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09/2011; , ISBN: 978-953-307-646-1
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ABSTRACT: The patient was a 72-year-old woman who had previously undergone treatment for femoral chondrosarcoma (histologically rated as myxofibrosarcoma). She suddenly developed left homonymous hemianopsia and was diagnosed with cerebral embolism. Because she had atrial fibrillation, we treated her for cardiogenic cerebral embolism. About 3 months later, however, she developed left hemiplegia, and head magnetic resonance imaging revealed multiple tumorous lesions affecting the previously detected infracted area and several new areas. We assumed that a tumor embolus had caused cerebral embolism, which resulted in growth of the tumor from the embolus and formation of a metastatic brain tumor. The metastatic foci formed from the tumor embolus were visualized by diagnostic imaging, and histological examination of the resected tumor confirmed that the brain tumor had occluded the brain vessel (tumorigenic cerebral embolism). No such case has been reported to date, and this case seems to be important.
Brain Tumor Pathology 09/2011; 29(1):63-7. · 1.19 Impact Factor
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ABSTRACT: MicroRNAs (miRNAs) are small noncoding RNAs that take part in diverse biological processes by suppressing target gene expression. Elevated expression of miR-21 has been reported in many types of human cancers. Radiotherapy is a standard adjuvant treatment for patients with glioblastoma. However, the resistance of glioblastoma cells to radiation limits the success of this treatment. In this study, we found that miR-21 expression was upregulated in response to ionizing radiation (IR) in U251 cells, which suggested that miR-21 could be involved in the response of U251 cells to radiation. We showed that a miR-21 inhibitor enhanced IR-induced glioblastoma cell growth arrest and increased the level of apoptosis, which was probably caused by abrogation of the G(2)-M arrest induced by IR. Further research demonstrated that the miR-21 inhibitor induced the upregulation of Cdc25A. Taken together, these findings suggest that miR-21 inhibitor can increase IR-induced growth arrest and apoptosis in U251 glioblastoma cells, at least in part by abrogating G(2)-M arrest, and that Cdc25A is a potential target of miR-21.
Brain Tumor Pathology 05/2011; 28(3):209-14. · 1.19 Impact Factor
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ABSTRACT: Even when we successfully perform a total extirpation of glioblastoma macroscopically, we often encounter tumor recurrence. We examined seven autopsy brains, focusing on tumor cell infiltration in the peripheral zone of a tumor, and compared our findings with the MR images. There has so far been no report regarding mapping of tumor cell infiltration and DNA histogram by flow cytometry, comparing the neuroimaging findings with the autopsy brain findings. The autopsy brain was cut in 10-mm-thick slices, in parallel with the OM line. Tissue samples were obtained from several parts in the peripheral zone (the outer area adjacent to the tumor edge as defined by postcontrast MRI) and then were examined by H&E, GFAP, and VEGF staining. We defined three infiltrating patterns based on number of infiltrated cells as follows: A zone, 100%-60% of the cells infiltrated tumor cells compared with tumor cell density of the tumor mass; B zone, 60%-20%; C zone, 20%-0%. In the autopsy brain, the tumor was easily identified macroscopically. We found that (1) the tumor cells infiltrated the peritumoral area; and (2) tumor cell infiltration was detected over an area measuring from 6 to 14 mm from the tumor border in the A zone. When performing surgery on glioblastoma, a macroscopic total extirpation of the tumor as defined by the contrast-enhanced area in MRI is therefore considered to be insufficient for successfully reducing tumor recurrence.
Brain Tumor Pathology 10/2010; 27(2):81-7. · 1.19 Impact Factor
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ABSTRACT: A 23-year-old Japanese woman presented with a newly developed spinal extradural arteriovenous fistula (AVF) during pregnancy. She had been followed up for a suspected spinal cavernous angioma and became unable to walk during the 29th week of her pregnancy. Magnetic resonance (MR) imaging showed a spinal extradural AVF at the T3 to T4 levels compressing the spinal cord. After delivery by cesarean section, her neurological symptoms gradually began to resolve, and she was able to resume walking without assistance. MR imaging confirmed spontaneous regression of the AVF. This case suggests that exacerbated neurological symptoms and AVF growth triggered by pregnancy can improve after delivery without interventional treatment. Careful follow up of neurological findings is required to prevent unnecessary interventional procedures in pregnant women with spinal AVF.
Neurologia medico-chirurgica 08/2009; 49(7):313-5. · 0.61 Impact Factor
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ABSTRACT: Spontaneous spinal epidural hematoma (SSEH) is rare. Its etiology remains controversial; however, spinal venous wall susceptibility to intravenous pressure change and the resultant venous rupture seem to be involved. The authors report a case of SSEH dorsal to the spine producing acute anterior spinal cord syndrome. A posterior SSEH between the C-3 and T-5 levels caused progressive tetraparesis and the disappearance of superficial body sensation below the level of C-8, although deep sensation remained completely intact. This neurological false localizing sign seems to have resulted from counterforce by preexisting asymptomatic cervical intervertebral disc herniation at the C6-7 levels inducing direct pressure on the anterior spinal cord. This case is the first reported instance of posterior cervical SSEH manifesting acute anterior spinal cord syndrome as its false localizing sign.
Journal of Neurosurgery Spine 07/2009; 10(6):574-7. · 1.53 Impact Factor
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ABSTRACT: Radiation-induced brain injury is a life-threatening or at least QOL-compromising pathological entity induced by therapeutic irradiation to malignant brain tumors. Although life-threatening late delayed radiation necrosis and radiation-induced leukoencephalopathy had been assumed to be major complications of radiation therapy to the brain classically, these complications seem to be less frequently seen in therapeutic irradiation to the brain recently because in many treatment protocols to brain tumors, irradiation field is now confined to tumors and their margins and adjuvant chemotherapy consisting of methothrexate etc. has been avoided as much as possible. Instead, less aggressive but still QOL-compromising encephalopathy has been recognized for the past 20 years. This encephalopathy occurs in senior adults several months after the extended field irradiation with even less amount of irradiation dose such as 40 Gy whole brain irradiation. This encephalopathy is characterized by cognitive impairment and brain atrophy which attenuates QOL of the patients. In this article, these radiation-induced brain injuries are reviewed clinically, etiologically and hisotopathologically based on reports in the literature.
Brain and nerve = Shinkei kenkyū no shinpo 03/2008; 60(2):123-9.
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ABSTRACT: We report two infant cases with atypical teratoid/rhabdoid tumor (AT/RT) located in the cerebellar vermis and spinal cord. MRI showed the tumors were isointense on T1-weighted images and mixed intensity of isointense and slight high intensity on T2-weighted images. Postcontrast MRI demonstrated clear margin of tumor and heterogeneous strong enhancement. It was difficult to differentiate the tumor from medulloblastoma by hematoxylin and eosin staining. However, immunohistochemical staining showed that these tumor cells react positively for cytokeratin, smooth muscle actin (SMA), and epithelial membrane antigen (EMA) and helped us with the differentiation. Electron microscopic study has confirmed the presence of mesenchymal components, such as filaments and desmosome junctions in the rhabdoid cells, but no neuronal components. The tumors rapidly increased in size, showing high MIB-1 index, and the prognosis was gave.
Brain Tumor Pathology 02/2008; 25(2):79-83. · 1.19 Impact Factor
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ABSTRACT: Although p53 controls cell death after various stresses, its role in neuronal death after brain ischemia is poorly understood. To address this issue, we subjected p53-deficient (p53-/- and p53+/-) mice (backcrossed for 12 generations with C57BL/6 mice) and wild-type mice (p53+/+) to transient global ischemia by the three-vessel occlusion method. Despite similar severity of ischemia, as shown by anoxic depolarization and cortical blood flow, neuronal death in the hippocampal cornus ammonis (CA)1 region was much more extensive in p53+/+ than in p53-/- mice (surviving neuronal count, 9.3%+/-3.0% versus 61.3%+/-34.0% of nonischemic p53+/+ controls, respectively, P<0.0037). In p53+/- mice, a similar trend was also observed, though not statistically significant (43.5% of nonischemic p53+/+ controls). In p53+/+ mice, p53-like immunoreactivity in hippocampal CA1 neurons was enhanced at 12 h after ischemia, and messenger ribonucleic acid for Bax, a direct downstream target of p53, was also increased. These results indicate that p53 potentiates ischemic neuronal death in vivo and suggest that this molecule could be a therapeutic target in neuronal death after cerebral ischemia.
Journal of Cerebral Blood Flow & Metabolism 11/2006; 26(10):1332-40. · 5.01 Impact Factor
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Takamitsu Fujimaki,
Masao Matsutani MD,
Osamu Nakamura, Akio Asai,
Nobuaki Funada,
Morio Koike,
Hiromu Segawa,
Kouichi Aritake,
Takanori Fukushima,
Shuntaro Houjo,
Akira Tamura,
Keiji Sano
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ABSTRACT: Bromodeoxyuridine (BUdR), a nonradioactive thymidine analogue, is taken up by cells in S-phase, and the ratio of BUdR-positive nuclei to the total number of cells counted is defined as the labeling index (LI). In this study, BUdR LI and the clinical course of 50 cerebral astrocytic tumors in adults were analyzed. The obtained LI distributed continuously in a broad range from 0% to 19%. The mean LI of 28 glioblastomas, 12 anaplastic astrocytomas, and ten astrocytomas were 8.5%, 4.2%, and 1.2%, respectively, and these differences were statistically significant (P = 0.05). In the analysis of LI and the recurrence-free period (RFP), regardless of the histologic findings, 23 patients with LI more than 5% had a median RFP of 9.0 months; the median RFP of nine patients with LI of 3% to 5% was 14.7 months. Nine of 13 patients with LI less than 3% have not yet recurred after a median follow-up of 36 months. These differences were also statistically significant by the generalized Wilcoxon test (P = 0.05). The proliferative potential reflected by the BUdR LI is a good clinical indicator for predicting the rate of tumor growth in cerebral astrocytic tumors. In combination with histologic diagnosis, BUdR LI could help in determining a patient's prognosis more precisely.
Cancer 06/2006; 67(6):1629 - 1634. · 4.77 Impact Factor
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ABSTRACT: Gliomas are classified based mainly on microscopic resemblance to their presumed glial origin such as astrocyte and oligodendrocyte. However, more objective diagnostic criteria are indispensable for the precise treatment of patients. For instance, loss of the short arm of chromosome 1 (1p) in oligodendrogliomas is recognized as an important marker for better response to chemotherapy and longer survival of the patients. To gain insight into their molecular biological background and to identify genes characterizing each subgroup, we investigated gene expression profile of the 4 glioma subsets, oligodendroglioma with and without 1p loss, diffuse astrocytoma and glioblastoma using DNA microarray. Remarkably, most of the genes showing distinctive expression in oligodendroglioma with 1p loss were also highly expressed in normal brain tissues and had neuron-related function, which included MYT1L, INA, RIMS2, SNAP97 and SNCB. Histological analysis also demonstrated that MYT1L, which were abundantly expressed in normal neuron, were certainly present in tumor cells. These results suggest that oligodendroglioma, especially with 1p loss, has more or less neuronal characteristics although oligodendroglioma is thought to originate form glial lineage cell. With further pathological studies, those neuron-related genes might be good diagnostic markers for oligodendroglioma of better prognosis as well.
Brain Pathology 02/2004; 14(1):34-42. · 3.99 Impact Factor
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ABSTRACT: We have characterised the blood vessels found in normal cerebral vasculature and in arteriovenous malformations (AVMs), based on the expression of smooth muscle cell (SMC)-specific proteins. The marker proteins used were smooth muscle alpha-actin and four myosin heavy chain isoforms (SM1, SM2, SMemb and NMHC-A). Specimens of AVM obtained during surgery, and normal cerebral vessels from autopsy cases were studied immunohistochemically and compared. The arterial components of AVM contained an abundance of SMCs of the contractile phenotype, which were positive for alpha-actin, SM1 and SM2, but not for SMemb and NMHC-A. These components showed the same staining pattern as mature normal arteries. Two different types of abnormal veins were found in the AVM specimens: large veins with a thick and fibrous wall (so-called 'arterialised' veins) and intraparenchymal thin-walled sinusoidal veins. The former expressed alpha-actin, SM1, SM2, and SMemb, the latter expressed alpha-actin, SM1, and SM2. These marker expression patterns resembled those of normal cerebral arteries, and the results were compatible with arterialisation of the cerebral veins caused by arteriovenous shunting. However, the expression of SMemb was found only in the arterialised type of veins, not in the sinusoidal type or the arteries that had sustained abnormal blood flow in the AVMs. The thick-walled veins in the AVMs showed the same staining pattern as normal veins of dural plexus origin (large subarachnoid veins and dural sinuses). It is therefore possible to assume that they originated from the dural plexus, and extended into the brain during the formation of AVMs.
Acta Neuropathologica 06/2003; 105(5):455-61. · 9.32 Impact Factor
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ABSTRACT: Delayed neuronal death in the hippocampal CA1 region after transient forebrain ischemia may share its underlying mechanism with neurodegeneration and other modes of neuronal death. The precise mechanism, however, remains unknown. In the postischemic hippocampus, conjugated ubiquitin accumulates and free ubiquitin is depleted, suggesting impaired proteasome function. The authors measured regional proteasome activity after transient forebrain ischemia in male Mongolian gerbils. At 30 minutes after ischemia, proteasome activity was 40% of normal in the frontal cortex and hippocampus. After 2 hours of reperfusion, it had returned to normal levels in the frontal cortex, CA3 region, and dentate gyrus, but remained low for up to 48 hours in the CA1 region. Thus, the 26S proteasome was globally impaired in the forebrain during transient ischemia and failed to recover only in the CA1 region after reperfusion. The authors also measured 20S and 26S proteasome activities directly after decapitation ischemia (at 5 and 20 minutes) by fractionating the extracts with glycerol gradient centrifugation. Without adenosine triphosphate (ATP), only 20S proteasome activity was detected in extracts from both the hippocampus and frontal cortex. When the extracts were incubated with ATP in an ATP-regenerating system, 26S proteasome activity recovered almost fully in the frontal cortex but only partially in the hippocampus. Thus, after transient forebrain ischemia, ATP-dependent reassociation of the 20S catalytic and PA700 regulatory subunits to form the active 26S proteasome is severely and specifically impaired in the hippocampus. The irreversible loss of proteasome function underlies the delayed neuronal death induced by transient forebrain ischemia in the hippocampal CA1 region.
Journal of Cerebral Blood Flow & Metabolism 07/2002; 22(6):705-10. · 5.01 Impact Factor
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ABSTRACT: Oligodendrogliomas frequently, but not always show sensitivity to chemotherapy and recent studies demonstrated that allelic loss of chromosome 1p is highly associated with this chemosensitivity. To gain insight into the molecular mechanism of such difference, we examined comprehensive gene expression profiles of 11 oligodendroglial tumors, six with and five without 1pLOH (loss of heterozygosity), and two normal brain tissues using the oligonucleotide microarray (GeneChip). Statistically significant numbers of genes were expressed differentially between the two genetic subsets. Clustering analysis separated the tumor subsets well. The tumors with 1pLOH had similar expression profiles to the normal brain for those differentially expressed genes. Many genes showing higher expression in tumors with 1pLOH were presumed to have functions in nervous tissues. Notably, the majority of the 123 genes showing significant expression reduction in tumors with 1pLOH were either on chromosome 1 (50%) or on 19 (10%), and the average expression reduction ratio was about 50% (0.54+/-0.13) possibly reflecting the chromosomal deletion. Thus, the biological difference between the genetic subsets of oligodendroglioma was indeed reflected to gene expression profile, which provided baseline information for further studies to elucidate the mechanism of chemosensitivity in gliomas.
Oncogene 07/2002; 21(25):3961-8. · 6.37 Impact Factor
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Keisuke Ueki,
Ryo Nishikawa,
Yoichi Nakazato,
Takanori Hirose,
Junko Hirato,
Nobuaki Funada,
Takamitsu Fujimaki,
Shuntaro Hojo,
Osami Kubo,
Takafumi Ide,
Masaaki Usui,
Chikayuki Ochiai,
Shoichi Ito,
Hiroshi Takahashi,
Akitake Mukasa, Akio Asai,
Takaaki Kirino
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ABSTRACT: The histological diagnosis of human gliomas is of great importance for estimating patient prognosis and guiding therapy but suffers from being subjective and, therefore, variable. We hypothesized that molecular genetic analysis could provide a more objective means to classify tumors and, thus, reduce diagnostic variability.
We performed molecular genetic analysis on 91 nonselected gliomas for 1p, 19q, 10q, TP53, epidermal growth factor receptor, and cyclin-dependent kinase 4 abnormalities and compared with the consensus diagnoses established among four independent neuropathologists.
There were six astrocytomas, seven anaplastic astrocytomas, 45 glioblastomas, 21 oligodendrogliomas, eight anaplastic oligodendrogliomas, three oligoastrocytomas, and one anaplastic oligoastrocytoma. Twenty-nine cases had either 1p or 19qloss of heterozygosity (LOH) while retaining both copies of 10q, of which 25 (86%) were histologically oligodendroglioma, anaplastic oligodendroglioma, oligoastrocytoma, or anaplastic oligoastrocytoma. As for the oligodendroglial tumors, unanimous agreement of the initial diagnoses was almost restricted to those cases with combined 1p/19qLOH, whereas all nine tumors without 1p loss initially received variable diagnoses. Interestingly, TP53 mutation was inversely related to 1pLOH in all gliomas (P = 0.0003) but not 19qLOH (P = 0.15).
These data demonstrate that molecular genetic analysis of 1p/19q/10q/TP53 has significant diagnostic value, especially in detecting oligodendroglial tumors. In addition, 1pLOH and TP53 mutations in gliomas may be markers of oligodendroglial and astrocytic pathways, respectively, which may separate gliomas with the same histological diagnosis, especially oligodendroglial tumors and glioblastomas. Testing for those molecular genetic alterations would be essential to obtain more homogeneous sets of gliomas for the future clinical studies.
Clinical Cancer Research 02/2002; 8(1):196-201. · 7.74 Impact Factor
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Toshihiro Mochizuki, Akio Asai,
Nobuhito Saito,
Sakae Tanaka,
Hideki Katagiri,
Tomoichiro Asano,
Makoto Nakane,
Akira Tamura,
Yoshiyuki Kuchino,
Chifumi Kitanaka,
Takaaki Kirino
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ABSTRACT: A growing body of evidence now suggests that programmed cell death (PCD) occurs via non-apoptotic mechanisms as well as by apoptosis. In contrast to apoptosis, however, the molecular mechanisms involved in the regulation of non-apoptotic PCD remain only poorly understood. Here we show that ceramide induces a non-apoptotic PCD with a necrotic-like morphology in human glioma cells. Characteristically, the cell death was not accompanied by loss of the mitochondrial transmembrane potential, cytosolic release of cytochrome c from mitochondria, or the activation of the caspase cascade. Consistent with these characteristics, this ceramide-induced cell death was inhibited neither by the overexpression of Bcl-xL nor by the pan-caspase inhibitor zVAD-fmk. However, strikingly, the ceramide-induced non-apoptotic cell death was inhibited by the activation of the Akt/protein kinase B pathway through the expression of a constitutively active version of Akt. The results for the first time indicate that the Akt kinase, known to play an essential role in survival factor-mediated inhibition of apoptotic cell death, is also involved in the regulation of non-apoptotic PCD.
Journal of Biological Chemistry 02/2002; 277(4):2790-7. · 4.77 Impact Factor
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ABSTRACT: Cavernous malformations (CVMs) and arteriovenous malformations (AVMs) were immunostained for three smooth muscle cell (SMC)-specific protein markers (smooth muscle !-actin, SM1 and SM2). Smooth muscle !-actin, a widely used marker of SMCs, is reportedly one of the earliest proteins expressed during differentiation of SMCs and expressed in some kinds of mesoderm-derived cells. In contrast, SM1, an isoform of myosin heavy chain (MHC), is detected only in SMCs. SM2 is another MHC isoform and expressed in the contractile phenotype of SMC. All 14 intraaxial CVMs were positive for smooth muscle !-actin, but SM1 was detected in only three of them and SM2 was not found. Their staining pattern resembled that of normal intraparenchymal and pial veins. All 15 cerebral AVMs and 5 out of 6 extraaxial CVMs from the cavernous sinus, orbit and scalp were positive for all three markers, as were the normal cerebral arteries. The venous components of AVMs, as well as the arterial components, expressed SM2, and were different from normal veins in the brain and intraaxial CVMs. This study shows that the histological analysis using the three markers for SMC is useful to differentiate intraaxial CVM from AVM and extraaxial CVMs.
Acta Neuropathologica 08/2001; 102(3):257-263. · 9.32 Impact Factor
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ABSTRACT: The p53 tumor-suppressor gene plays a critical role in radiation-induced apoptosis. Several genes, including Bax and Fas, are involved in p53-mediated apoptosis, and their over-expression enhances the degree of radiation-induced apoptosis. Apaf-1 and caspase-9 have been reported to be downstream components of p53-mediated apoptosis, suggesting that these genes play a role in radiation-induced apoptosis. In this study, we transduced U-373MG cells harboring mutant p53 with the Apaf-1 and/or caspase-9 genes via adenoviral (Adv) vectors concomitant with X-ray irradiation and evaluated the degree of apoptosis. The percentage of apoptotic cells in U-373MG cells co-infected with the Adv for Apaf-1 (Adv-APAF-1) and that for caspase-9 (Adv-Casp9) and treated with irradiation (24%) was much higher than that in cells co-infected with Adv-APAF-1 and Adv-Casp9 and not treated with irradiation (0.86%) and that in cells infected with either Adv-APAF-1 or Adv-Casp9 and treated with irradiation (2.0% or 2.6%, respectively). The apoptosis induced by co-transduction of Apaf-1 and caspase-9 and irradiation was repressed in cells that were co-infected with the Adv for Bcl-XL but not in cells co-infected with the Adv for Bcl-2. These results indicate that Apaf-1 and caspase-9 play a role in radiation-induced apoptosis in cancer cells harboring mutant p53.Bcl-XL may be critically involved in the radioresistance of cancer cells by repressing Apaf-1– and caspase-9–mediated apoptosis. Expression of Apaf-1 and caspase-9 in tumors may be an important determinant of the therapeutic effect of irradiation in cancer treatment. © 2001 Wiley-Liss, Inc.
International Journal of Cancer 07/2001; 93(2):252 - 261. · 5.44 Impact Factor
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ABSTRACT: Selective neuronal death of the hippocampal CAI area after mild ischemia is known as delayed neuronal death (DND). Progression of DND was evaluated using 7 T MRI in gerbils. In the CAI, the T2 relaxation time started to increase on day 3 and was significantly higher on day 4 than that of the control gerbils. However, the apparent diffusion coefficient of water (ADC) was significantly lower on day 1 than in the control and continued to decline up to day 4. Changes in T2 coincided with loss of MAP2 immunoreactivity, while the ADC decrease preceded these changes. After 1 month, the ADC had returned to within the normal range, while T2 had decreased to below the control level. These results suggest that MRI is useful for monitoring DND.
Neuroreport 10/2000; 11(15):3333-3336. · 1.66 Impact Factor
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ABSTRACT: Purpose: Although chemotherapeutic protocols that include chloroethylnitrosoureas (CENUs), such as 1-(4-amino-2-methyl-5-pyrimidinyl)
methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), have been a mainstay
of treatment for glioblastomas, the clinical outcomes have been unsatisfactory. More effective chemotherapeutic protocols
for these tumors will require clear delineation of more cytocidal and cytostatic chemotherapeutic drugs. Methods and Results: In this study, we measured the cytocidal effects of ACNU, cisplatin, actinomycin D, and staurosporine, administered within
their therapeutic dose ranges, in the treatment of glioblastoma cells. As assessed by WST-1 colorimetric assay, the number
of viable cells decreased markedly in T98G cultures treated with actinomycin D or staurosporine, to less than 20% of the level
in control cultures at 72 h, but did not decrease or even increased after 6 days of treatment with ACNU. After treatment with
cisplatin for 5 days, cell viability decreased to 30% of control. As assessed by fluorescence microscopic examination of nuclear
staining by Hoechst 33258 and by electron microscopy, the majority of dead cells treated with actinomycin D, staurosporine,
or cisplatin had morphologic features of apoptosis. Caspase-3 activity increased more than 20-fold in cells treated with actinomycin
D, staurosporine, or cisplatin but increased less than fivefold in ACNU-treated cells. In addition to caspase-3 activation,
western blot analysis demonstrated cleavage of caspase-2 during the apoptotic process. These findings indicate that actinomycin
D and staurosporine potently induce apoptosis, whereas ACNU exerts mainly a cytostatic rather than a cytocidal effect. Conclusion: Actinomycin D and staurosporine and their derivatives are potentially effective chemotherapeutic agents against glioblastoma
cells at least in vitro.
Cancer Chemotherapy and Pharmacology 12/1999; 45(2):149-156. · 2.83 Impact Factor
