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  • 1
    Online Resource
    Online Resource
    Genomic analysis reveals secondary glioblastoma after radiotherapy in a subset of recurrent medulloblastomas
    Springer Science and Business Media LLC ; 2018
    In:  Acta Neuropathologica Vol. 135, No. 6 ( 2018-6), p. 939-953
    Details
    In: Acta Neuropathologica, Springer Science and Business Media LLC, Vol. 135, No. 6 ( 2018-6), p. 939-953
    Type of Medium: Online Resource
    ISSN: 0001-6322 , 1432-0533
    URL: Article
    DOI: 10.1007/s00401-018-1845-8
    RVK:
    XA 10000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2018
    detail.hit.zdb_id: 1458410-4
    detail.hit.zdb_id: 1079-0
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  • 2
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    Abstract 5513: Targeting brain tumor initiating cells in atypical teratoid/rhabdoid tumors: Aldehyde dehydrogenase inhibition with disulfiram
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 5513-5513
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 5513-5513
    Abstract: Atypical teratoid/rhabdoid tumors (AT/RT) are one of the most malignant pediatric brain tumors with a dismal prognosis. Cells with high aldehyde dehydrogenase (ALDH) activity from brain tumors have a number of characteristics that are expected of brain tumor initiating cells (BTICs). This study aimed to evaluate the therapeutic potential of ALDH inhibition using disulfiram (DSF) against BTICs from AT/RT. Primary cultured BTICs from AT/RT were stained with Aldefluor and isolated by fluorescence activated cell sorting. Therapeutic effect of DSF against BTICs from AT/RT was confirmed using in vitro and in vivo studies. AT/RT showed high expression of ALDH. DSF significantly inhibited ALDH enzyme activity of AT/RT cells. DSF decreased self-renewal ability, cell viability, proliferation potential and induced apoptosis and cell cycle arrest on ALDH+ AT/RT cells. DSF showed more potent cytotoxic effect to ALDH+ AT/RT cells compared to standard anti-cancer agents including ifosfamide, carboplatin and etoposide. Importantly, DSF reduced metabolite (metabolism?) of ALDH+ AT/RT cells by increasing NAD+ ratio and regulating SIRT1, NF-κB, Lin28A/B and miRNA let-7g. Notably, treatment with DSF did not have considerable effect on the normal neural stem cells and fibroblasts. Animals in the DSF-treated group demonstrated a significant survival benefit (105 days of median survival in the DSF-treated group versus 91 days in the control group, p = 0.0219). Our study demonstrated the therapeutic potential of DSF against BTICs from AT/RT and suggested the possibility of ALDH inhibition for clinical application. Note: This abstract was not presented at the meeting. Citation Format: Seung Ah Choi, Jung Won Choi, Kyu-Chang Wang, Ji Hoon Phi, Ji Yeoun Lee, Yong Hwy Kim, Young-Hoon Kim, Sung-Hye Park, Seung-Ki Kim. Targeting brain tumor initiating cells in atypical teratoid/rhabdoid tumors: Aldehyde dehydrogenase inhibition with disulfiram. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 5513. doi:10.1158/1538-7445.AM2014-5513
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2014-5513
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
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  • 3
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    Abstract 5326: ID3 contributes to cerebrospinal fluid seeding and poor prognosis of medulloblastoma
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 5326-5326
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 5326-5326
    Abstract: Seeding of medulloblastoma is the most influential prognostic factor for survival, but little has been known about the molecular mechanism of seeding in medulloblastoma. Inhibitor of differentiation (ID) genes are implicated as promoter of tumor progression and metastasis in many human cancers. We investigated the expression and functional roles of ID genes in terms of seeding and prognosis of medulloblastoma. Significantly higher ID3 expression was observed in medulloblastoma with seeding than in tumors without seeding. In vitro studies using D283 medulloblastoma cells and ID3-siRNA showed that ID3 knockdown resulted in decreased proliferation, enhanced apoptosis, and suppressed migration. We made a seeding model of medulloblastoma in mice and injected a stable cell line with ID3 knockdown with shRNA. ID3 knockdown in vivo inhibited growth of primary tumor and development of leptomeningeal seeding and prolonged survival of animals compared with controls. A mRNA mini-array revealed that ID3 knockdown leads to up-regulation (TIMP3, ITGB4, COL12A1, ADAMTS8) and down-regulation (TNC, CTGF, ICAM1) of several genes related to cellular invasion and migration. High ID3 expression was associated with poor survival of patients with medulloblastoma as with seeding at presentation. These findings indicated that ID3 plays an important role in seeding of medulloblastoma and may be a target of therapeutic intervention for enhancing survival of the patients in the poor-prognostic group. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5326. doi:1538-7445.AM2012-5326
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-5326
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
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  • 4
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    Smooth-muscle progenitor cells isolated from patients with moyamoya disease: novel experimental cell model : Laboratory investigation
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2014
    In:  Journal of Neurosurgery Vol. 120, No. 2 ( 2014-02), p. 415-425
    Details
    In: Journal of Neurosurgery, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 120, No. 2 ( 2014-02), p. 415-425
    Abstract: Moyamoya disease (MMD) is a cerebrovascular occlusive disease affecting bilateral internal carotid termini. Smooth-muscle cells are one of the major cell types involved in this disease process. The characteristics of circulating smooth-muscle progenitor cells (SPCs) in MMD are poorly understood. The authors purified SPCs from the peripheral blood of patients with MMD and sought to identify differentially expressed genes (DEGs) in SPCs from these patients. Methods The authors cultured and isolated SPCs from the peripheral blood of patients with MMD (n = 25) and healthy control volunteers (n = 22). After confirmation of the cellular phenotype, RNA was extracted from the cells and DEGs were identified using a commercially available gene chip. Real-time quantitative reverse transcription polymerase chain reaction was performed to confirm the putative pathogenetic DEGs. Results The SPC-type outgrowth cells in patients with MMD invariably showed a hill-and-valley appearance under microscopic examination, and demonstrated high α–smooth muscle actin, myosin heavy chain, and calponin expression (96.5% ± 2.1%, 42.8% ± 18.6%, and 87.1% ± 8.2%, respectively), and minimal CD31 expression (less than 1%) on fluorescence-activated cell sorter analysis. The SPCs in the MMD group tended to make more irregularly arranged and thickened tubules on the tube formation assay. In the SPCs from patients with MMD, 286 genes (124 upregulated and 162 downregulated) were differentially expressed; they were related to cell adhesion, cell migration, immune response, and vascular development. Conclusions With adequate culture conditions, SPCs could be established from the peripheral blood of patients with MMD. These cells showed specific DEGs compared with healthy control volunteers. This study provides a novel experimental cell model for further research of MMD.
    Type of Medium: Online Resource
    ISSN: 0022-3085 , 1933-0693
    URL: Article
    DOI: 10.3171/2013.9.JNS131000
    RVK:
    XA 10000
    RVK:
    XA 55270
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2014
    detail.hit.zdb_id: 3089-2
    detail.hit.zdb_id: 2026156-1
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  • 5
    Online Resource
    Online Resource
    Identification of brain tumour initiating cells using the stem cell marker aldehyde dehydrogenase
    Elsevier BV ; 2014
    In:  European Journal of Cancer Vol. 50, No. 1 ( 2014-01), p. 137-149
    Details
    In: European Journal of Cancer, Elsevier BV, Vol. 50, No. 1 ( 2014-01), p. 137-149
    Type of Medium: Online Resource
    ISSN: 0959-8049
    URL: Article
    DOI: 10.1016/j.ejca.2013.09.004
    RVK:
    XA 42017.A
    RVK:
    XA 42017
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2014
    detail.hit.zdb_id: 1120460-6
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  • 6
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    Abstract 3318: A distinct subpopulation within CD133 positive brain tumor cells shares characteristics with endothelial progenitor cells
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 3318-3318
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 3318-3318
    Abstract: The cell surface marker CD133 was proposed as a brain tumor stem cell marker. However there have been substantial controversies regarding the necessity and role of CD133 in tumorigenesis. This study aimed to characterize CD133 positive cells in brain tumors. Fresh human brain tumor specimens and whole blood were collected from the same patients [medulloblastoma (N=6), glioblastoma (N=4), ependymoma (N=1), and atypical teratoid/rhabdoid tumor (ATRT, N=2)]. Dual FACS staining for CD133/CD34, functional assay of CD133 positive cells from different origin for tumorigenesis and angiogenesis were done. We also investigated the in vivo tumorigenic potential and histological characteristics of four distinct groups on the basis of expression of CD133/CD34 markers (CD133+, CD133+/CD34+, CD133+/CD34-, and CD133-). CD133 positive brain tumor cells coexpressed significantly higher positivity for CD34 (67.97 ± 5.34 % in CD133 (+) cells vs. 11.96 ± 1.48 % in CD133 (−) cells, P & lt;0.001). CD133 positive brain tumor cells formed neurosphere-like spheroids and differentiated into multiple nervous system lineages contrary to CD133 positive blood cells. Furthermore they showed biological characteristics of endothelial cells including vWF expression, LDL uptake and tube formation in vitro, unlike CD133 negative brain tumors cells. Pathologic analysis of the brains implanted with CD133+ glioma cells showed large, highly proliferative and vascular tumors with widespread necrosis and hemorrhage. Notably pure BTSC (CD133+/CD34-) or EPC (CD133+/CD34+) fraction alone did not generate tumor. Our data suggest the presence of a distinct subpopulation of CD133 positive cells isolated from human brain tumors, with characteristics of EPCs. Therefore, interpreting the results of experiments carried out with “CD133-positive BTSCs” should be extrapolated with caution. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3318. doi:10.1158/1538-7445.AM2011-3318
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-3318
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
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  • 7
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    Online Resource
    Abstract 5343: Identification of brain tumor initiating cells using the stem cell marker aldehyde dehydrogenase 1
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 5343-5343
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 5343-5343
    Abstract: Aldehyde dehydrogenase 1 (ALDH1) has been identified in stem cells from both normal and cancerous tissue. This study aimed to evaluate the potential of ALDH1 as a universal brain tumor initiating cell (BTIC) marker applicable to primary brain tumors and their biological role in maintaining stem cell status. Cells from various primary brain tumors (24 pediatric and 6 adult brain tumors) were stained with Aldefluor and sorted by flow cytometry. We investigated the impact of ALDH1 expression on BTIC characteristics in vitro and on tumorigenic potential in vivo. Primary cultured brain tumor cells showed universal expression of ALDH1, with 0.3 to 28.9% of the cells in various tumors identified as ALDH1+. ALDH1+ cells generate neurospheres with high proliferative potential, express neural stem cell markers (nestin and musashi) and differentiate into multiple nervous system lineages. ALDH1+ cells are phenotypically distinct from CD133+ cells, and they show high expression of induced pluripotent stem cell-related genes. Notably, targeted knockdown of ALDH1 by shRNA interference in BTICs potently disturbed their self-renewing ability. After three months, ALDH1+ cells gave rise to tumors in 93% of mice whereas ALDH1- cells did not. The characteristic pathology of mice brain tumors from ALDH1+ cells was similar to that of human brain tumors, and these cells are highly proliferative in vivo. Our data suggest that primary brain tumors contain distinct subpopulations of cells that have high expression levels of ALDH1 and BTIC characteristics. ALDH1 might be a potential therapeutic target applicable to primary brain tumors. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5343. doi:1538-7445.AM2012-5343
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-5343
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
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  • 8
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    Online Resource
    Congenital solitary infantile myofibromatosis involving the spinal cord : Case report
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2013
    In:  Journal of Neurosurgery: Pediatrics Vol. 11, No. 1 ( 2013-01), p. 82-86
    Details
    In: Journal of Neurosurgery: Pediatrics, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 11, No. 1 ( 2013-01), p. 82-86
    Abstract: Infantile myofibromatosis, a rare mesenchymal disorder that develops in early childhood, is classified by the number of lesions that occur: solitary or multicentric. Involvement of the CNS is unusual in either type. Infantile myofibromatosis in the spine is exceptional, and most published cases represent a secondary invasion. Here, the authors report on an 8-month-old girl presenting with weakness below the ankle and an intraspinal mass extending from T-6 to the conus. The patient underwent only partial surgical removal of the lesion, and the pathology was confirmed as infantile myofibromatosis. After the operation, weakness in the lower extremities gradually improved; however, she could not walk at the time of the final follow-up. On follow-up MRI performed 19 months after the operation, the residual lesion remained unchanged with decreased enhancement.
    Type of Medium: Online Resource
    ISSN: 1933-0707 , 1933-0715
    URL: Article
    DOI: 10.3171/2012.9.PEDS12245
    RVK:
    XA 55270.2
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2013
    detail.hit.zdb_id: 2403990-1
    detail.hit.zdb_id: 2403985-8
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  • 9
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    Abstract 3450: Growth-inhibitory effect of neurotrophin-3-secreting adipose tissue-derived mesenchymal stem cells on the D283-MED human medulloblastoma cell line
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 3450-3450
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 3450-3450
    Abstract: Medulloblastoma (MBL), the most common malignant pediatric brain tumor, is incurable in about one-third of patients and can lead to long-term disabilities despite current multimodal treatments. We evaluate the in vitro, growth-inhibitory effect of neurotrophin-3 (NT-3)-secreting stem cells on an MBL cell line and propose that this cell therapy may have therapeutic effects for MBL. NT-3-secreting stem cells were produced by nucleofecting pIRES2.EGFP-NT3 into human adipose tissue-derived mesenchymal stem cells (hAT-MSCs). Double-layered co-culture experiments with the NT-3-secreting hAT-MSCs and D283-MED MBL cells were performed, and NT-3-induced apoptosis was studied by the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) test. The growth-inhibitory effects of these stem cells on human MBL in vitro were confirmed by 3-(4, 5-dimethylathiazol-2-yl)-2, 5-dephenyl-tetrazolium bromide (MTT) assay. We confirmed by western blotting that D283-MED cells express tyrosine kinase C, a specific receptor for NT-3, and we showed by fluorescence microscopy and RT-PCR that transfected hAT-MSCs express NT-3. The double-layered co-culture of D283-MED with NT-3-secreting hAT-MSCs induced a concentration-dependent increase in apoptosis in the tumor cell line. Consequently, the high concentrations of NT-3-secreting hAT-MSCs significantly (P & lt; 0.001) increased the death of D283-MED cells in vitro. The present studies demonstrate the potential of NT-3-secreting hAT-MSCs as an effective therapeutic cell therapy for human MBL in vitro, but in vivo experiments and clinical studies will be required in the future. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3450. doi:10.1158/1538-7445.AM2011-3450
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-3450
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
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  • 10
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    Abstract 3107: The role of LIN28 in atypical teratoid rhabdoid tumor (ATRT) pathogenesis
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 3107-3107
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 3107-3107
    Abstract: Atypical teratoid rhabdoid tumor (ATRT) is a highly malignant brain tumor developing almost exclusively in children. It belongs to the embryonal brain tumor group which consists of primitive tumors recapitulating early embryogenesis of nervous system. It is known that loss of INI protein expression is the hallmark of ATRT pathogenesis. LIN28 is a key gene in embryonic development and maintenance of pluripotency in stem cells. Considering the primitive nature and young age onset of ATRT, LIN28 may be an important co-player in ATRT pathogenesis. We explored the expression and functional role of LIN28 in ATRT. In tumor tissues, LIN28 is highly expressed in ATRT compared with medulloblastomas, another embroynal tumor, whereas primary let-7 microRNA is down-regulated in ATRT. ATRT also showed higher expression of CCND1 and MYC and lower expression of CDKN1C. Knockdown of LIN28 with siRNA in ATRT cell lines resulted decreased cell viability, proliferation, and migration capability. Suppression of CCND1 and MYC expression and enhanced expression of CDKN1C were also observed. Knockdown of LIN28 lead to decreased expression of other pulripotency genes (OCT4 and NANOG) and signature of mesenchymal-epithelial transition was observed after suppression of LIN28. We then introduced wild-type INI1 into ATRT cells by transfection. Restoration of INI in ATRT cell lines lead to decreased expression of LIN28 and CCND1. These results showed that LIN28 is regulated by INI1 and that loss of INI1 protein in ATRT results in unopposed expression of LIN28 and related oncogenes such as CCND1, leading to tumorigenesis. Therefore, the strategic role of LIN28 in ATRT may be utilized as an important therapeutic target. Citation Format: Ji Hoon Phi, Seung Ah Choi, Yong Hwy Kim, Young-Hoon Kim, Chul-Kee Park, Kyu-Chang Wang, Seung-Ki Kim. The role of LIN28 in atypical teratoid rhabdoid tumor (ATRT) pathogenesis. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3107. doi:10.1158/1538-7445.AM2014-3107
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2014-3107
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
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