Accès ouvert déclaré
2013
article
ANGIOGENESIS AND INVASION
H. Abuhusain, A. Matin, Q. Qiao, Huming Shen, B. Daniels, M. Laaksonen, C. Teo, A. Don, K. McDonald, A. Jahangiri, M. De Lay, Kate Lu, C. Park, S. Carbonell, G. Bergers, M. K. Aghi, M. Anand, C. Tucker-Burden, J. Kong, D. J. Brat, E. Bae, L. Smith, G. Muller-Greven, R. Yamada, M. Nakano-Okuno, X. Feng, D. Hambardzumyan, I. Nakano, C. L. Gladson, M. Berens, S. Jung, S. Kim, J. Kiefer, J. Eschbacher, H. Dhruv, K. Vuori, C. Hauser, R. Oshima, D. Finlay, P. Aza-Blanc, M. Bessarabova, Y. Nikolsky, D. Emig, L. Rivera, J. Chang, K. Burrell, S. Singh, R. Hill, G. Zadeh, C. Li, Yuxia Chen, X. Mei, K. Sai, Zhongqun Chen, J. Wang, M. Wu, P. Marsden, S. Das, E. Eskilsson, K. M. Talasila, G. V. Rosland, L. Leiss, H. S. Saed, N. Brekka, Per Øystein Sakariassen, M. Lund-Johansen, P. O. Enger, R. Bjerkvig, H. Miletic, Verena Gawrisch, Maike Rüttgers, P. Weigell, E. Kerkhoff, M. Riemenschneider, U. Bogdahn, A. Vollmann-Zwerenz, P. Hau, T. Ichikawa, M. Onishi, K. Kurozumi, T. Maruo, K. Fujii, J. Ishida, Y. Shimazu, T. Oka, E. A. Chiocca, I. Date, R. Jain, B. Griffith, Kassan- Dra Khalil, L. Scarpace, T. Mikkelsen, S. Kalkanis, L. Schultz, S. Jalali, C. Chung, W. Foltz, C. Jiang, H. Wang, N. Kijima, N. Hosen, N. Kagawa, N. Hashimoto, Y. Chiba, M. Kinoshita, H. Sugiyama, T. Yoshimine, R. Klank, S. Decker, C. Forster, M. Price, K. SantaCruz, J. McCarthy, J. Ohlfest, D. Odde, B. Kaur, Y. Huang, Q. Lin, H. Mao, Y. Wang, M. Kogiso, P. Baxter, C. Man, Z. Wang, Yingling Zhou, X.-N. Li, J. Liang, Y. Piao, J. de Groot, Shannon McDonell, V. Henry, L. Holmes, Signe Regner Michaelsen, M.-T. Stockhausen, S. Poulsen, R. Jahedi, F. Azuaje, D. Stieber, S. Foerster, J. Varughese, Christian Ritter, Simone P. Niclou, A. Soentgerath, P. Euskirchen, P. C. Huszthy, L. Prestegarden, Kai Ove Skaftnesmo, O. Keunen, J. Nigro, Olav Karsten Vintermyr, S. Mork, Nandhu Mohan-Sobhana, B. Hu, J. De Jesus, B. Hollingsworth, M. Viapiano, C. Carlin, C. Gladson, M. Nakada, T. Furuta, H. Sabit, Y. Chikano, Y. Hayashi, H. Sato, T. Minamoto, J.-i. Hamada, F. Fack, H. Espedal, N. Obad, E. Gotlieb, S. Bougnaud, A. Golebiewska, A. Oudin, Nicolaas H. C. Brons, P. O'Halloran, T. Viel, K. Schwegmann, L. Wachsmuth, S. Wagner, K. Kopka, P. Dicker, C. Faber, M. Jarzabek, S. Hermann, M. Schafers, Dianne O’Brien, J. Prehn, A. Jacobs, A. Byrne, S. Inoue, L. S. Olsen, M. Stockhausen, H. S. Poulsen, K. H. Plate, A. Scholz, R. Henschler, P. Baumgarten, P. Harter, M. Mittelbronn, D. Dumont, Y. Reiss, S. Rahimpour, C. Yang, J. Frerich, Z. Zhuang, D. Renner, F. Jin, I. Parney, A. Johnson, R. Rockne, A. Hawkins-Daarud, J. Jacobs, Cam Bridge, M. Mrugala, J. Rockhill, K. Swanson, H. Schneider, E. Szabo, K. Seystahl, M. Weller, Y. Takahashi, M. Ouchida, Kohei Fuji, M. Umakoshi, Hun Ju Sim, Paul Gruenbacher, L. Jakeman, J. J. Parker, K. Dionne, P. Canoll, B. DeMasters, A. Waziri
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11Institutions déclarées
3Pays d’affiliation déclarés
Rattachement africain : us, jp, au.
Niveau de preuve : code pays fourni par la source.
Le résumé fourni par la source
INTRODUCTION: Recently, anti-angiogenic therapies have moved into the forefront of GBM targeted therapies, especially following the success of anti-VEGF treatment in increasing progression-free survival and quality of life for patients.However, with the recurrence of GBMs, anti-VEGF treatment seems insufficient at blocking glioma induced angiogenesis single-handedly.Sphingosine-1-phosphate (S1P), a known pro-angiogenic lipid molecule formed by the enzyme sphingosine kinase 1 (Sphk1), has been shown to contribute to breast cancer induced angiogenesis.High SphK1 expression has been shown in two independent studies to predict an unfavorable prognosis in GBM.S1P data in GBM and its role in angiogenesis is limited, therefore requires further research.METHODS: We assessed the levels of SphK1 and S1P in normal grey matter (n ¼ 20), diffuse astrocytomas (n ¼ 26), anaplastic astrocytomas (n ¼ 10), and GBM (n ¼ 20) tissue samples using quantitative PCR and liquid chromatography-mass spectrometry (LC-MS), respectively.Cell based assays examining angiogenesis were performed, targeting SphK1 with siRNA and selective SphK1 inhibitors, including a stereoisomer control.An independent cohort of 50 GBM tissue samples, 35 matched GBM plasma samples, and 20 normal plasma samples were analyzed for S1P using LC-MS, and correlated with patient survival.RESULTS: S1P levels increased, alongside SphK1 expression, as glioma grade increased and compared to normal tissue.Knockdown of SphK1 with siRNA and inhibitor, but not stereoisomer control, affected U87MG induced angiogenesis for HMEC-1 cell lines significantly.S1P in GBM tissue was elevated in short term survivors, but not statistically significant.However, S1P in GBM plasma was elevated compared to normal plasma, and correlated with survival outcome.CONCLUSIONS: S1P is significantly elevated in GBM, a highly vascular tumor, and contributes to U87MG induced angiogenesis independent of VEGF in a cell based assay.The potential role of S1P as a marker for survival requires further validation.However, S1P shows exciting potential as an antiangiogenic target.
Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.
Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- ANGIOGENESIS AND INVASION
- Date Crossref
- 01/11/2013
- Éditeur
- Oxford University Press (OUP)
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Les institutions déclarées
Une affiliation ne permet pas de déduire la nationalité d’un auteur.
Les sujets associés
Sphingolipid Metabolism and SignalingAngiogenesis and VEGF in CancerCaveolin-1 and cellular processes