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)

Rapid growth of a glioblastoma during therapy for multiple myeloma is reported. A 53-year-old man was admitted to our hospital with a right costal tumor, which was resected. The diagnosis was plasmocytoma. Urine protein electrophoresis showed a monoclonal peak in the region of gamma-globulin, and examination of the bone marrow revealed 17.8% of atypical plasma cells. Brain magnetic resonance (MR) imaging detected two small lesions, but these could not be identified as brain tumor. He received chemotherapy (melphalan 10 mg/day and predonin 30 mg/day for 4 days) and was discharged. Two weeks after discharge, he was readmitted because of left hemiparesis. T1-weighted MR imaging showed two large hypointense lesions in the right frontal lobe, with ring-like enhancement following Gd-DTPA infusion. 1H-MR spectroscopy showed typical findings of tumor with increased choline and lactic acid peaks. 201Tl SPECT revealed high accumulation in both early and delayed images. Right carotid angiography showed a hypervascular tumor with venous filling and mass effect. The lesions were resected via right frontal craniotomy, followed by intraoperative radiation and placement of an Ommaya reservoir. Histological examination showed the tumors were glioblastoma. The brain between the tumors also showed the typical appearance of glioblastoma, suggesting that the lesions were continuous. Postoperatively, the patient's left hemiparesis disappeared. He received local irradiation and chemotherapy and was then discharged. Coexistence of glioblastoma and multiple myeloma is rare. The cause may be genetic abnormality, but immunodeficiency due to multiple myeloma, surgical damage, or chemotherapy may have contributed to the rapid growth of the glioblastoma.
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PMID:[Rapid growth of glioblastoma during therapy for multiple myeloma: case report]. 974 4

We report a surgical case of a 54-year-old woman with a radiation induced glioblastoma. At the age of 34, the patient was diagnosed to have a non-functioning pituitary adenoma. It was partially removed followed by 50 Gy focal irradiation with a 5 x 5 cm lateral opposed field. Twenty years later, she suffered from rapidly increasing symptoms such as aphasia and right hemiparesis. MRI showed a large mass lesion in the left temporal lobe as well as small mass lesions in the brain stem and the right medial temporal lobe. These lesions situated within the irradiated field. Magnetic resonance spectroscopy revealed relatively high lactate signal and decreased N-acetyl aspartate, choline, creatine and phosphocreatine signals. Increased lactate signal meant anaerobic metabolism that suggested the existence of a rapidly growing malignant tumor. Thus, we planned surgical removal of the left temporal lesion with the diagnosis of a radiation induced malignant glioma. The histological examination revealed a glioblastoma with radiation necrosis. MIB-1 staining index was 65%. Postoperatively, her symptoms improved, but she died from pneumonia 1 month after the surgery. An autopsy was obtained. The lesion of the left temporal lobe was found to have continuity to the lesion in the midbrain, the pons and the right temporal lobe as well. High MIB-1 staining index suggested that a radiation induced glioblastoma had high proliferative potential comparing with a de novo and a secondary glioblastoma.
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PMID:[Radiation induced glioblastoma: a case report]. 1084 10

A 47-year-old woman presented with headache and left homonymous hemianopsia. T1-weighted magnetic resonance (MR) imaging with contrast medium showed a mass lesion with ring-like enhancement in the right temporo-occipital lobe. The patient underwent surgery, focal irradiation, and chemotherapy. The histological diagnosis was glioblastoma. Four months after the operation, the patient again developed headache and left homonymous hemianopsia in addition to vomiting and mild left hemiparesis. MR imaging showed recurrence of the tumor and hydrocephalus. The patient underwent a second craniotomy and placement of a ventriculoperitoneal shunt. Intraoperative findings revealed that the transverse-sigmoid sinus was occluded by tumor invasion. The patient died of intraventricular dissemination 2 months after the second operation. Autopsy revealed metastases in the spleen and lungs. Glioblastoma with metastases to the spleen is very rare. The prognosis for patients is poor. Excessive therapy should not be used for patients with extracranial metastases from glioblastoma.
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PMID:Glioblastoma with metastasis to the spleen--case report. 1456 Aug 51

The current WHO classification recognizes two distinct variants of glioblastoma multiforme (GBMs): giant cell glioblastoma (GCG) and gliosarcoma, based on histological heterogeneity. Unlike conventional GBMs, GCGs preferentially occur in younger individuals and are associated with a better prognosis, a few reports documenting prolonged survival up to 17 years after diagnosis. However, transformation to gliosarcoma is possible and has been already reported. Radio-induced glioblastoma, which meets Cahan's criteria for radio-induced tumor, is very rare; the first case was published by Kleriga et al. We report a rare case observed in a 46-year-old man with a past history of right nose leiomyosarcoma treated 40 years earlier by surgery and interstitial and external beam radiation. At admission, the patient presented left hemiparesis revealing a right frontal GCG confirmed by pathology after cranial surgery. We describe this case firstly because of its rare histological variety and discuss its clinical, radiological, histopathological, therapeutic and prognostic characteristics with literature data. Secondly, because of its occurrence 40 years after external radiotherapy, which could suggest the hypothesis of radio-induced glioblastoma.
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PMID:[Frontal giant cell glioblastoma: radio-induced tumor? Case report and literature review]. 1806 29

Pleomorphic xanthoastrocytoma (PXA) has been considered an astrocytic tumor with a relatively favorable prognosis. However, PXA cases having several recurrent patterns with poor prognosis have been reported in recent years, and a new concept of anaplastic PXA has been proposed. The present case was a 59-year-old woman who presented with tumor bleeding onset and cerebrospinal fluid dissemination. The patient had sudden-onset right hemiparesis, aphasia, and consciousness disturbance and was admitted to a local area hospital. After emergency surgery had removed the hematoma, postoperative contrast-enhanced CT scan revealed a left temporal tumor. A second surgery was therefore performed for initial tumor removal 2 months later. Histopathological findings showed that the tumor was typical PXA with strong pleomorphism and xanthomatous changes and contained an ependymoma-like component in the center area. However, endothelial proliferation and mitosis were more remarkable compared to ordinary PXA. The MIB-1 labeling index was 9.8% high. From these findings, the histopathological diagnosis was anaplastic PXA. The patient underwent surgery to remove recurrent tumors 5 and 16 months later. The patient died 36 months after the first onset, and CT revealed glioblastoma-like findings and cerebrospinal fluid dissemination. This case report is the first case in which PXA presented with tumor bleeding onset. Histopathological findings suggested anaplastic PXA from the first surgical specimens, and PXA recurred many times. We thus believe that the patient displayed primary anaplastic PXA rather than secondary anaplastic PXA that results in malignant transformation.
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PMID:A case of anaplastic pleomorphic xanthoastrocytoma presenting with tumor bleeding and cerebrospinal fluid dissemination. 1809 20

Congenital glioblastoma multiforme is a rare primary brain tumor that has a unique biology distinct from pediatric and adult variants. In this report, we present a case of congenital glioblastoma with complicated management course. A literature review of previously reported cases is included to illustrate the epidemiology and natural history of this disease. A 9-month-old male infant developed acute lethargy, hemiparesis and unilaterally dilated pupil. Imaging studies revealed a large hemispheric tumor, resulting in significant midline shift suggestive of impending herniation. Emergent tumor cystic fluid drainage was performed at initial presentation. A frontotemporoparietal craniotomy was performed on the following day to attempt a gross total resection. Adjuvant chemotherapy consisting of oral temozolomide was administered. The patient eventually succumbed 4 months later due to aggressive tumor progression. Congenital glioblastoma should be included in the differential diagnosis of infants with large intracranial tumors. Although surgical intervention may increase survival, the overall outcome remains poor despite maximal multimodal treatment.
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PMID:Congenital glioblastoma multiforme: case report and review of the literature. 1850 17

Recurrence of clear cell ependymoma is not a rare condition, but malignant transformation of clear cell ependymoma has not yet been well presented. The authors report a 44-year-old man who presented with progressive right hemiparesis. A brain tumor in the left frontal premotor area was removed and an initial pathological diagnosis of oligodendroglioma was made. The tumor recurred 4 months later, and reoperation of the tumor and adjuvant local radiotherapy were performed. The patient subsequently underwent surgical removal of recurrent tumors on another four occasions (6 times in total) during a period of 11 years and finally died of the original disease. Histopathological studies of all surgical and autopsy specimens were carried out. The first and second surgical specimens did not contain any ependymal rosettes or pseudorosettes, and thus a diagnosis of oligodendroglioma was made. However, the third surgical specimen showed pseudorosettes. At this time, the tumor had an ultrastructural appearance compatible with ependymoma. Thereafter, the recurrent tumors showed anaplastic features such as nuclear pleomorphisms and necrosis with pseudopallisading. The autopsy specimens resembled a feature of glioblastoma but the tumor was sharply demarcated from the surrounding parenchyma.
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PMID:Malignant transformation of supratentorial clear cell ependymoma. 1864 67

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

A 73-year-old male presented with a glioblastoma that was detected at the initial stage in the developmental process. He suffered cerebral infarction. Follow-up magnetic resonance (MR) imaging showed no abnormality. Ten months later, he had transient right hemiparesis. Diffusion-weighted and fluid-attenuated inversion recovery (FLAIR) MR imaging showed a hyperintense area in the left frontal lobe. The diagnosis was cerebral infarction and antiplatelet drug treatment was begun. The patient's right hemiparesis subsided. Ten days later, right hemiparesis reappeared. Diffusion-weighted and FLAIR MR imaging showed an enlarged hyperintense area in the left frontal lobe. Three weeks after the onset of right hemiparesis, MR imaging revealed an irregular ring-enhanced mass lesion that had further increased in size. The diagnosis was brain abscess and antibiotic treatment was initiated. However, the lesion did not respond and had further enlarged 5 weeks after the onset of right hemiparesis. The lesion was partially removed and the histological diagnosis was glioblastoma with Ki-67 labeling index of 26%. After surgical treatment, the patient received irradiation of 60 Gy and chemotherapy with temozolomide. Follow-up MR imaging showed regrowth of the tumor and aggravation of edema. The rapid progression of the tumor ultimately resulted in the patient's death 12 months after the onset of right hemiparesis. Diffusion-weighted imaging is a good method for the early detection of glioblastoma.
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PMID:Glioblastoma detected at the initial stage in its developmental process -case report-. 2050 2

Bevacizumab is expected to constitute a new treatment modality for radiation necrosis. In the present cases, we observed a recurrence of radiation necrosis after temporary improvement by bevacizumab treatment. Re-treatment with bevacizumab controlled the necrosis again. A 39-year-old male and a 57-year-old female were diagnosed with glioblastoma and lung cancer metastasis, respectively. The former patient underwent partial resection of the glioblastoma, followed by boron neutron capture therapy (BNCT) and 30 Gy of fractionated X-ray radiotherapy. Eleven months after BNCT, he suffered from left hemiparesis and convulsions with enlargement of a perifocal edema. The latter patient underwent stereotactic radiosurgery twice for the same tumor. Three months after the second radiosurgery, she had an uncontrollable convulsion and right hemiplegia with a massive perifocal edema. Both lesions were suggested to be radiation necroses by positron emission tomography using amino acids as a tracer. Neither patient responded to corticosteroids, anticoagulants, or vitamin E. They underwent treatment with 5 mg/kg bevacizumab biweekly, for a total of 6 cycles. The size of the perifocal edema was clearly reduced in response to the treatments. The neurological status of the patients improved concomitant with therapy. However, the clinical status of both patients was aggravated several months after the bevacizumab was stopped, and the perifocal edemas enlarged again. The patients underwent a second treatment with bevacizumab, and the perifocal edemas again decreased. Although radiation necrosis may recur several months after bevacizumab treatment, repeated bevacizumab treatments also appear to be effective.
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PMID:Repeated treatments with bevacizumab for recurrent radiation necrosis in patients with malignant brain tumors: a report of 2 cases. 2069 73


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