Development of cerebellar malignant astrocytoma at site of a medulloblastoma treated 11 years earlier

1978 ◽  
Vol 49 (3) ◽  
pp. 445-449 ◽  
Author(s):  
Enrique Klériga ◽  
Joanna Hollenberg Sher ◽  
Sanath-Kumar Nallainathan ◽  
Sherman C. Stein ◽  
Michael Sacher

✓ A child treated for a desmoplastic medulloblastoma of the left cerebellar hemisphere at the age of 10 months developed a malignant astrocytoma in the same site 11 years later. Theories of origin of the second tumor, particularly in relation to concepts of the genesis of medulloblastoma in general, are discussed.

1986 ◽  
Vol 65 (2) ◽  
pp. 245-248 ◽  
Author(s):  
Marie-Magdeleine Ruchoux ◽  
Francoise Gray ◽  
Romain Gherardi ◽  
Annette Schaeffer ◽  
Jean Comoy ◽  
...  

✓ A 49-year-old woman presented with orthostatic hypotension. Vertebral angiography and ventriculography revealed a tumor of the left cerebellar hemisphere. Ventriculoperitoneal shunting was followed by complete disappearance of the orthostatic hypotension. The tumor was subsequently removed and microscopic study showed Lhermitte-Duclos disease. Orthostatic hypotension has been rarely reported in association with tumors of the posterior fossa except for those tumors destroying the medullary centers and interrupting the baroreceptor reflex arc. This case is of interest because the tumor was restricted to the cerebellum. The authors have found no previous case in which orthostatic hypotension was a presenting symptom of Lhermitte-Duclos disease.


1978 ◽  
Vol 48 (4) ◽  
pp. 622-627 ◽  
Author(s):  
Richard L. Sogg ◽  
Sarah S. Donaldson ◽  
Craig H. Yorke

✓ A 9-year-old schoolgirl received 6007 rads to the suprasellar region for craniopharyngioma. Five years later, a malignant astrocytoma developed in the right temporal lobe. We cite clinical and experimental evidence to support our suspicion that the glioma may have been induced by radiation.


2001 ◽  
Vol 94 (2) ◽  
pp. 301-308 ◽  
Author(s):  
Masanori Kurimoto ◽  
Yutaka Hirashima ◽  
Tsuneaki Ogiichi ◽  
Hideo Hamada ◽  
Hironaga Kamiyama ◽  
...  

Object. Patients with neurofibromatosis Type 1 (NF1) have a predisposition to development of a variety of benign and malignant tumors including neurofibromas, astrocytomas, pheochromocytomas, and malignant peripheral nerve sheath tumors. The availability of an astrocytoma cell line derived from NF1 would be useful in studies in which sporadic astrocytomas could be compared with NF1-derived astrocytomas. In this article the authors describe a novel astrocytoma cell line, TM-31, that they established from a tumor removed in a 42-year-old woman with NF1. Methods. The TM-31 cell line was prepared from a surgical specimen of malignant astrocytoma and was serially subcultured over 250 times throughout a 6-year period without showing any sign of cell senescence. Immunocytochemical analyses demonstrated that TM-31 cells are negative for glial fibrillary acidic protein but positive for vimentin and S-100 protein. The TM-31 cells display little neurofibromin expression when subjected to immunoblotting, indicating that there is an NF1 gene mutation. Polymerase chain reaction—single-strand conformational polymorphism analysis revealed that TM-31 cells harbor a p53 point mutation in exon 7, codon 238. Chemosensitivity testing of TM-31 cells revealed a resistance to 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea, although they are sensitive to cisplatin and etoposide. In addition, TM-31 cells displayed no morphological differentiation after all-transretinoic acid and dibutyryl cyclic adenosine monophosphate treatments. Pharmacological inhibition of farnesyltransferase of the Ras oncoprotein led to decreased proliferative activity and inhibition of anchorage-independent growth of TM-31 cells in soft agar. Conclusions. The TM-31 cell line is an immortalized astrocytoma cell line derived from a tumor obtained in a patient with NF1. Ras activation may be the major event of proliferative activity and of the transformed phenotype of TM-31 cells, and the farnesyltransferase inhibitor may be potentially important as a novel antiproliferative therapy for NF1-derived astrocytomas.


2002 ◽  
Vol 97 (1) ◽  
pp. 190-196 ◽  
Author(s):  
Ali H. Mesiwala ◽  
John D. Kuratani ◽  
Anthony M. Avellino ◽  
Theodore S. Roberts ◽  
Marcio A. Sotero ◽  
...  

✓ The issue of whether seizures can arise in the cerebellum remains controversial. The authors present the first known case of focal subcortical epilepsy with secondary generalization thought to arise from a dysplastic lesion within the cerebellum. A newborn infant presented with daily episodes of left eye blinking, stereotyped extremity movements, postural arching, and intermittent altered consciousness lasting less than 1 minute. These episodes began on his 1st day of life and progressively increased in frequency to more than 100 events per day. Antiepileptic medications had no effect, and interictal and ictal scalp electroencephalography (EEG) recordings demonstrated bilateral electrical abnormalities. Magnetic resonance imaging revealed a mass in the left cerebellar hemisphere, and ictal and interictal single-photon emission computerized tomography revealed a focal perfusion abnormality in the region of the cerebellar mass. The patient subsequently underwent intraoperative EEG monitoring with cortical scalp electrodes and cerebellar depth electrodes. Intraoperative EEG recordings revealed focal seizure discharges that arose in the region of the cerebellar mass and influenced electrographic activity in both cerebral hemispheres. Resection of this mass and the left cerebellar hemisphere led to complete resolution of the patient's seizures and normalization of the scalp EEG readings. Neuropathological findings in this mass were consistent with ganglioglioma. A review of the literature on the cerebellar origins of epilepsy is included.


1979 ◽  
Vol 51 (4) ◽  
pp. 562-564 ◽  
Author(s):  
Sverre J. Mørk ◽  
Martin Berg-Jensen ◽  
Åge Haugen

✓ This report presents clinicopathological documentation of a nerve-cell tumor in the right cerebellar hemisphere in a young woman. The nomenclature and some other aspects of tumors containing neuronal cells are discussed.


2002 ◽  
Vol 96 (5) ◽  
pp. 909-917 ◽  
Author(s):  
Shoichi Nagai ◽  
Kazuo Washiyama ◽  
Masanori Kurimoto ◽  
Akira Takaku ◽  
Shunro Endo ◽  
...  

Object. It has been suggested that nuclear factor (NF)-κB, a pleiotropic transcription factor, controls cell proliferation. The authors examined NF-κB activity and its participation in the growth of human malignant astrocytoma. Methods. The authors examined NF-κB activity in human malignant astrocytoma cell lines and high-grade astrocytoma tissues by using electrophoretic mobility shift assays and immunohistochemical studies, respectively. In addition, messenger (m)RNA expression of p50 and RelA, which are representative subunits of NF-κB, and IκBα, which is a representative inhibitory protein of NF-κB, were analyzed using Northern blot hybridization in the astrocytoma cell lines. Furthermore, alterations in DNA synthesis and cell growth in the astrocytoma cell lines were examined after inhibition of NF-κB activity by RelA antisense oligodeoxynucleotide. The authors found NF-κB activity in all astrocytoma cell lines and high-grade astrocytoma tissues that were examined, but not in the fetal astrocyte strain or in normal cerebral tissue. Expression of p50, RelA, and IκBα mRNA was found in the fetal astrocyte strain and normal adult brain tissue, in addition to the astrocytoma cell lines. The relative levels of expression of these mRNAs were similar among these cell lines, the cell strain, and normal tissue. The RelA antisense oligodeoxynucleotide specifically reduced the levels of RelA mRNA expression and NF-κB activity in the astrocytoma cell lines, thus significantly inhibiting their DNA synthesis and cell growth. Conclusions. Human malignant astrocytoma cells have aberrant NF-κB activity, which promotes their growth. This activity is not associated with aberrant expression of p50 and RelA.


2003 ◽  
Vol 98 (1) ◽  
pp. 14-20 ◽  
Author(s):  
Matthew J. McGirt ◽  
Ketan R. Bulsara ◽  
Thomas J. Cummings ◽  
Kent C. New ◽  
Kenneth M. Little ◽  
...  

Object. The prognostic value of differentiating between recurrent malignant glioma and a lesion due to radiation effect by performing stereotactic biopsy has not been assessed. Thus, this study was undertaken to determine such value. Methods. Between 1995 and 2001, 114 patients underwent magnetic resonance (MR) imaging—guided stereotactic biopsy to differentiate lesions caused by a recurrence of malignant astrocytoma and by radiation effect. All patients had previously undergone tumor resection (World Health Organization Grade III or IV) followed by radiotherapy. Disease diagnosis based on biopsy and patient characteristics were assessed as predictors of survival according to results of a multivariate Cox regression analysis. The diagnosis determined with the aid of biopsy was compared with that established during a subsequent resection in 26 patients. Survival following stereotactic biopsy was markedly increased in patients suffering from radiation effect compared with those harboring recurrent malignant glioma (p < 0.0001). In patients with radiation effect on biopsy, an increasing patient age (p < 0.05), having had two compared with one prior resection (p < 0.05), and a decreasing time from radiotherapy to biopsy (p < 0.001) were factors associated with decreased survival. Nevertheless, in patients with biopsy-defined radiation effect at second progression or with an age younger than 50 years the survival rate remained higher than that in patients with recurrent tumor on biopsy (p < 0.01). A biopsy-based diagnosis of radiation effect obtained less than 5 months after radiotherapy was not associated with an increased rate of patient survival compared with a diagnosis of recurrent malignant glioma on biopsy (p = 0.286). Eighty-six percent of lesions initially determined to be due to radiation effect on biopsy fewer than 5 months after radiotherapy were characterized as recurrent glioma by a mean of 11 months later. In contrast, only 25% of lesions initially diagnosed as attributable to radiation effect on biopsy more than 5 months after radiotherapy were classified as recurrent glioma a mean of 12 months later (p < 0.05). Conclusions. With the aid of stereotactic biopsy the authors demonstrated prognostic significance in differentiating recurrent malignant astrocytoma from a lesion due to radiation effect in patients presenting more than 5 months after having undergone radiotherapy. In patients who presented earlier than 5 months after radiotherapy, radiation effect on biopsy was not associated with an improved rate of survival compared with that in patients harboring recurrent malignant astrocytoma.


2002 ◽  
Vol 96 (5) ◽  
pp. 900-908 ◽  
Author(s):  
Takeshi Uemura ◽  
Kouzo Moritake ◽  
Yasuhiko Akiyama ◽  
Yoriyoshi Kimura ◽  
Takashi Shingu ◽  
...  

Object. Deuterium oxide (D2O), or heavy water, affects a variety of biological activities different from those of water. The authors examined the antitumoral effect of D2O on brain neoplasms and demonstrated D2O-mediated cytotoxicity by using a Rous sarcoma virus—induced murine malignant astrocytoma cell line, RSVM. The mechanism of the observed cytotoxicity may involve D2O-induced apoptosis and cell-cycle modulation. Methods. The authors performed an assay with methylthiazol tetrazolium bromide and a trypan blue dye exclusion test to confirm in vitro D2O-mediated cytotoxicity for RSVM cells. At D2O concentrations of 10 to 50%, the cytotoxic effect was dose and time dependent. Flow cytometry analysis revealed programmed cell death (apoptosis) and the accumulation of RSVM cells during the G2/M phase. By applying the terminal deoxynucleotidyl transferase—mediated deoxyuridine triphosphate nick-end labeling method, fluorescein isothiocyanate—annexin V and propidium iodide double staining, and caspase-family protease activity analysis, the authors demonstrated both DNA fragmentation and enhancement of caspase activity after a 48-hour treatment with D2O, thus indicating that D2O induces apoptosis in RSVM cells. Apoptotic DNA fragmentation was completely abolished by the caspase inhibitor Z-VAD-FMK (benzyloxycarbonil-Val-Ala-Aps-fluoromethylketone). The findings indicate that the caspase activation pathway may be involved in D2O-induced apoptosis. Conclusions. The authors found that D2O is cytotoxic to malignant astrocytoma cells. The mechanism of D2O-mediated cytotoxicity involved the induction of apoptosis and cell accumulation during the G2/M phase. This D2O-induced apoptosis is modulated through the caspase activation pathway.


1973 ◽  
Vol 39 (6) ◽  
pp. 777-779 ◽  
Author(s):  
R. Michael Scott ◽  
H. Thomas Ballantine

✓ A patient who underwent subtotal resection of a cerebellar astrocytoma had a recurrence of his original symptoms 39 years later. Surgery disclosed a malignant glioma arising in the original operative site in the right cerebellar hemisphere.


1996 ◽  
Vol 85 (5) ◽  
pp. 892-900 ◽  
Author(s):  
Paul G. Matz ◽  
Stephen M. Massa ◽  
Philip R. Weinstein ◽  
Christopher Turner ◽  
S. Scott Panter ◽  
...  

✓ Induction of the hemeoxygenase-1 (ho-1) stress gene is of importance for rapid heme metabolism and protection against oxidative injury in vitro and in vivo. Although ho-1 expression is observed in glia following exposure to whole blood and oxyhemoglobin, expression is mild, and other stress genes are not induced simultaneously in this setting. Hemeoxygenase-1 can be induced by several other physiological stresses in addition to heme. In the brain, ho-1 induction has been observed in the penumbra following focal cerebral ischemia. Because lysed blood is a spasmogen, the authors studied focal hyperexpression of the ho-1 gene after injection of lysed blood, whole blood, or saline into the cisterna magna of adult rats. Immunocytochemical analysis of HO-1 was performed at 1, 2, 3, and 4 days after the injections. Because the 70-kD inducible heat shock protein (HSP70) is induced by cellular stress, alternate sections were immunostained for HSP70 to assess whether focal hyperexpression was a stress phenomenon. An oligonucleotide probe was also used for in situ hybridization to demonstrate that ho-1 messenger (m)RNA was present. Focal HO-1 immunostained areas were observed after lysed blood injection only and were located mainly in the basal cortex and cerebellar hemisphere, although focal hyperexpression was also found in many other regions. The intensity of staining and the number of regions were maximum at 1 day. Double-labeled immunofluorescence revealed that many HO-1—immunoreactive cells were microglia. The HSP70 immunostaining of adjacent sections from the same animals demonstrated focal regions of immunoreactivity whose topography corresponded exactly with the topography of the HO-1—immunostained areas. Conventional histology in regions of HO-1 hyperexpression was often normal. In situ hybridization using the same oligonucleotide demonstrated that ho-1 mRNA was induced in focal areas of forebrain and in large regions of cerebellum within 6 hours of injection. These results demonstrate that focal hyperexpression of the ho-1 stress gene occurs after lysed blood injection and appears to be an indicator of cellular stress and injury in regions in which infarction does not occur. These results also suggest that cellular injury that occurs after injection of lysed blood may go undetected using conventional histology. Although direct heme metabolism was not investigated, our results indicate that rapid metabolism of heme, both intracellular and extracellular, may prove to be beneficial after subarachnoid hemorrhage.


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