Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Neurotrophins and neuronal versus glial differentiation in medulloblastomas and other pediatric brain tumors (1998)
    Springer
    Acta neuropathologica 95 (1998), S. 325-332 
    Details
    ISSN: 1432-0533
    Keywords: Key words Pediatric brain tumor ; Primitive ; neuroectodermal tumpor ; Trk receptor ; Neurotrophin ; Cell differentiation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Medulloblastomas are highly malignant and poorly understood childhood neoplasms. To determine if neurotrophins might influence the phenotypic properties of medulloblastoma in a paracrine or autocrine manner, 51 pediatric brain tumors including 20 biopsy specimens of these primitive neuroectodermal tumors (PNETs) and 31 other pediatric brain tumors were studied. Immunohistochemistry was used with antibodies to nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and NT-3, their cognate high affinity receptors as well as to neuronal and glial markers. TrkA, TrkB, and TrkC were observed in 5 (25%), 8 (40%), and 17 (85%), respectively, of these medulloblastomas while NGF, BDNF, and NT-3 were observed in 6 (30%), 8 (40%), and 3 (15%), respectively, and antibodies to neurofilament (NF) and glial fibrillary acidic proteins (GFAP) stained 16 (80%) and 11 (55%), respectively. TrkA and NGF were not observed in the same biopsy samples, while TrkB and BDNF were co-distributed in 6 of the cases, all of which expressed NF proteins. TrkC and NT-3 were co-distributed in 3 of the medulloblastomas, and these areas overlapped with NF protein-positive tumor cells in all 3 cases. In contrast to medulloblastomas, TrkA and NGF co-distributed in other pediatric brain tumors, and both Trk receptors and their neurotrophins co-distributed with GFAP-positive tumor cells in 13 (42%) of the non-PNET pediatric brain tumors. The absence of medulloblastomas that contain NGF and TrkA is consistent with in vitro data demonstrating that NGF-mediated TrkA signaling induces apoptosis. Finally, this study also suggests that BDNF and NT-3 may act in a paracrine or autocrine manner through TrkB and TrkC receptors, respectively, to induce neuronal differentiation in medulloblastomas.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050806
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Acute experimental allergic encephalomyelitis in radiation bone marrow chimeras between high and low susceptible strains of mice (1986)
    Springer
    Immunogenetics 24 (1986), S. 309-315 
    Details
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Acute experimental allergic encephalomyelitis (EAE) is an autoimmune disease involving the central nervous system (CNS) that can be elicited in susceptible strains of mice by the subcutaneous inoculation of mouse spinal cord homogenate (MSCH) in conjunction with complete Freund's adjuvant. In order to localize the physiological compartment conveying susceptibility to mice for EAE induction, hematopoietic radiation chimeras were prepared between the highly responsive SJL and low responder B10.S strains. Upon challenge with SJL MSCH preparations, high incidence of clinical disease was exhibited by B10.S → SJL chimeras but not by SJL → B10.S mice, suggesting that non-bone-marrow-derived factors were influencing development of disease. The incidence of histological lesions in the CNS was high for virtually all experimental and control groups except normal B10.S and B10.S → B10.S reconstituted mice. In contrast, challenge with B10.S MSCH induced a high clinical incidence of EAE in both B10.S → SJL and SJL → B10.S chimeras, indicating a possible interstrain difference in the immunogenicity of relevant CNS antigens.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00395536
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Family history of cancer and seizures in young children with brain tumors: a report from the Childrens Cancer Group (United States and Canada) (1993)
    Springer
    Cancer causes & control 4 (1993), S. 455-464 
    Details
    ISSN: 1573-7225
    Keywords: Astrocytoma ; case-control study ; childhood brain tumors ; family history ; North America ; primitive neuroectodermal tumor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: The occurrence of cancer and neurological disorders in first- and second-degree relatives of children in the United States and Canada diagnosed with brain tumor before age six was investigated. A pair-matched casecontrol study with 155 astrocytoma and 166 primitive neuroectodermal tumor (PNET) cases was performed. Cases were identified through the Childrens Cancer Group. Controls were selected by random-digit dialing and matched to cases on age, race, and telephone area code and exchange. Childhood cancers were more common in PNET relatives compared with the general population (standardized incidence ratio [SIR]=2.5, 95 percent confidence interval [CI] 1.1–4.8, P=0.02) and with control relatives (odds ratio [OR]=3.0, CI=0.5–30, P=0.29). For astrocytoma, nonsignificant excesses of brain tumor, leukemia/lymphoma, and childhood cancer occurred among case relatives compared with control relatives, but not compared with the general population. Astrocytoma cases were significantly more likely than controls to have a relative with seizures (OR=2.5, CI=1.2–4.9, P=0.009), especially childhood seizures (OR=3.4, CI=1.2–12, P=0.02), epilepsy (OR=3.0, CI=0.9–13, P=0.08), and febrile convulsions (OR=4.5, CI=0.9–43, P=0.07). A family history of stroke was not a risk factor for either type of brain tumor. These results suggest that some childhood brain tumors may result from a genetic susceptibility and that some risk factors may affect childhood astrocytoma and PNET differently.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00050865
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Molecular cytogenetic studies of pediatric ependymomas (1998)
    Springer
    Journal of neuro-oncology 37 (1998), S. 25-33 
    Details
    ISSN: 1573-7373
    Keywords: ependymoma ; childhood brain tumor ; chromosome 6 ; chromosome 17 ; chromosome 22
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cytogenetic and molecular studies of ependymomas have previously demonstrated deletions of chromosomes 17 and 22 as frequent abnormalities, implicating inactivation of tumor suppressor genes in the pathogenesis of these tumors. In the present study, we analyzed 22 childhood ependymomas by standard cytogenetic analysis, fluorescence in situ hybridization (FISH) and polymerase chain reaction (PCR)-based microsatellite analysis of chromosomes 17 and 22. Microsatellite analysis of chromosome 6 was performed to identify submicroscopic deletions implicated by the cytogenetic studies. Among the 22 cases, we demonstrated loss of chromosome 22 in 2 patients, deletion of chromosome 17 in 2 patients, and rearrangements or deletions of chromosome 6 in 5 patients. These data do not suggest that loss of a gene on chromosome 17p plays a primary role in the initiation of pediatric ependymomas. This is in contrast to what has been reported for pediatric CNS primitive neuroectodermal tumors and malignant astrocytomas, in which deletion of 17p is regarded as a primary event. Furthermore, loss of chromosome 22 may define a subset of ependymomas more commonly seen in adults. Cytogenetic studies in this series, however, suggest that a region on the long arm of chromosome may be involved in the development and/or progression of ependymomas in children.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005925613992
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Cerebellar sclerosis in pediatric cancer patients (1987)
    Springer
    Journal of neuro-oncology 4 (1987), S. 353-360 
    Details
    ISSN: 1573-7373
    Keywords: cerebellum ; methotrexate ; leukemia ; cerebellar sclerosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cerebal cortical sclerosis is an acquired condition that has rarely been described in cancer patients. We reviewed necropsy findings in all children with cancer who died at the Children's Hospital of Philadelphia during the 20 year period 1963–1982 and found cerebellar sclerosis in 14 children with cancer (12 with acute lymphoblastic leukemia, 1 each with neuroblastoma and osteogenic sarcoma). The lesions were focal (3), multifocal (9) or diffuse (2). They occurred more frequently in children with acute lymphoblastic leukemia who had received intravenous methotrexate therapy. Ten of these 12 children had also received whole brain irradiation. The pathogenesis of the cerebellar sclerosis is unknown, but it is possible that extrinsic cerebellar compression by tumor or chronically increased intracranial pressure may have played a role in 6, ischemia/hypoxia in 3, and methotrexate toxicity in 2. No clear associations could be ascertained in 3. Methotrexate may be a previously unrecognized cause of cerebellar cortical injury. In addition, oncologic treatment regimens that include other central nervous system-penetrating drugs and irradiation may sensitize cerebellar cortex and make it more susceptible to other cerebellar sclerosis-causative factors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00195606
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Outcome of children with primary intramedullary spinal cord tumors (1987)
    Springer
    Child's nervous system 3 (1987), S. 89-92 
    Details
    ISSN: 1433-0350
    Keywords: Spinal cord neoplasms ; Children ; Outcome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The influence of clinical and treatment factors on the outcome of children with primary intramedullary spinal cord tumors (PST) was evaluated by reviewing the records of 26 children diagnosed during the 15-year period 1970–1984. Five-year survival was 39%, but 5-year event-free survival (EFS) was only 14%. Eighteen-month EFS was 53% (9/17) among children with low-grade astrocytoma, 100% (2/2) with ependymoma, and 0 of 7 with anaplastic astrocytoma or ganglioglioma. There was no significant difference in the 18-month EFS by location of tumor, duration of symptoms, or extent of surgical removal. Five of 9 children with locally recurrent PST had a second operation, and 4 were alive a median of 56 months later. PST disseminated to the leptomeninges or the III ventricle in 5 children: 2 at diagnosis, 2 as the first sign of disease relapse, and 1 after local recurrence. Given the poor outcome of our children, different methods of treatment for children with tumors in this location should be evaluated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00271131
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Brain stem necrosis after preradiation high-dose methotrexate (1985)
    Springer
    Child's nervous system 1 (1985), S. 355-358 
    Details
    ISSN: 1433-0350
    Keywords: Brain necrosis ; Radiation necrosis ; High-dose methotrexate ; Methotrexate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Both cranial radiation therapy (RT) and high-dose systemic methotrexate (MTX) are used to treat intracranial neoplasms, but both may cause neurologic damage. MTX may be less neurotoxic if given before rather than after radiotherapy. We cared for a 5-year-old girl with a pineocytoma who had progressive brain stem dysfunction 4 months after MTX therapy, followed by local radiation therapy. CT studies were consistent with radiation necrosis that was confirmed at autopsy. MTX used in conjunction with cranial irradiation can result in severe neurotoxicity, even if the drug is given first.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00270824
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...