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  • Book
    Erwin G. Van Meir, editor.
    Summary: Covers three areas of research in brain tumors: a) animal models for brain tumors, including spontaneous occurrence of brain tumors in mammals, transgenic models in rodents and transplant models; b) Prognostic factors and biomarkers; c) Therapeutic targets and targeting approaches to brain tumors.

    Contents:
    Part I. Animal Models for central nervous tumors
    Modeling gliomas using PDGF-expressing retroviruses
    Modeling brain tumors using avian retroviral gene transfer
    Using neurofibromatosis type 1 mouse models to understand human pediatric low-grade gliomas
    Transgenic mouse models of CNS tumors: using genetically engineered murine models to study the role of p21 Ras in glioblastoma multiforme
    PTEN-deficient mouse models for high-grade astrocytomas
    The Nfl-/+; Trp53-/+cis mouse model of anaplastic astrocytoma and secondary glioblastoma : dissecting genetic susceptibility to brain cancer
    Modeling astrocytomas in a family of inducible genetically engineered mice : implications for preclinical cancer drug development
    Human brain tumor cell and tumor tissue transplantation models
    Transformed human brain cells in culture as a model for brain tumors
    Rat glioma models for preclinical evaluation of novel therapeutic and diagnostic modalities
    Neuro-oncogenesis induced by nitroso compounds in rodents and strain-specific genetic modifiers of predisposition
    The murine GL261 glioma experimental model to assess novel brain tumor treatments
    Spontaneous occurrence of brain tumors in animals: opportunities as preclinical model systems
    Part II. Prognostic factors and biomarkers
    p53 pathway alterations in brain tumors
    The PTEN/P13 kinase pathway in human glioma
    Value of 1p/19q and other LOH markers for brain tumor diagnosis, prognosis, and therapy
    Discovery of genetic markers for brain tumors by comparative genomic hybridization
    Genomic identification of significant targets in brain cancer
    Oncomodulatory role of the human cytomegalovirus in glioblastoma
    Aberrant EGFR signaling in glioma
    Mechanisms of brain tumor angiogenesis
    Vaso-occlusive mechanisms that intiate hypoxia and necrosis in glioblastoma: the role of thrombosis and tissue factor
    Transcription profiling of brain tumors: tumor biology and treatment stratification
    Proteomic profiling of human brain tumors
    Proteomic discovery of biomarkers in the cerebrospinal fluid of brain tumor patients
    Epigenetic profiling of gliomas
    Micronase in the central nervous system and potential roles of RNA interference in brain tumors
    Of Escherichia coli and man : understanding glioma resistance to temozolomide therapy
    Brain tumor stem cell markers
    Part III. Therapeutic targets and targeting approaches
    Clinical agents for the targeting of brain tumor vasculature
    Bone marrow-derived cells in GBM neovascularization
    Vascular targeting of brain tumors--bridging the gap with phage display
    Impact of the blood-brain barrier on brain tumor imaging and therapy
    Targeting CXCR4 in brain tumors
    Molecular targeting of IL-13R[alpha]2 and EphA2 receptor in GBM
    Molecular targets for antibody-mediated immunotherapy of malignant glioma
    Stat3 oncogenic signaling in glioblastoma multiforme
    Inhibition of Ras signaling for brain tumor therapy
    HGF/c-Met signaling and targeted therapeutics in brain tumors
    Combinatorial therapeutic strategies for blocking kinase pathways in brain tumors
    Targeting the TRAIL apoptotic pathways for glioblastoma therapies
    The NF-[kappa]B signaling pathway in GBMs : implications for apoptotic and inflammatory responses and exploitation for therapy
    Targeting endoplasmic reticulum stress for malignant glioma therapy
    Brain cancer stem cells as targets of novel therapies
    The use of retinoids as differentiation agents against medulloblastoma
    Herpes simplex virus 1 (HSV-1) for glioblastoma multiforme therapy
    The development of targeted cancer gene-therapy adenoviruses for high-grade glioma treatment
    Harnessing T-cell immunity to target brain tumors
    Glioma invasion : mechanisms and therapeutic challenges.
    Digital Access Springer 2009
  • Article
    Matsuda M, Yoshida N, Aoki N, Wakabayashi K.
    Ann N Y Acad Sci. 1978 Jun 20;312:74-92.
    Cold-insoluble globulin is normally present in plasma and serum at concentrations of 27.52 +/- 4.60 and 23.46 +/- 5.18 mg/dl, respectively (means +/- SD). The concentration of CIg in blood samples was significantly decreased in DIC syndromes (14.69 +/- 6.55 mg/dl; p less than 0.001). A strong, positive correlation was found with AT-III (r = 0.68) and a less striking one with Plg. Although alpha 2-PI was shown to be significantly decreased in DIC syndromes (p less than 0.001), a weak, inverse correlation was found between CIg and alpha 2-PI (r = -0.29). Immunologically cross-reactive substances were found to be widely distributed in association with the cells and tissues of mesenchymal origin, including fibroblasts, adipose cells, smooth muscle cells, and basement membranes. The glomerular basement membrane was an exception and is currently believed to be of different origin. In the kidney, fluorescence was found in the mesangium. Cold-insoluble globulin is also present as a component of cryofibrinogen that forms a solid gel at low temperatures. Sodium dodecyl sulfate polyacrylamide gel electrophoresis revealed that CIg in this fraction was rather homogeneous. Although closely migrating doublets were occasionally seen in the 440,000-dalton region on gels of unreduced samples, monomeric derivatives with a molecular weight of 220,000 or less, which have been claimed to occur in circulating plasma, were not observed. Thus, intact dimeric CIg appears to be the form of the molecule that complexes with fibrinogen. Cold-insoluble globulin is the fraction that was shown to exist as an independent entity from fibrinogen at an ambient temperature by immunoelectrophoresis and ultracentrifugation. However, very rapid formation of highly polymerized complexes in the sol phase at low temperatures was manifested by the finding of a sharp increase in light-scattering intensity using the technique of quasielastic light scattering. A control study on a mixture of normal CIg and fibrinogen disclosed no appreciable change in the temperature range between 37 and 8.5 degrees C. A comparative study on a mixture of cryofibrinogen-derived CIg and normal fibrinogen revealed an intermediate light-scattering pattern. After 2 hr at 8 degrees C, this mixture reached a state of equilibrium, where no further polymerization occurred. The secondary structures of normal and cryofibrinogen-derived CIg, determined by circular dichroism, showed no appreciable difference. A noteworthy finding was the almost complete absence of alpha-helices and a relatively high proportion of beta-structure in both forms of CIg. Amino termini of the fibrinogen moiety of cryofibrinogen were found to consist of alanine, tyrosine, and a small quantity of aspartic acid, consistent with the NH2 terminal moiety composition of normal fibrinogen but not of soluble fibrin monomer complex.
    Digital Access Access Options