression-free survival, overall survival) of the patients included in this analysis resemble those of the general study cohort. The patient groups did not differ in the promoter methylation status of methyl guanine methyltransferase (MGMT). Overall frequency of distant recurrences was 20%. Analysis of recurrence patterns revealed no difference between the groups in the size of the recurrent tumor or in the differential effect on the distance of the recurrences from the preoperative tumor location. The data show the feasibility of groupwise recurrence pattern analysis. An effect of TMZ treatment on the recurrence pattern in the EORTC 26981/22981/NCIC CE.3 study could not be demonstrated.
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PMID:A novel tool to analyze MRI recurrence patterns in glioblastoma. 1867 55

A 53-year-old man was admitted to our hospital after suffering four attacks with loss of consciousness and/or topographic agnosia. Three months after the first attack, the cerebrospinal fluid analysis showed no abnormal findings. IgG-autoantibodies and IgM-autoantibodies against glutamate receptor epsilon2 (GluRepsilon2) were detected in cerebrospinal fluid and serum respectively. At that time, we diagnosed him as having limbic encephalopathy. Brain MRI revealed a high intensity lesion on T2-weighted and FLAIR images in the medial regions of the bilateral temporal lobes and splenium. A diffusion-weighted image revealed high intensity lesions which were also weakly enhanced by Gd-DTPA in the deep white matter beside the posterior horns. The patient then developed numbness in the right hand. The cerebralspinal fluid analysis, four months after the onset of the disease, exhibited slight pleocytosis and elevated protein. IgG-autoantibodies against GluRepsilon2 were detected in the serum. The lesions beside the posterior horns were ring-like enhanced more strongly. Brain biopsy led to a diagnosis of glioblastoma. We suggest that patients with autoantibodies against GluRepsilon2 should be carefully diagnosed with limbic encephalopathy associated with autoimmune mechanisms even if radiological findings are typical of the disease.
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PMID:[A case of glioblastoma misdiagnosed initially due to positive finding of anti-glutamate receptor antibody]. 1871 84

Radiation induced tumors are well-known but rare complications of radiotherapy. Meningiomas are the most common radiation-induced (RI) cranial tumors, followed by gliomas and sarcomas, while other tumors as haemangioblastomas remain extremely exceptional. We present 7 patients with RI brain tumors diagnosed and treated at our institution between 1990 and 2006. Retrospective review of their clinical charts is supplied. All patients were irradiated during childhood as a treatment for another disease, and fulfilled the criteria of RI neoplasia. Four patients developed meningiomas and three developed other tumors (one glioblastoma, one softtissue sarcoma and one hemangioblastoma). In all cases a complete surgical removal was achieved. Preoperative assessment based on MRI supplied the correct diagnosis in six patients. The most important risks factors described in the literature for developing RI tumors are the age at which radiotherapy was administered and the dose of radiation applied. Differential diagnosis of RI tumors includes any tumor appearing after radiotheraphy, especially recurrences of the primary disease, as RI neoplasias are a rare complication. Even in cases with complete surgical resection, prognosis of this clinical entity is basically related to the histology of the RI tumor.
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PMID:[Radiation-induced cranial tumors: clinical series and literature review]. 1904 87

The coincidence of multiple sclerosis (MS) and glioblastoma has been reported in several anecdotal reports. Little is known concerning the effects of radio- and/or chemotherapy on demyelinating brain lesions in MS patients. Moreover, there are no data concerning the effect of concomitant radiochemotherapy according to the STUPP protocol on the course ofMS in patients with coexisting glioblastoma. A 43-year-old male patient was diagnosed for relapsing-remitting MS in 1997. He received interferon and glatiramer acetate for immunomodulatory treatment and was stable until 2006 (EDSS < 1.5), when neurological deterioration occurred. He developed a left-sided hemiparesis, and an MRI showed right temporal contrast-enhancing mass lesion. A subsequent tumor resection was performed and histology revealed a glioblastoma. At the beginning of radiochemotherapy, treatment for multiple sclerosis (glatiramer acetate) was stopped. The tumor responded well to treatment and was clinically as well as radiologically stable until 9 months after diagnosis of glioblastoma. The typical radiological MS lesions remained unchanged. The patient died 12 months after diagnosis of glioblastoma due to tumor progression. This report demonstrates that concomitant radiochemotherapy according to the STUPP protocol, was safe in our patient with respect to the radiological as well as the clinical course of multiple sclerosis.
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PMID:Concomitant radiochemotherapy in a patient with multiple sclerosis and glioblastoma. 1880 66

We present a case of de novo fibrosarcoma in a 43-year-old male, with MRI documented evolution from a 5 mm hyperintense area to 5 cm tumor mass in a 12-month period. The diagnosis of low-grade fibrosarcoma was established by three experienced neuropathologists. The patient underwent gross total resection with adjuvant fractionated conformal radiotherapy. Following first recurrence 3 months later, the patient was reoperated and stereotactic radiosurgery of a residual tumor was performed thereafter. The pathological diagnosis was similar, but with additional extensive radiation effects. Six months later the patient underwent aggressive surgical resection for second recurrence. The pathological diagnosis was WHO grade IV glioblastoma. The etiology of this highly unusual progression from primary mesenchymal neoplasm to high-grade glioma is discussed.
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PMID:Rapid growth of primary cerebral fibrosarcoma with conversion to glioblastoma at second recurrence. 1908 30

Multicentric glioblastoma is a uncommon brain malignant tumour.We report the case of a 43-years-old woman, born in Ukraine and living in Italy, who manifested an initial isolated epileptic seizure and subsequent atypical psychiatric symptoms. Clinical neurological examination, Brain Computed Tomography and standard EEG examinations were negative at the moment of admission. A month later, she presented apathy, apraxia, psychomotor slowdown and expressive aphasia. A Magnetic Resonance Imaging examination showed a bi-frontal lesion. The patient underwent to two neurosurgical removals of the lesions: histological examination demonstrated the presence of a grade IV glioblastoma.Clinical onset, diagnostic and therapeutic problems are discussed.In case of atypical psychiatric presentation, it should be taken into consideration neoplastic, inflammatory or infective causes. Despite the absence of focal neurological signs and basal CT scan and EEG alterations, complementary imaging examinations, such as MRI and contrast enhancement CT, are necessary, especially when the conditions become quickly worse.
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PMID:A rare case of multicentric synchronous bi-frontal glioma in a young female. Diagnostic and therapeutic problems: a case report. 1916 37

Recently, there has been greater awareness that combination radiation and temozolomide used to treat glioblastomas may cause increased contrast enhancement on the first post radiation MRI scan. However, this increased enhancement may stabilize or decrease over time and represent pseudo-progression (psPD) rather than true progressive disease. It has never been shown that this phenomenon is greater with combination therapy than radiation alone. To address this question, we reviewed MRI scans in glioblastoma patients treated with radiation alone versus patients treated with radiation and concomitant temozolomide and compared the frequency of psPD in the two groups. Eighteen of 47 patients (38%) treated with radiation alone demonstrated enlargement on their first post-radiation MRI scan and 11 of these 18 (61%) proved to have psPD as defined by no further enlargement on stable therapy for 3 months following radiation. Twenty-four of 45 patients (53%) treated with radiation and temozolomide had enlargement on their first post-radiation MRI scan and 13 of these 24 (54%) had psPD. Median overall survival (OS) in patients with psPD treated with radiation alone was 15.6 versus 12.8 months in those without psPD. Median OS in patients treated with radiation and concomitant temozolomide who had psPD was 24.4 versus 15.9 months in those who did not have psPD. We were unable to detect a difference in OS between the four groups. Presence of psPD, independent of treatment, was associated with prolonged progression-free survival (P = 0.05) but not OS. psPD may be more common in combination therapy but most likely by a small margin.
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PMID:Effect of adding temozolomide to radiation therapy on the incidence of pseudo-progression. 1922 65

To assess incidence and degree of regrowth in glioblastoma between surgery and radiation therapy (RT) and to correlate regrowth with presurgical imaging and survival, we examined images of 32 patients with newly diagnosed glioblastoma who underwent MR spectroscopic imaging (MRSI), perfusion-weighted imaging (PWI), and diffusion-weighted imaging (DWI) prior to surgery, after surgery, and prior to RT/temozolomide. Contrast enhancement (CE) in the pre-RT MR image was compared with postsurgical DWI to differentiate tumor growth from postsurgical infarct. MRSI and PWI parameters were analyzed prior to surgery and pre-RT. Postsurgical MRI indicated that 18 patients had gross total and 14 subtotal resections. Twenty-one patients showed reduced diffusion, and 25 patients showed new or increased CE. In eight patients (25%), the new CE was confined to areas of postsurgical reduced diffusion. In the other 17 patients (53%), new CE was found to be indicative of tumor growth or a combination of tumor growth and surgical injury. Higher perfusion and creatine within nonenhancing tumor in the presurgery MR were associated with subsequent tumor growth. High levels of choline and reduced diffusion in pre-RT CE suggested active metabolism and tumor cell proliferation. Median survival was 14.6 months in patients with interim tumor growth and 24 months in patients with no growth. Increased volume or new onset of CE between surgery and RT was attributed to tumor growth in 53% of patients and was associated with shorter survival. This suggests that reducing the time between surgery and adjuvant therapy may be important. The acquisition of metabolic and physiologic imaging data prior to adjuvant therapy may also be valuable in assessing regions of new CE and nonenhancing tumor.
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PMID:Tumor regrowth between surgery and initiation of adjuvant therapy in patients with newly diagnosed glioblastoma. 1922 57

The dose distribution and failure pattern after treatment with the external beam boron neutron capture therapy (BNCT) protocol were retrospectively analyzed. BSH (5 g/body) and BPA (250 mg/kg) based BNCT was performed in eight patients with newly diagnosed glioblastoma. The gross tumor volume (GTV) and clinical target volume (CTV)-1 were defined as the residual gadolinium-enhancing volume. CTV-2 and CTV-3 were defined as GTV plus a margin of 2 and 3 cm, respectively. As additional photon irradiation, a total X-ray dose of 30 Gy was given to the T2 high intensity area on MRI. Five of the eight patients were alive at analysis for a mean follow-up time of 20.3 months. The post-operative median survival time of the eight patients was 27.9 months (95% CI=21.0-34.8). The minimum tumor dose of GTV, CTV-2, and CTV-3 averaged 29.8+/-9.9, 15.1+/-5.4, and 12.4+/-2.9 Gy, respectively. The minimum tumor non-boron dose of GTV, CTV-2, and CTV-3 averaged 2.0+/-0.5, 1.3+/-0.3, and 1.1+/-0.2 Gy, respectively. The maximum normal brain dose, skin dose, and average brain dose were 11.4+/-1.5, 9.6+/-1.4, and 3.1+/-0.4 Gy, respectively. The mean minimum dose at the failure site in cases of in-field recurrence (IR) and out-field recurrence (OR) was 26.3+/-16.7 and 14.9 GyEq, respectively. The calculated doses at the failure site were at least equal to the tumor control doses which were previously reported. We speculate that the failure pattern was related to an inadequate distribution of boron-10. Further improvement of the microdistribution of boron compounds is expected, and may improve the tumor control by BNCT.
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PMID:Dose distribution and clinical response of glioblastoma treated with boron neutron capture therapy. 1937 33


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