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  • 1
    Call number: QZ200:483 ; B060:87 ; B060:88 ; 01-PROE:320 ; 01-KID:605
    Keywords: Neoplasms / epidemiology ; Neoplasms / etiology ; Neoplasms / prevention & control ; Neoplasms / therapy
    ISBN: 92-832-0411-5
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    B060:87 departmental collection or stack – please contact the library
    B060:88 departmental collection or stack – please contact the library
    01-PROE:320 departmental collection or stack – please contact the library
    01-KID:605 departmental collection or stack – please contact the library
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  • 2
    Call number: H0700:41
    Keywords: Nervous System Neoplasms
    Pages: xv, 230 p.
    ISBN: 0387193804
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  • 3
    Call number: QZ241:3(2)/21
    Keywords: Central nervous system / Tumors ; Tumors / Classification ; Neoplasms, Nervous Tissue / classification ; Neoplasms, Nervous Tissue / pathology ; Neoplasms, Nervous Tissue / pathology ; Central Nervous System Neoplasms / classification ; Central Nervous System Neoplasms / pathology ; Central Nervous System Neoplasms / pathology
    Notes: Rev. ed. of: Histological typing of tumours of the central nervous system / K.J. Zülch, in collaboration with pathologists in 14 countries. 1979.
    Pages: xii, 112 p. : col. ill.
    Edition: 2nd ed.
    ISBN: 3540569715
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  • 4
    Call number: 04-Med:238 ; H0400:21 ; H0600:184 ; B060:98
    Keywords: Neoplasms / pathology ; Nervous System Neoplasms / pathology ; Nervous System Neoplasms / genetics ; Brain Neoplasms / secondary
    Notes: Later edition with title: WHO classification of tumours of the central nervous system
    Pages: 314 p. : ill.
    ISBN: 92-832-2409-4
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    H0400:21 departmental collection or stack – please contact the library
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  • 5
    ISSN: 1432-1173
    Keywords: Schlüsselwörter: Tumor-Suppressor-Gen – p53 – Melanom – Spinozelluläres Karzinom – Basaliom – M. Bowen ; Key words: Tumour suppressor gene – p53 – Melanoma – Squamous cell carcinoma – Basalioma – Bowen's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract. The product of the p53 tumour suppressor gene is a sequence-specific DNA-binding protein that acts as a transcription factor and can inhibit transformation in vitro. Mutational inactivation of p53 is the most frequent genetic alteration found in human cancer. Point mutations of the p53 gene have been detected in about 50% of squamous cell carcinomas, basaliomas and cases of Bowen's disease. A significant portion of these mutations were CC→TT or C→T transitions suggestive of UV involvement in mutagenesis. Increased concentrations of p53 protein were immunohistochemically detected in cutaneous malignant melanomas, but p53 mutations are rare in this tumour.
    Notes: Zusammenfassung. Das Produkt des p53-Tumorsuppressor-Gens reguliert als Transskriptionsfaktor negativ das Zellwachstum und kann in vitro die Teilung transformierter Zellen hemmen. Inaktivierung des p53 durch Mutationen gehört zu den häufigsten genetischen Veränderungen in menschlichen Tumoren. Beim spinozellulären Karzinom, Basaliom und Bowenkarzinom wurden Punktmutationen in etwa 50% der Fälle nachgewiesen. Dabei fanden sich gehäuft CC→TT- und C→T-Transitionen, die typischerweise durch UV-Bestrahlung hervorgerufen werden. In malignen Melanomen wurden zwar erhöhte Konzentrationen des p53-Proteins immunohistochemisch nachgewiesen; p53-Mutationen sind hingegen sehr selten.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0533
    Keywords: Cerebral Ischemia ; Protein Biosynthesis ; Autoradiography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The incorporation ofl-[3-3H]tyrosine into cat brain proteins was investigated after 1 h of complete ischemia and 7 h of recirculation. Autoradiographs from the cerebral hemispheres, the brain stem and cerebellum revealed that the vast majority of neuronal and glial cells had resumed protein synthesis. Focal reduction of amino acid incorporation was restricted to a few cortical areas within the cerebral hemispheres. A significant number of neurons with no detectable [3H]tyrosine incorporation was only found in the dentate gyrus. The postischemic recovery of protein synthesis supports electrophysiological findings which indicate that nerve cells may survive extended periods of ischemia if the cerebral circulation can be adequately restored.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0533
    Keywords: Retroviral vectors ; Oncogene-ras-myc ; Grafting ; Brain tumors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Introduction into fetal rat brain cells of a replication-defective retroviral vector harboring v-Ha-ras and v-gag-myc rapidly causes the induction of highly malignant undifferentiated neuroectodermal tumors following transplantation into the brains of syngeneic hosts [Wiestler, et al. (1992) Cancer Res. 52: 3760–3767]. In the present study, we have investigated the modulating effect of the developmental stage of neural target cells and of the dose of the retroviral vector used in the grafting experiments. Exposure of fetal cells from embryonic day (E)12 or E14 produced a 100% incidence of malignant neuroectodermal tumors which led to the death of recipient animals after a median latency period of 32 days. A 100-fold reduction of the virus dose from 2.062×106 to 2.062×104 focus-forming units/ml resulted in a lower tumor incidence of 25%. Of six neural grafts exposed to v-Ha-ras and v-myc at E16, only one showed evidence of tumorigenesis (low-grade astrocytoma and hemangioma). All other transplants were morphologically normal for observation periods of 26 weeks, indicating a marked loss of transforming activity of ras and myc in more advanced stages of brain development. In retrovirus-exposed donor cells which caused the development of neural tumors in recipient rats, malignant transformation was also evident during culture in vitro, usually after 9–12 days. Oncogene complementation was also studied in the newborn rat brain. After microinjection of the retroviral vector into the brain at postnatal day (P)0, P1 and P3, 5 out of 20 animals (25%) developed a total of seven brain tumors. Histopathologically, three of these neoplasms were malignant neuroectodermal tumors which, in contrast to those induced in fetal brain transplants showed evidence of focal glial and/or neuronal differentiation. In addition, we observed one oligodendroglioma, two hemangiomas and a malignant hemangioendothelioma. These data indicate that neural precursor cells and endothelia of the rat brain represent the major target cells for the complementary action of ras and myc and that the use of target cells from later developmental stages (E16 and postnatal) leads to the induction of both primitive and more differentiated neoplasms.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0533
    Keywords: Key words Fas ; Glioblastoma ; Astrocytoma ; Apoptosis ; Necrosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Fas/APO-1 (CD95)-mediated apoptosis is one of the major mechanisms of programmed cell death. We have previously shown by reverse transcriptase-polymerase chain reaction that Fas is frequently expressed in malignant gliomas [Tachibana et al. (1995) Cancer Res 55: 5528–5530]. In this study, we assessed Fas expression in astrocytomas using a polyclonal anti-Fas antibody. Immunoreactivity to Fas was detected in 1 out of 9 (11%) low-grade astrocytomas (WHO grade II), 2 of 11 (18%) anaplastic astrocytomas (WHO grade III) and in 13 of 15 (87%) glioblastomas (WHO grade IV). In glioblastomas, Fas expression was almost exclusively observed in glioma cells surrounding foci of necrosis. In these perinecrotic areas, there was also an accumulation of glioma cells undergoing apoptosis, as detected by in situ nick-end labeling. This suggests that Fas-mediated apoptosis may play a role in the pathogenesis of necrosis which constitutes a histological hallmark of glioblastoma multiforme.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0533
    Keywords: Key words APO2 ligand ; CD95 ligand ; Glioma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract APO2 ligand (APO2L) is a CD95 ligand (CD95L)-related cytokine of the tumor necrosis factor family that interacts with agonistic (DR4, DR5) and antagonistic (DcR1, DcR2) receptors. Cultured malignant glioma cells preferentially express agonistic receptors and are susceptible to APO2L-induced apoptosis. Here, we report that 8 of 8 human glioma cell lines expressed APO2L mRNA and protein in vitro. Immunohistochemistry using a monoclonal antibody to APO2L revealed that all 23 primary astrocytic brain tumors analyzed, including low-grade astrocytomas and glioblastomas, express APO2L in vivo. With the exception of reactive astrocytes, non-neoplastic glia and neurons in the cerebrum lacked immunoreactivity of APO2L. Thus, in addition to the CD95/CD95L system, a second death ligand/death receptor pair may regulate susceptibility to apoptosis in human glial neoplasms.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-0533
    Keywords: Key wordsp16 ; CDK4 ; RB ; Glioblastoma ; Progression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Primary glioblastomas develop rapidly de novo through a genetic pathway characterized by amplification/overexpression of EGFR and of MDM2 genes. Secondary glioblastomas develop more slowly through progression from low grade or anaplastic astrocytoma and show a high incidence of a p53 mutation. In the present study, primary and secondary glioblastomas were analyzed for p16 deletions and CDK4 amplification by differential PCR and for loss of expression of the retinoblastoma (RB) gene by immunohistochemistry. Except for one case, alterations in the structure or expression of p16, CDK4 and RB were mutually exclusive. The overall incidence of aberrant expression of these genes coding for components of the cell-cycling-regulatory system was similar in primary (14/28; 50%) and secondary glioblastomas (9/23; 39%). However, p16 deletions were significantly more frequent in the former (10/28; 36%) than in the latter (1/23, 4%; P = 0.0075), suggesting that this alteration constitutes an additional genetic hallmark of the primary (de novo) glioblastoma.
    Type of Medium: Electronic Resource
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