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  • American Association for Cancer Research (AACR)  (8)
  • 1
    Online Resource
    Online Resource
    Abstract 3333: Therapeutic efficacy and safety of TRAIL-producing human adipose tissue-derived mesenchymal stem cells against experimental brainstem glioma
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 3333-3333
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 3333-3333
    Abstract: Mesenchymal stem cells (MSCs) have an extensive migratory capacity for gliomas, which is comparable to that of neural stem cells. Among the various types of MSCs, human adipose tissue-derived MSCs (hAT-MSC) emerge as one of the most attractive vehicles for gene therapy because of their high throughput, lack of ethical concerns, and availability and ease of isolation. We evaluated the therapeutic potential and safety of genetically engineered hAT-MSCs encoding the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) against brainstem gliomas. hAT-MSCs were isolated from human fat tissue, characterized, and transfected with TRAIL using nucleofector. The therapeutic potential of TRAIL-producing hAT-MSCs (hAT-MSC.TRAIL) was confirmed using in vitro and in vivo studies. The final fate of injected hAT-MSCs was traced in long-survival animals. The characterization of hAT-MSCs revealed the expression of MSC-specific cell-type markers and their differentiation potential into neuronal lineage. Short-term outcomes included a 56.3% reduction of tumor volume (P & lt; 0.001) with increased apoptosis (3.03-fold, P & lt; 0.05) in animals treated with hAT-MSC.TRAIL compared with the control groups. Long-term outcomes included a significant survival benefit in the hAT-MSC.TRAIL-treated group (26 days of median survival in the control group vs 84 days in the hAT-MSC.TRAIL-treated group, P & lt; 0.0001), without any evidence of mesenchymal differentiation in vivo. Our study demonstrated the therapeutic efficacy and safety of nonvirally engineered hAT-MSCs against brainstem gliomas. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3333.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM10-3333
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 2
    Online Resource
    Online Resource
    Abstract 3056: Combined disulfiram and radiation therapy against atypical teratoid/rhabdoid tumor
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Research Vol. 76, No. 14_Supplement ( 2016-07-15), p. 3056-3056
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 76, No. 14_Supplement ( 2016-07-15), p. 3056-3056
    Abstract: Disulfiram (DSF) has been studied as an anticancer drug and radiosensitizer. In our previous study, the therapeutic potential of DSF against atypical teratoid/rhabdoid tumor (AT/RT), one of the most aggressive forms of childhood cancer, had been confirmed using in vitro and in vivo studies. To develop more effective and safer therapy in AT/RT, we evaluated the sensitizing potential of DSF on radiation therapy (RT). The effect of DSF in low concentration alone and in combination with RT was investigated in vitro and vivo. Clonogenic assay, western blot analysis, autophagy assay and γ-H2AX foci staining were performed using several primary cultured AT/RT cells and cell lines. Also, in vivo study was performed using AT/RT orthotopic xenograft mouse model. Combination therapy with DSF and RT potently reduced clonogenicity and down-regulated protein expression of survivin and BCL2. The combination treatment strongly promoted the autophagic cell death and produced abundant γ-H2AX foci in all AT/RT cells. Moreover, the combination treatment significantly reduced the tumor growth and prolonged the survival rate compared to single treatment in AT/RT mouse model. Taken together, our results demonstrated that the combination therapy with DSF and RT has a synergistic therapeutic effect on AT/RT, suggesting a potential clinical application for AT/RT patients. Citation Format: Yeoung Eun Lee, Seung Ah Choi, Pil Ae Kwak, Kyu-Chang Wang, Ji Hoon Phi, Ji Yeoun Lee, Sangjoon Chong, Youn Joo Moon, Anshika Jangra, Kyeung Min Joo, Seung-Ki Kim. Combined disulfiram and radiation therapy against atypical teratoid/rhabdoid tumor. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3056.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2016-3056
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 3
    Online Resource
    Online Resource
    Abstract 3195: Synergistic effects of combined treatment with hAT-MSC.sTRAIL and panobinostat in brainstem glioma
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Research Vol. 76, No. 14_Supplement ( 2016-07-15), p. 3195-3195
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 76, No. 14_Supplement ( 2016-07-15), p. 3195-3195
    Abstract: Human adipose-derived mesenchymal stem cells expressing secreted form of the tumor necrosis factor-related apoptosis-inducing ligand (hAT-MSC.sTRAIL) have demonstrated therapeutic activity against various tumors. However, sTRAIL resistance remains a challenge in developing anticancer strategies. To solve this problem, many studies have tried to combine drugs to produce synergism or sensitize resistant cancer cells. Histone deacetylase inhibitors (HDACi) have been known to induce expression of TRAIL death receptors 4 and 5 (DR4/DR5). Herein, we evaluated the use of combined therapy of hAT-MSC.sTRAIL with HDAC inhibitor, panobinostat, in enhancing sensitivity to hAT-MSC.sTRAIL mediated apoptosis against the brainstem glioma. A sTRAIL was introduced into the characterized hAT-MSCs using electroporation. To confirm appropriate treatment concentration of panobinostat to the glioblastoma cells, dose titration was tested using cell viability assay. The therapeutic effect of single or combination treatment against glioblastoma was evaluated using primary cultured glioblastoma cells and cell lines. Orthotopic xenograft brainstem glioma mouse model was established using engineered firefly luciferase expressing tumor cells for bioluminescence in vivo imaging. Panobinostat induced anti-proliferative effects in dose and time-dependent manner (IC50 range, 0.05-0.2 μM) and effectively enhanced the expression of TRAIL DR4 and DR5, but not decoy receptors. Combined hAT-MSC.sTRAIL and panobinostat significantly decreased the tumor cell growth compared to each alone. Intriguingly, the combination treatment not only induced apoptosis but also autophagy. Using a preclinical brainstem mouse model, we confirmed that the combination of hAT-MSC.sTRAIL and panobinostat was safe and induced regression of tumor volume. Furthermore, the combination therapy prolonged the survival of brainstem glioma-bearing mice. Our results suggested that combination therapy of panobinostat enhanced the anti-cancer effect of hAT-MSC.sTRAIL and represent potential therapeutic approach to the brainstem glioma. Citation Format: Seung Ah Choi, Chanhee Lee, Pil Ae Kwak, Kyu-Chang Wang, Ji Hoon Phi, Ji Yeoun Lee, Sangjoon Chong, Seung-Ki Kim. Synergistic effects of combined treatment with hAT-MSC.sTRAIL and panobinostat in brainstem glioma. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3195.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2016-3195
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 4
    Online Resource
    Online Resource
    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
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
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  • 5
    Online Resource
    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
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    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 6
    Online Resource
    Online Resource
    Abstract 2649: Human adipose tissue-derived mesenchymal stem cells can target brain tumor initiating cells.
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 8_Supplement ( 2013-04-15), p. 2649-2649
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 8_Supplement ( 2013-04-15), p. 2649-2649
    Abstract: Abstract The discovery of neural stem cells offers paradigm shift in brain tumor research. In neuro-oncology, the biology of neural stem cells has been pursued in two ways: as cancer stem cells to understand the origin and maintenance of brain tumors and as a potential cell-based vehicle for gene therapy. In addition to neural stem cells, mesenchymal stem cells (MSCs) have been reported to possess tumor-tropic migratory capacities. However, there is scanty data on migratory capacity of MSC toward brain tumor initiating cells (BTICs). This study focuses on investigating the ability of human adipose tissue derived MSCs (hAT-MSCs) to target BTICs and their cross-talk in the microenvironment. BTICs were isolated from three different kinds of brain tumors (medulloblastoma, atypical teratoid/rhabdoid tumor (ATRT), glioblastoma). The migration capacities of hAT-MSCs toward BTICs were examined both in vitro transwell assay and in vivo bioluminescence imaging analysis. To investigate the crosstalk between hAT-MSCs and BTICs, various cytokines were analyzed. Using co-culture system of hAT-MSCs and BTICs, we analyzed the mRNA expression patterns of cytokine receptors (CCR2, CCR4, CCR5, CCR7, CCR9, CCR10, XCR1, CXCR1, IL-8R, CXCR4, CX3CR1, IL1R1, IL6R, MET, PDGFRB, KDR, CD44, IFNAR1 and TEK) by qRT-PCR and protein level of their ligand in co-cultured media by Bio-Plex human cytokine ELISA. We confirmed the migratory capacity of t hAT-MSCs toward BTICs in vitro and BTICs-derived xenograft brain tumors in vivo live imaging. mRNA expression of receptors (CCR4, CCR5, CCR10, XCR1, CXCR1, IL-8R, CXCR4, PDGFRB, KDR, CD44, IFNAR1 and TEK) increased two- to eighteen-fold higher levels. The cytokine analysis revealed that the ligand levels of hAT-MSCs (medulloblastoma: VEGF, IL6, IL8, CCL3, CCL2 and TEK; ATRT: VEGF, CCL3 and TEK; glioblastoma: CCL2, PDGF, TEK and IGF1) and the ligand levels BTICs (medulloblastoma: CCL5 and CXCL4; ATRT: IL-8 and CXCL4; glioblastoma: CXCL4 and IGF1) were elevated in the co-cultured media. Our findings demonstrated that hAT-MSCs can target BTICs. Cross-talk between hAT-MSCs cytokine receptor and BTICs ligand (medulloblastoma: CCR5/CCL5 and CXCR4/CXCL4; ATRT: IL-8R/IL-8 and CXCR4/CXCL4; glioblastoma: CXCR4/CXCL4 and IGF1R/IGF1) play cardinal role in this process. Citation Format: Seung Ah Choi, Kyu-Chang Wang, Ji Hoon Phi, Ji Yeoun Lee, Jung Won Choi, Hyung Ah Kim, Se Hee Kim, Yong Hwy Kim, Sung Eun Kwon, Young-Hoon Kim, Seung-Ki Kim. Human adipose tissue-derived mesenchymal stem cells can target brain tumor initiating cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2649. doi:10.1158/1538-7445.AM2013-2649
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2013-2649
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 7
    Online Resource
    Online Resource
    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
    detail.hit.zdb_id: 410466-3
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  • 8
    Online Resource
    Online Resource
    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
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
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