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  • Journal of Neurosurgery Publishing Group (JNSPG)  (5)
  • 1
    Online Resource
    Online Resource
    Marked inhibition of glioblastoma target cell tumorigenicity in vitro by retrovirus-mediated transfer of a hairpin ribozyme against deletion-mutant epidermal growth factor messenger RNA
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2000
    In:  Journal of Neurosurgery Vol. 92, No. 2 ( 2000-02), p. 297-305
    Details
    In: Journal of Neurosurgery, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 92, No. 2 ( 2000-02), p. 297-305
    Abstract: Object. The goal of this study was to evaluate the activity of certain hairpin ribozymes against deletion-mutant epidermal growth factor receptor ( Δ EGFR) messenger (m)RNA in glioblastomas multiforme (GBMs). A distinct 801-bp deletion mutation associated with amplification of the EGFR gene is present in a large subgroup of primary GBMs and confers enhanced tumorigenicity in vivo. As a result of the deletion mutation, the fusion junction of the gene is created directly upstream of a GTA triplet, which is subsequently transcribed into a ribozyme target codon (GUA). Methods. In attempts to intercept Δ EGFR gene expression at the mRNA level, the authors designed three different hairpin ribozymes derived from the negative strands of satellite RNAs in tobacco ringspot virus, chicory yellow mottle virus (sCYMV1), and arabis mosaic virus against this target and evaluated their efficiency and specificity in a cell-free system. The sCYMV1, identified as the most active anti-Δ EGFR hairpin ribozyme motif, was cloned into the retroviral plasmid N2A+tRNA i met . High-titer recombinant retrovirus-containing supernatants ( 〉 10 5 colony-forming units/ml) derived from an amphotropic GP+envAM 12 packaging cell line transfected with the N2A+tRNA i met -anti-ΔEGFR-sCYMV1 construct were used to introduce the sCYMV1 hairpin ribozyme into U-87MG.ΔEGFR glioblastoma cells, which overexpress exogenous ΔEGFR. Using a virus/target cell ratio of 40:1 in the absence of drug selection, the ribozyme transfer resulted in a greater than 90% reduction of Δ EGFR mRNA levels, a 69% inhibition of ΔEGFR-mediated proliferation advantage, and a greater than 95% decrease of colony formation in soft agar under relative serum starvation conditions in vitro; transfer of a control mutant ribozyme that was rendered incapable of cleaving its target yielded none of these effects. Conclusions. These findings indicate that the anti-ΔEGFR-sCYMV1 hairpin ribozyme is capable of specifically inhibiting the expression of Δ EGFR and reversing the ΔEGFR-associated malignant phenotype of GBM cells. This strategy may constitute a promising gene therapy approach for a molecularly defined subgroup of GBMs.
    Type of Medium: Online Resource
    ISSN: 0022-3085
    URL: Article
    DOI: 10.3171/jns.2000.92.2.0297
    RVK:
    XA 10000
    RVK:
    XA 55270
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2000
    detail.hit.zdb_id: 2026156-1
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  • 2
    Online Resource
    Online Resource
    Inverse correlation of epidermal growth factor receptor messenger RNA induction and suppression of anchorage-independent growth by OSI-774, an epidermal growth factor receptor tyrosine kinase inhibitor, in glioblastoma multiforme cell lines
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2004
    In:  Journal of Neurosurgery Vol. 100, No. 3 ( 2004-03), p. 523-533
    Details
    In: Journal of Neurosurgery, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 100, No. 3 ( 2004-03), p. 523-533
    Abstract: Object. Quantitative and qualitative alterations in the epidermal growth factor receptor (EGFR) commonly occur in many cancers in humans, including malignant gliomas. The aim of the current study was to evaluate molecular and cellular effects of OSI-774, a novel EGFR tyrosine kinase inhibitor, on nine glioblastoma multiforme (GBM) cell lines. Methods. The effects of OSI-774 on expression of EGFR messenger (m)RNA and protein, proliferation, anchorage-independent growth, and apoptosis were examined using semiquantitative reverse transcription—polymerase chain reaction, immunocytochemical analysis, Coulter counting, soft agar cloning, and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling/fluorescence-activated cell sorting, respectively. All p53 genes were completely and bidirectionally sequenced. Suppression of anchorage-independent growth by OSI-774 was inversely correlated to the induction of EGFR mRNA during relative serum starvation (r = −0.74) and was unrelated to p53 status. Overall, suppression of anchorage-independent growth was a considerably stronger effect of OSI-774 than inhibition of proliferation. The extent of OSI-774—induced apoptosis positively correlated with both proliferation and anchorage-independent growth of GBM cell lines (r = 0.75 and 0.79, respectively). In a single cell line derived from a secondary GBM, exposure to concentrations of greater than or equal to 1 Émol/L resulted in a substantial net cell loss during proliferation studies. Conclusions. The induction of EGFR mRNA may constitute a cellular mechanism to counteract the inhibitory effect of OSI-774 on the anchorage-independent growth of GBM cells. In contrast, no considerable correlation could be established between baseline expression levels of EGFR (both mRNA and protein) in GBM cell lines and their biological response to OSI-774. The OSI-774 induced greater ( p53 -independent) apoptosis in more malignant GBM phenotypes and may be a promising therapeutic agent against secondary GBM.
    Type of Medium: Online Resource
    ISSN: 0022-3085
    URL: Article
    DOI: 10.3171/jns.2004.100.3.0523
    RVK:
    XA 10000
    RVK:
    XA 55270
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2004
    detail.hit.zdb_id: 2026156-1
    Location Call Number Limitation Availability
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  • 3
    Online Resource
    Online Resource
    Inverse correlation of epidermal growth factor receptor messenger RNA induction and suppression of anchorage-independent growth by OSI-774, an epidermal growth factor receptor tyrosine kinase inhibitor, in glioblastoma multiforme cell lines
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2004
    In:  Neurosurgical Focus Vol. 16, No. 2 ( 2004-02), p. 1-11
    Details
    In: Neurosurgical Focus, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 16, No. 2 ( 2004-02), p. 1-11
    Abstract: Quantitative and qualitative alterations in the epidermal growth factor receptor (EGFR) commonly occur in many cancers in humans, including malignant gliomas. The aim of the current study was to evaluate molecular and cellular effects of OSI-774, a novel EGFR tyrosine kinase inhibitor, on nine glioblastoma multiforme (GBM) cell lines. Methods The effects of OSI-774 on expression of EGFR messenger (m)RNA and protein, proliferation, anchorage-independent growth, and apoptosis were examined using semiquantitative reverse transcription–polymerase chain reaction, immunocytochemical analysis, Coulter counting, soft agar cloning, and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling/fluorescence-activated cell sorting, respectively. All p53 genes were completely and bidirectionally sequenced. Suppression of anchorage-independent growth by OSI-774 was inversely correlated to the induction of EGFR mRNA during relative serum starvation (r = −0.74) and was unrelated to p53 status. Overall, suppression of anchorage-independent growth was a considerably stronger effect of OSI-774 than inhibition of proliferation. The extent of OSI-774–induced apoptosis positively correlated with both proliferation and anchorage-independent growth of GBM cell lines (r = 0.75 and 0.79, respectively). In a single cell line derived from a secondary GBM, exposure to concentrations of greater than or equal to 1 μmol/L resulted in a substantial net cell loss during proliferation studies. Conclusions The induction of EGFR mRNA may constitute a cellular mechanism to counteract the inhibitory effect of OSI-774 on the anchorage-independent growth of GBM cells. In contrast, no considerable correlation could be established between baseline expression levels of EGFR (both mRNA and protein) in GBM cell lines and their biological response to OSI-774. The OSI-774 induced greater ( p53 -independent) apoptosis in more malignant GBM phenotypes and may be a promising therapeutic agent against secondary GBM.
    Type of Medium: Online Resource
    ISSN: 1092-0684
    URL: Article
    DOI: 10.3171/foc.2004.16.2.12
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2004
    detail.hit.zdb_id: 2026589-X
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  • 4
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    Online Resource
    Candidate genes for sensitivity and resistance of human glioblastoma multiforme cell lines to erlotinib : Laboratory investigation
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2009
    In:  Journal of Neurosurgery Vol. 111, No. 2 ( 2009-08), p. 211-218
    Details
    In: Journal of Neurosurgery, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 111, No. 2 ( 2009-08), p. 211-218
    Abstract: The authors have previously reported that erlotinib, an EGFR tyrosine kinase inhibitor, exerts widely variable antiproliferative effects on 9 human glioblastoma multiforme (GBM) cell lines in vitro and in vivo. These effects were independent of EGFR baseline expression levels, raising the possibility that more complex genetic properties form the molecular basis of the erlotinib-sensitive and erlotinib-resistant GBM phenotypes. The aim of the present study was to determine candidate genes for mediating the cellular response of human GBMs to erlotinib. Methods Complementary RNA obtained in cell lines selected to represent the sensitive, somewhat responsive, and resistant phenotypes were hybridized to CodeLink Human Whole Genome Bioarrays. Results Expression analysis of 814 prospectively selected genes involved in major proliferation and apoptosis signaling pathways identified 19 genes whose expression significantly correlated with phenotype. Functional annotation analysis revealed that 2 genes ( DUSP4 and STAT1 ) were significantly associated with sensitivity to erlotinib, and 10 genes ( CACNG4 , FGFR4 , HSPA1B , HSPB1 , NFATC1 , NTRK1 , RAC1 , SMO , TCF7L1 , and TGFB3 ) were associated with resistance to erlotinib. Moreover, 5 genes ( BDNF , CARD6 , FOSL1 , HSPA9B , and MYC ) involved in antiapoptotic pathways were unexpectedly found to be associated with sensitivity. Gene expressions were confirmed by quantitative polymerase chain reaction. Conclusions Based on an analysis of gene expressions in cell lines with sensitive, somewhat responsive, and resistant phenotypes, the authors propose candidate genes for GBM response to erlotinib. The 10 gene candidates for conferring GBM resistance to erlotinib may represent therapeutic targets for enhancing the efficacy of erlotinib against GBMs. Five additional genes warrant further investigation into their role as putative cotargets of erlotinib.
    Type of Medium: Online Resource
    ISSN: 0022-3085 , 1933-0693
    URL: Article
    DOI: 10.3171/2008.9.JNS08551
    RVK:
    XA 10000
    RVK:
    XA 55270
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2009
    detail.hit.zdb_id: 2026156-1
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  • 5
    Online Resource
    Online Resource
    Characteristics of thoracolumbar intramedullary subependymomas : Clinical article
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2009
    In:  Journal of Neurosurgery: Spine Vol. 10, No. 1 ( 2009-01), p. 54-59
    Details
    In: Journal of Neurosurgery: Spine, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 10, No. 1 ( 2009-01), p. 54-59
    Abstract: Thoracolumbar intraspinal subependymomas are very rare intramedullary low-grade tumors. The authors report on the clinical and morphological features of 2 cases of thoracolumbar intraspinal subependymomas and provide midterm follow-up data. Methods The clinical and radiological profiles of 2 patients with progressive spinal cord dysfunction due to thoracolumbar intraspinal subependymomas were retrospectively studied and compared with previously reported cases. Results Patients with intraspinal subependymomas initially presented with back pain and long-tract signs. The tumors were hyperintense on T2-weighted MR imaging, isointense on T1-weighted imaging, and noncontrast enhancing. Within 1 of the tumors, a medial septum was present on axial T2-weighted imaging. The tumors were intramedullary but grew exophytically and were amenable to gentle surgical separation from normal neural structures. Therefore, gross-total resection was feasible, and neurological outcome was good. No further adjuvant therapy was conducted. On follow-up (at 58 and 18 months, respectively), no tumor recurrence was observed. Conclusions Symptomatic thoracolumbar intraspinal subependymomas with a distinct appearance on MR imaging are amenable to complete excision with favorable neurological outcome. In this study no tumor recurrence was observed at midterm follow-up in either patient, neither of whom underwent adjuvant therapy.
    Type of Medium: Online Resource
    ISSN: 1547-5654
    URL: Article
    DOI: 10.3171/2008.10.SPI08311
    RVK:
    XA 55270.1
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2009
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