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  • 1
    Call number: QZ200:530/1(4 rev) ; QZ380:188(4 rev) ; A240:19 ; A240:26 ; G340:34 ; B340:68 ; L201:7 ; L401:5 ; M100:582 ; G033:100
    Keywords: Central Nervous System Neoplasms / genetics ; Central Nervous System Neoplasms / pathology ; Brain Neoplasms / pathology
    Notes: The WHO Classification of Tumours of the Central Nervous System presented in this book reflects the views of a Working Group that convened for a Consensus and Editorial Meeting at the German Cancer Research Center, Heidelberg 21-24 June 2015.
    Pages: 408 p. : ill.
    Edition: 4th rev. ed.
    ISBN: 9789283244929
    Signatur Availability
    QZ200:530/1(4 rev) available
    QZ380:188(4 rev) available
    A240:19 departmental collection or stack – please contact the library
    A240:26 departmental collection or stack – please contact the library
    G340:34 departmental collection or stack – please contact the library
    B340:68 departmental collection or stack – please contact the library
    L201:7 departmental collection or stack – please contact the library
    L401:5 departmental collection or stack – please contact the library
    M100:582 departmental collection or stack – please contact the library
    G033:100 departmental collection or stack – please contact the library
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  • 2
    Call number: QZ200:530/1(4) ; QZ380:188(4) ; B060:152 ; B060:153 ; B060:163 ; G100:23 ; G033:68
    Keywords: Central Nervous System Neoplasms / classification ; Central Nervous System Neoplasms / pathology ; Brain Neoplasms / classification ; Brain Neoplasms / pathology
    Notes: Earlier edition with title: Pathology and genetics of tumours of the nervous system.
    Pages: 309 p. : ill.
    Edition: 4th ed.
    ISBN: 978-92-832-2430-2
    Signatur Availability
    QZ200:530/1(4) available
    QZ380:188(4) on loan
    B060:152 departmental collection or stack – please contact the library
    B060:153 departmental collection or stack – please contact the library
    B060:163 departmental collection or stack – please contact the library
    G100:23 departmental collection or stack – please contact the library
    G033:68 departmental collection or stack – please contact the library
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  • 3
    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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  • 4
    ISSN: 1432-0533
    Keywords: Key words Astrocytoma ; Glioblastoma ; Glioma ; progression ; p53 mutation ; Gemistocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Low-grade diffuse astrocytomas have an intrinsic tendency for malignant progression but the factors determining the kinetics of this process are still poorly understood. We report here the case of a male patient who developed a fibrillary astrocytoma at the age of 33 years and who underwent six surgical interventions over a period of 17 years without radiotherapy or chemotherapy. The first three biopsies spanned a period of 11 years and led to the diagnosis of low-grade, diffuse astrocytoma (WHO grade II), with a growth fraction (MIB-1 labeling index) of 2.3–3.7%. The fourth to sixth biopsies showed histological features of anaplastic astrocytoma (WHO grade III), with growth fractions between 5.0 and 10.5%. The fraction of gemistocytic neoplastic astrocytes also increased, from 0.3% in the first biopsy to 17.5% in the last biopsy and preceded the increase in proliferative activity and transition to anaplastic astrocytoma. The fraction of tumor cells immunoreactive to BCL-2 increased from 0.3% to 8.2%. A p53 mutation in codon 273 (CGT→TGT, Arg→Cys) was identified in the first biopsy and persisted throughout the course of the disease. However, the fraction of cells with p53 protein accumulation increased significantly during progression, from 3.2% in the first biopsy to 13.7% in the last. The absence of additional genetic alterations (PTEN mutations, loss of chromosome 10 and 19q) may be responsible for the slow progression and lack of glioblastoma features even after a 17-year disease duration.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1335
    Keywords: Gastric carcinogenesis ; N-methyl-N-nitrosourea ; DNA methylation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The formation ofO 6-methyldeoxyguanosine (O 6-MedGuo) was determined by an immuno-slot-blot assay in DNA of various tissues of F344 rats exposed toN-methyl-N-nitrosourea (MNU) in the drinking water at 400 ppm for 2 weeks. Although the pyloric region of the glandular stomach is a target organ under these experimental conditions, the extent of DNA methylation was highest in the forestomach (185 μmolO 6-MedGuo/mol guanine). Fundus (91 μmol/mol guanine) and pylorus (105 μmol/mol guanine) of the glandular stomach, oesophagus (124 μmol/mol guanine) and duodenum (109 μmol/mol guanine) showed lower levels ofO 6-MedGuo but differed little between each other. Thus, no correlation was observed between target organ specificity and the extent of DNA methylation. This is in contrast to the gastric carcinogen,N-methyl-N′-nitro-N-nitrosoguanidine (MNNG), which preferentially alkylates DNA of the pylorus, the main site of induction of gastric carcinomas by this chemical. In contrast to MNU, the non-enzymic decomposition of MNNG is accelerated by thiol compounds (reduced glutathione,l-cysteine), which are present at much higher concentrations in the glandular stomach than in the forestomach and oesophagus. During chronic exposure to MNNG (80 ppm), mucosal cells immunoreactive toO 6-MedGuo are limited to the luminal surface [Kobori et al. (1988) Carcinogenesis 9:2271–2274]. Although MNU (400 ppm) produced similar levels ofO 6-MedGuo in the pylorus, no cells containing methylpurines were detectable by immunohistochemistry, suggesting a more uniform methylation of mucosal cells by MNU than by MNNG. After a single oral dose of MNU (90 mg/kg) cells containing methylpurines were unequivocally identified using antibodies toO 6-MedGuo and the imidazole-ring-opened product of 7-methyldeoxyguanosine. In the gastric fundus, their distribution was similar to those methylated by exposure to MNNG, whereas the pyloric region contained immunoreactive cells also in the deeper mucosal layers. After a 2-week MNU treatment, the rate of cell proliferation, as determined by bromodeoxyuridine immunoreactivity, was only slightly enhanced in the oesophagus and in the fundus, but markedly in the forestomach and the pyloric region of the glandular stomach. It is concluded that the overall extent of DNA methylation, the distribution of alkylated cells within the mucosa and the proliferative response all contribute to the organ-specific carcinogenicity of MNU.
    Type of Medium: Electronic Resource
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