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ABSTRACT: Oncogenic protein provokes cell cycle arrest termed premature senescence. In this process Ras has been known to induce cyclin-dependent kinase inhibitor (CKI) p16INK4A in primary fibroblasts. Here, we present a novel finding that human chimeric oncoprotein SYT-SSX1 induces CKI p21WAF1/CIP1 (p21) for suppression of cell growth. In human synovial sarcoma cell lines, the expression levels of p21 were high and the transcriptional activity of the p21 gene promoter was significantly elevated. The transient expression of SYT-SSX1-induced activation of the p21 gene promoter in human diploid fibroblasts. The N-terminus deletion form of SYT-SSX1, which failed to bind to hBRM one of the chromatin remodeling factors, preserved the p21 induction ability. This effect of SYT-SSX1 was similar in extent in both wild-type and p53-deficient HCT116 cell lines. Furthermore, the introduction of mutation in Sp1/Sp3 binding sites of the p21 gene promoter abolished the SYT-SSX1-induced transcriptional activity of its promoter. In SW13 cells, the stable expression of SYT-SSX1 suppressed cell growth in culture. These results suggest that SYT-SSX1 is able to induce p21 in a manner independent on hBRM and p53 but dependent on Sp1/Sp3.Keywords: p21WAF1/CIP1, Sp1, synovial sarcoma, SYT-SSX
Oncogene 08/2005; 24(54):7984-7990. · 6.37 Impact Factor
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ABSTRACT: The late region of the three primate polyomaviruses (JCV, BKV, and SV40) encodes a small, highly basic protein known as agnoprotein. While much attention during the last two decades has focused on the transforming proteins encoded by the early region (small and large T-antigens), it has become increasingly evident that agnoprotein has a critical role in the regulation of viral gene expression and replication, and in the modulation of certain important host cell functions including cell cycle progression and DNA repair. The importance of agnoprotein is underscored by its expression during lytic infection of glial cells by JCV that occurs in progressive multifocal leukoencephalopathy (PML), and also in some JCV-associated human neural tumors particularly medulloblastoma. In this review, we will discuss the structure and function of agnoprotein in the viral life cycle during the course of lytic infection and the consequences of agnoprotein expression for the host cell.
Journal of Cellular Physiology 08/2005; 204(1):1-7. · 3.87 Impact Factor
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Huai-Ying Zheng,
Tomokazu Takasaka,
Kazuyuki Noda,
Akira Kanazawa,
Hideo Mori,
Tomoyuki Kabuki,
Kohsuke Joh,
Tsutomu Oh-ishi,
Hiroshi Ikegaya, Kazuo Nagashima,
William W Hall,
Tadaichi Kitamura,
Yoshiaki Yogo
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ABSTRACT: JC polyomavirus (JCPyV) causes progressive multifocal leukoencephalopathy (PML) in patients with decreased immune competence. To elucidate genetic changes in JCPyV associated with the pathogenesis of PML, multiple complete JCPyV DNA clones originating from the brains of three PML cases were established and sequenced. Although unique rearranged control regions occurred in all clones, a low level of nucleotide variation was also found in the coding region. In each case, a parental coding sequence was identified, from which variant coding sequences with nucleotide substitutions would have been generated. A comparison between the parental and variant coding sequences demonstrated that all 12 detected nucleotide substitutions gave rise to amino acid changes. Interestingly, seven of these changes were located in the surface loops of the major capsid protein (VP1). Finally, 16 reported VP1 sequences of PML-type JCPyV (i.e. derived from the brain or cerebrospinal fluid of PML patients) were compared with their genotypic prototypes, generated as consensus sequences of representative archetypal isolates belonging to the same genotypes; 13 VP1 proteins had amino acid changes in the surface loops. In contrast, VP1 proteins from isolates from the urine of immunocompetent and immunosuppressed patients rarely underwent mutations in the VP1 loops. The present findings suggest that PML-type JCPyV frequently undergoes amino acid substitutions in the VP1 loops. These polymorphisms should serve as a new marker for the identification of JCPyV isolates associated with PML. The biological significance of these mutations, however, remains unclear.
Journal of General Virology 08/2005; 86(Pt 7):2035-45. · 3.36 Impact Factor
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Tadaki Suzuki,
Yuki Okada,
Shingo Semba,
Yasuko Orba,
Satoko Yamanouchi,
Shuichi Endo,
Shinya Tanaka,
Toshitsugu Fujita,
Shun'ichi Kuroda, Kazuo Nagashima,
Hirofumi Sawa
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ABSTRACT: The human polyomavirus JC virus (JCV) is the causative agent of a fatal demyelinating disease, progressive multifocal leukoencephalopathy, and encodes six major proteins, including agnoprotein. Agnoprotein colocalizes with microtubules in JCV-infected cells, but its function is not fully understood. We have now identified fasciculation and elongation protein zeta 1 (FEZ1) as a protein that interacted with JCV agnoprotein in a yeast two-hybrid screen of a human brain cDNA library. An in vitro binding assay showed that agnoprotein interacted directly with FEZ1 and microtubules. A microtubule cosedimentation assay revealed that FEZ1 also associates with microtubules and that agnoprotein induces the dissociation of FEZ1 from microtubules. Agnoprotein inhibited the promotion by FEZ1 of neurite outgrowth in PC12 cells. Conversely, overexpression of FEZ1 suppressed JCV protein expression and intracellular trafficking in JCV-infected cells. These results suggest that FEZ1 promotes neurite extension through its interaction with microtubules, and that agnoprotein facilitates JCV propagation by inducing the dissociation of FEZ1 from microtubules.
Journal of Biological Chemistry 08/2005; 280(26):24948-56. · 4.77 Impact Factor
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Tadaki Suzuki,
Yuki Okada,
Shingo Semba,
Yasuko Orba,
Satoko Yamanouchi,
Shuichi Endo,
Shinya Tanaka,
Toshitsugu Fujita,
Shun'ichi Kuroda, Kazuo Nagashima,
Hirofumi Sawa
[show abstract]
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ABSTRACT: The human polyomavirus JC virus (JCV) is the causative agent of a fatal demyelinating disease, progressive multifocal leukoencephalopathy,
and encodes six major proteins, including agnoprotein. Agnoprotein colocalizes with microtubules in JCV-infected cells, but
its function is not fully understood. We have now identified fasciculation and elongation protein zeta 1 (FEZ1) as a protein
that interacted with JCV agnoprotein in a yeast two-hybrid screen of a human brain cDNA library. An in vitro binding assay showed that agnoprotein interacted directly with FEZ1 and microtubules. A microtubule cosedimentation assay
revealed that FEZ1 also associates with microtubules and that agnoprotein induces the dissociation of FEZ1 from microtubules.
Agnoprotein inhibited the promotion by FEZ1 of neurite outgrowth in PC12 cells. Conversely, overexpression of FEZ1 suppressed
JCV protein expression and intracellular trafficking in JCV-infected cells. These results suggest that FEZ1 promotes neurite
extension through its interaction with microtubules, and that agnoprotein facilitates JCV propagation by inducing the dissociation
of FEZ1 from microtubules.
Journal of Biological Chemistry 06/2005; 280(26):24948-24956. · 4.77 Impact Factor
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Yuki Okada,
Tadaki Suzuki,
Yuji Sunden,
Yasuko Orba,
Shingo Kose,
Naoko Imamoto,
Hidehiro Takahashi,
Shinya Tanaka,
William W Hall, Kazuo Nagashima,
Hirofumi Sawa
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ABSTRACT: The nuclear envelope is one of the chief obstacles to the translocation of macromolecules that are larger than the diameter of nuclear pores. Heterochromatin protein 1 (HP1) bound to the lamin B receptor (LBR) is thought to contribute to reassembly of the nuclear envelope after cell division. Human polyomavirus agnoprotein (Agno) has been shown to bind to HP1alpha and to induce its dissociation from LBR, resulting in destabilization of the nuclear envelope. Fluorescence recovery after photobleaching showed that Agno increased the lateral mobility of LBR in the inner nuclear membrane. Biochemical and immunofluorescence analyses showed that Agno is targeted to the nuclear envelope and facilitates the nuclear egress of polyomavirus-like particles. These results indicate that dissociation of HP1alpha from LBR and consequent perturbation of the nuclear envelope induced by polyomavirus Agno promote the translocation of virions out of the nucleus.
EMBO Reports 06/2005; 6(5):452-7. · 7.36 Impact Factor
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ABSTRACT: The Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1), which is critical for EBV-induced B-cell transformation, is also abundantly expressed during the lytic cycle of viral replication. However, the biological significance of this strong LMP1 induction remains unknown. We engineered a bacterial artificial chromosome clone containing the entire genome of Akata strain EBV to specifically disrupt the LMP1 gene. Akata cell clones harboring the episomes of LMP1-deleted EBV were established, and the effect of LMP1 loss on virus production was investigated. We found that the degree of viral DNA amplification and the expression levels of viral late gene products were unaffected by LMP1 loss, demonstrating that the LMP1-deleted EBV entered the lytic replication cycle as efficiently as the wild-type counterpart. This was confirmed by our electron microscopic observation that nucleocapsid formation inside nuclei occurred even in the absence of LMP1. By contrast, loss of LMP1 severely impaired virus release into culture supernatants, resulting in poor infection efficiency. The expression of truncated LMP1 in Akata cells harboring LMP1-deleted EBV rescued the virus release into the culture supernatant and the infectivity, and full-length LMP1 partially rescued the infectivity. These results indicate that inducible expression of LMP1 during the viral lytic cycle plays a critical role in virus production.
Journal of Virology 05/2005; 79(7):4415-24. · 5.40 Impact Factor
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ABSTRACT: Human T-lymphotropic virus type I (HTLV-I) is known to be the causative agent of the chronic myelopathy, HTLV-I--associated myelopathy (HAM), and on rare occasions infection is also associated with the development of polyneuropathy. Here the authors present an HTLV-I--positive family of whom four members developed a chronic demyelinating polyneuropathy without HAM. Four female patients in a family from Hokkaido in Japan developed distal dominant paresthesia and muscle weakness in the second and third decades of their life. Neurological findings at ages ranging from 50 to 65 years included mild painful sensorimotor disturbances with atrophy of the distal parts of the extremities but without pyramidal signs or hyperactive tendon reflexes. Magnetic resonance imaging (MRI) findings of brain and spinal cord were unremarkable. Serum HTLV-I antibody levels were elevated at 1:8192 to 1:32,768, whereas those in cerebrospinal fluid were low at 1:4 to 1:8. Electrophysiological studies revealed polyphasic compound muscle action potentials with denervation potentials on nerve conduction studies and neurogenic patterns by electromyography, which were consistent with signs of chronic motor dominant demyelinating polyneuropathy. Sural nerve biopsy showed decreased myelinated fibers, occurrence of globule formation, myelin ovoid and remyelinated fibers, and an infiltration of CD68-positive macrophages with occasional CD4-positive T cells in the nerve fascicles. The polyneuropathy was responsive to steroid therapy. Analyses of serological human leukocyte antigen (HLA) types indicated that none of the patients possessed a high-risk HLA type known to be associated with adult T-cell leukemia (ATL), whereas they did have high responsive alleles to HTLV-I env similar to that observed in HAM. Nucleotide sequence analysis of the HTLV-I tax region demonstrated the B subgroup in all patients. This study suggests that HTLV-I infection can result in the development of a familial form of polyneuropathy that is associated with distinct HLA class I alleles, which might possibly involve a distinct virus subtype.
Journal of NeuroVirology 05/2005; 11(2):199-207. · 2.31 Impact Factor
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ABSTRACT: Methyl-2-cyanoacrylate, a widely used material for coating cerebral aneurysm, was recently withdrawn. The aim of the present study was to develop an alternative coating material for cerebral aneurysm, which is safe, effective and stable within the brain. In the first experiment, an aneurysm model of the common carotid artery was produced in a rabbit by the local application of elastase. The aneurysm produced was covered by no material (Group A), a cellulose cotton sheet and conventional methyl-2-cyanoacrylate (Group B), a newly produced polyglycolic acid felt and fibrin glue (Group C), or a cellulose cotton sheet and fibrin glue (Group D). Histological examination showed that the materials resulted in the formation of tight connective tissue around the artery, and that the material was completely replaced by the connective tissue after 12 weeks. This change was found exclusively in Group C, but not in Group A or the other materials, although a temporary thickening of the intima was also observed at the site of the elastase application in Group C. In Group D, a long-term, marked thickening of the intima was observed. In the second experiment, using an intracranial internal carotid artery from a beagle, the applied polyglycolic acid felt and fibrin glue to the intracranial artery induced the formation of connective tissue around the artery that was completely absorbed 16 weeks after surgery. There were no signs of intimal thickening or of adverse reactions in nervous tissue. The present results suggest that polyglycolic acid felt and fibrin glue is a possible candidate for a safe, effective biomaterial to wrap or coat cerebral aneurysm.
Neuropathology 04/2005; 25(1):66-76. · 2.02 Impact Factor
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ABSTRACT: Polyomavirus JC (JCV) infection causes the fatal human demyelinating disease, progressive multifocal leukoencephalopathy. Although the initial interaction of JCV with host cells occurs through direct binding of the major viral capsid protein (VP1) with cell-surface molecules possessing sialic acid, these molecules have not yet been identified. In order to isolate monoclonal antibodies which inhibit attachment of JCV, we established an immunoscreening system using virus-like particles consisting of the VP1. Using this system, among monoclonal antibodies against the cell membrane fraction from JCV-permissive human neuroblastoma IMR-32 cells, we isolated a monoclonal antibody designated as 24D2 that specifically inhibited attachment and infection of JCV to IMR-32 cells. The antibody 24D2 recognized a single molecule of around 60 kDa in molecular weight in the IMR-32 membrane fraction. Immunohistochemical staining with 24D2 demonstrated immunoreactivity in the cell membrane of JCV-permissive cell lines and glial cells of the human brain. These results suggested that the molecule recognized by 24D2 plays a role in JCV infection, and that it might participate as a receptor or a co-receptor in JCV attachment and entry into the cells.
Biochemical and Biophysical Research Communications 03/2005; 327(1):242-51. · 2.48 Impact Factor
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ABSTRACT: Methyl-2-cyanoacrylate, a widely used material for coating cerebral aneurysm, was recently withdrawn. The aim of the present study was to develop an alternative coating material for cerebral aneurysm, which is safe, effective and stable within the brain. In the first experiment, an aneurysm model of the common carotid artery was produced in a rabbit by the local application of elastase. The aneurysm produced was covered by no material (Group A), a cellulose cotton sheet and conventional methyl-2-cyanoacrylate (Group B), a newly produced polyglycolic acid felt and fibrin glue (Group C), or a cellulose cotton sheet and fibrin glue (Group D). Histological examination showed that the materials resulted in the formation of tight connective tissue around the artery, and that the material was completely replaced by the connective tissue after 12 weeks. This change was found exclusively in Group C, but not in Group A or the other materials, although a temporary thickening of the intima was also observed at the site of the elastase application in Group C. In Group D, a long-term, marked thickening of the intima was observed. In the second experiment, using an intracranial internal carotid artery from a beagle, the applied polyglycolic acid felt and fibrin glue to the intracranial artery induced the formation of connective tissue around the artery that was completely absorbed 16 weeks after surgery. There were no signs of intimal thickening or of adverse reactions in nervous tissue. The present results suggest that polyglycolic acid felt and fibrin glue is a possible candidate for a safe, effective biomaterial to wrap or coat cerebral aneurysm.
Neuropathology 02/2005; 25(1):66 - 76. · 2.02 Impact Factor
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ABSTRACT: Tanycytic ependymomas are a subtype of ependymomas that were formally recognized as a new pathological entity in the latest World Health Organization (WHO) classification of 2000. They occur mostly in the spinal cord. Only a few reports have analyzed the proliferative potentials of these tumors; however, it has been reported that the MIB-1 labeling index of tanycytic ependymoma is lower than that of other subtypes of WHO grade II ependymomas. We report a rare case of cervicomedullary junction tanycytic ependymoma associated with marked cyst formation. A 62-year-old man had a history of progressive gait disturbance, diplopia, and swallowing disturbance over a one-month period prior to admission. Magnetic resonance imaging (MRI) showed a cystic mass with a mural nodule at the cervicomedullary junction with Gd-DTPA enhancement. Cyst-subarachnoid shunt was performed using a far lateral approach. After 6 years, however, the man was readmitted to the hospital because of reaccumulation of the cyst. Partial removal of a mural nodule and a cyst-subarachnoid shunt were performed simultaneously by a midline suboccipital approach. The pathological diagnosis was tanycytic ependymoma. Postoperatively, the patient recovered well and was discharged from the hospital without further treatment. Most of the tumor cells had small, round nuclei; pleomorphism was minimal. The cytoplasm was dilated. The tumor cells were positive for EMA and s-100, and negative for CD-34. GFAP was not determined due to difficulty caused by background glial processes. The MIB-1 labeling index was less than 1%. Ultrastructurally, the tumor cells had ependymal cell features, such as desmosomes and microvilli. Based on these findings, the pathological diagnosis was tanycytic ependymoma.
Brain Tumor Pathology 02/2005; 22(1):29-33. · 1.19 Impact Factor
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ABSTRACT: Two cases of clear cell ependymoma (CCE) of the fourth ventricle are reported in a 49-year-old woman with dysphagia and a 59-year-old woman with dizziness and gait disturbance. CCE is a relatively new variant of ependymoma added to the WHO classification of tumors in 1993. Tumor cells display an oligodendroglioma-like appearance with a clear perinuclear halo. Most infratentorial CCE tumors are located in the cerebellum. There are only three cases, including the present two cases, that have been reported to affect the fourth ventricle.
Neuropathology 01/2005; 24(4):330-5. · 2.02 Impact Factor
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Mulan Jin,
Hirofumi Sawa,
Tadaki Suzuki,
Kazuko Shimizu,
Yoshinori Makino,
Shinya Tanaka,
Takayuki Nojima,
Yasunori Fujioka,
Makoto Asamoto,
Noriaki Suko,
Miri Fujita, Kazuo Nagashima
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ABSTRACT: It has been reported that Simian virus 40 (SV40) is linked to human beings by inoculation of contaminated poliovaccines and may have a role in the etiology of malignant mesothelioma. However, there have been no reports describing the relationship between SV40 and malignant mesothelioma in Japan. A study was undertaken to investigate whether SV40 was related to patients of malignant mesothelioma in Japan by the polymerase chain reaction (PCR) assay, DNA sequence analysis, and immunohistochemical methods. Paraffin-embedded samples of the 18 autopsied patients with pleural malignant mesothelioma were collected from five hospitals in Japan. After isolation of DNA from paraffin blocks, PCR analyses followed by sequencing were performed using three different sets of primers for detection of SV40 large T antigen (TAg) gene. All 18 malignant mesothelioma samples were also immunohistochemically evaluated for expression of SV40 TAg protein with two different anti-SV40 TAg antibodies. SV40 TAg genome was detected in eight malignant mesothelioma cases. Only one of three primer pairs successfully amplified SV40 genome in the samples, whereas all pairs yielded a PCR product in the controls, suggesting a low content of virus DNA. No immunopositive staining for SV40 TAg was found in any of the samples. This study shows that SV40 genome was present in a subset of Japanese malignant mesothelioma patients who were unlikely to have received a contaminated polio vaccine based on their age.
Journal of Medical Virology 01/2005; 74(4):668-76. · 2.82 Impact Factor
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Toshiko Nagashima,
Takayo Chuma,
Yukio Mano,
Yu-ichi Goto,
Yukiko K Hayashi,
Narihiro Minami,
Ichizo Nishino,
Ikuya Nonaka,
Toshiaki Takahashi,
Hirofumi Sawa,
Masashi Aoki, Kazuo Nagashima
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ABSTRACT: Dysferlinopathy and rigid spine syndrome occurring in a 50-year-old man is reported. The patient noticed stiffness of knee and ankle joints, which gradually extended to neck, wrist and elbow joints leading to difficulty in anterior flexion. Muscular weakness and wasting of the lower extremities had developed since age 40, accompanied by a limitation of anterior bending of the spine. Elevated serum CK was noticed. Muscle CT revealed atrophy with moderate fatty replacement of muscles in the neck, shoulder and pelvic girdle, and marked replacement in the para-vertebral muscles, posterior compartment of hamstrings and calf muscles. Electromyography showed a typical myogenic pattern, and muscle biopsy disclosed dystrophic changes, compatible with limb-girdle muscular dystrophy 2B. Loss of dysferlin expression was verified by immunohistochemistry, which was confirmed by a mini-multiplex Western blotting system. Gene analyses of the dysferlin gene disclosed compound heterozygotes for frameshift (G3016 + 1A) and a missense mutation (G3370T). This study might propose some clues to resolve the combination of musular dystrophies and rigid spine syndrome.
Neuropathology 01/2005; 24(4):341-6. · 2.02 Impact Factor
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ABSTRACT: Cell migration is a well organized process regulated by the extracellular matrix-mediated cytoskeletal reorganization. The signaling adaptor protein Crk has been shown to regulate cell motility, but its precise role is still under investigation. Herein, we report that Crk associates with ERM family proteins (including ezrin, radixin, and moesin), activates RhoA, and promotes cell motility toward hyaluronic acid. The binding of Crk with ERMs was demonstrated both by transient and stable protein expression systems in 293T cells and 3Y1 cells, and it was shown that v-Crk translocated the phosphorylated form of ERMs to microvilli in 3Y1 cells by immunofluorescence and immunoelectron microscopy. This v-Crk-dependent formation of microvilli was suppressed by inhibitors of Rho-associated kinase, and the activity of RhoA was elevated by coexpression of c-Crk-II and ERMs in 3Y1 cells. In concert with the activation of RhoA by Crk, Crk was found to associate with Rho-GDI, which has been shown to bind to ERMs. Furthermore, upon hyaluronic acid treatment, coexpression of c-Crk-II and ERMs enhanced cell motility, whereas the sole expression of c-Crk-II or either of the ERMs decreased the motility of 3Y1 cells. These results suggest that Crk may be involved in regulation of cell motility by a hyaluronic acid-dependent mechanism through an association with ERMs.
Journal of Biological Chemistry 12/2004; 279(45):46843-50. · 4.77 Impact Factor
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ABSTRACT: Fibrous hamartoma of infancy (FHI) in the spinal cord is very rare. It is characterized histopathologically by three elements: fibrous, adipose, and myxoid mesenchymal tissues.
A 10-month-old boy presented with paraparesis. Magnetic resonance imaging showed a large intradural mass that occupied the space between the T10 and L4 levels.
We performed partial removal of the mass. Histopathological examination of the lesion revealed that it was composed of collagen bundles and fibrous tissue interspersed with adipose tissue, mesenchymal tissue, and glial tissue, and it was diagnosed as FHI.
FHI in the central nervous system, especially in the spine, is very rare, and the presence of glial tissue admixed with particular components of FHI is quite exceptional.
Neurosurgery 10/2004; 55(3):712. · 2.79 Impact Factor
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ABSTRACT: Dynamin associates with a variety of SH3 domain-containing molecules via a C-terminal proline-rich motif and takes part, with them, in endocytic processes. Here, we have investigated a new dynamin-associating molecule, formin-binding protein 17 (FBP17), involved in deforming the plasma membrane and in endocytosis. FBP17 formed tubular invaginations originating from the plasma membrane. Its N-terminal Fer/CIP4 homology domain, a coiled-coil domain, and a proline-rich motif were required for tubular invagination and self-assembly, by which tubular invagination might be induced. Using anti-FBP17 antibody, we detected positive immunoreactions in the testis that were restricted to the germ cells. We also detected FBP17 in the brain by immunoblotting and in situ hybridization. When COS cells expressing enhanced green fluorescent protein-tagged FBP17 were incubated with fluorescently labeled transferrin, epidermal growth factor, and cholera toxin, these molecules co-localized with FBP17-induced tubular invaginations, suggesting that FBP17 is involved in dynamin-mediated endocytosis in both a clathrin-dependent and -independent manner. These observations therefore indicate that FBP17 interacts with dynamin and regulates endocytosis by forming vesicotubular structures.
Journal of Biological Chemistry 10/2004; 279(38):40091-9. · 4.77 Impact Factor
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ABSTRACT: Five cases of pilomyxoid astrocytoma (PmA) characterized by a monophasic pattern with a myxoid background were selected for a clinicopathological study from 23 cases previously diagnosed as pilocytic astrocytoma (PA). All PmA patients were either infants or young children (mean age 2.1 years), and all tumors were located in the optic chiasm/hypothalamus region. All cases received chemotherapy, which reduced tumor size, and the location of the tumor became confined to the optic chiasm. In two cases, tumor recurrence occurred 3 and 7 years after chemotherapy. Histology of the recurrent tumors showed the biphasic pattern of classical PA. Hence, we conclude that PmA might be an infantile form of PA and speculate that a subset of PmA in the optic pathway/hypothalamus originates from the optic chiasm, possibly derived from radial glia existing in the embryonic optic chiasm.
Acta Neuropathologica 09/2004; 108(2):109-14. · 9.32 Impact Factor
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ABSTRACT: We report a case of a 71-year-old man who presented with cerebellar dysfunction. He was diagnosed as having squamous cell carcinoma of the lung (T2N3M0, Stage IIIB). No anti-onconeural antibodies were found in his serum. Cerebral spinal fluid (CSF) examination showed mild mononuclear pleocytosis alone. Magnetic resonance imaging (MRI) of the brain and spinal cord revealed no abnormalities. At autopsy, there was complete disappearance of Purkinje cells with reactive astrocytosis. These findings are compatible with paraneoplastic cerebellar degeneration (PCD). To our knowledge, no case of PCD has been reported previously in patients with squamous cell carcinoma of the lung.
Internal Medicine 08/2004; 43(7):602-6. · 0.94 Impact Factor
