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He AMPK agonist AICAR inhibits the growth of EGFRvIII-expressing glioblastomas by inhibiting lipogenesis. Proc Natl Acad Sci U S A 2009, 106:12932?2937.doi:10.1186/1476-4598-11-22 Cite this article as: Euw et al.: Antitumor effects of the investigational selective MEK inhibitor TAK733 against cutaneous and uveal melanoma cell lines. Molecular Cancer 2012 11:22.Submit your next manuscript to BioMed
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Ed migration and invasion in vitro. In vivo, tumors expressing high galectin-1 levels showed enhanced invasion and decreased host survival. Conclusions: In conclusion, cells at the margin of glioblastoma, in comparison to tumor core cells, have enhanced expression of mediators of invasion. Galectin-1 is likely one such mediator. Previous studies, along with the current one, have proven galectin-1
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Ed migration and invasion in vitro. In vivo, tumors expressing high galectin-1 levels showed enhanced invasion and decreased host survival. Conclusions: In conclusion, cells at the margin of glioblastoma, in comparison to tumor core cells, have enhanced expression of mediators of invasion. Galectin-1 is likely one such mediator. Previous studies, along with the current one, have proven galectin-1
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Nium Pharmaceuticals, Inc., the manufacturer of TAK733. Acknowledgements This work was funded by The Seaver Institute, the Melanoma Research Foundation, the Melanoma Research Alliance, the Louise Belley and Richard Schnarr Fund, the Wesley Coyle Memorial Fund, the Garcia-Corsini Family Fund, the Keiter Family Foundation and the Caltech-UCLA Joint Center for Translational Medicine (all to A.R.). Au
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Orithm. Galectin-1 was ranked at the top of this list. We thus took advantage of our own patient-derived glioblastoma xenograft model [25] in order to further decipher the roles of galectin-1 on GBM cell migration features. The system we have developed mitigates the effect of three important confounders from human samples. First, tissue is frozen within one minute of removal, ensuring high quality
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Genetic alterations in melanoma. N Engl J Med 2005, 353:2135?147. 4. Van Raamsdonk CD, Bezrookove V, Green G, Bauer J, Gaugler L, O'Brien JM, Simpson EM, Barsh GS, Bastian BC: Frequent somatic mutations of GNAQ in uveal melanoma and blue naevi. Nature 2009, 457:599?02. 5. Van Raamsdonk CD, Griewank KG, Crosby MB, Garrido MC, Vemula S, Wiesner T, Obenauf AC, Wackernagel W, Green G, Bouvier N, et al
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Thur GA, Hutson TE, Moschos SJ, Flaherty KT, et al: Survival in BRAF V600mutant advanced melanoma treated with vemurafenib. N Engl J Med 2012, 366:707?14. Lin WM, Baker AC, Beroukhim R, Winckler W, Feng W, Marmion JM, Laine E, Greulich H, Tseng H, Gates C, et al: Modeling genomic diversity and tumor dependency in malignant melanoma. Cancer Res 2008, 68:664?73. Haigis KM, Kendall KR, Wang Y, Cheung
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Les, CA, USA. 5 Millennium Pharmaceuticals, Inc., Cambridge, MA, USA. 6Division of Hematology-Oncology, 11?34 Factor Building, UCLA Medical Center, 10833 Le Conte Avenue, Los Angeles, CA 90095-1782, USA.Western blottingWestern blotting was performed as previously described [31]. Primary antibodies included pAkt (Ser473), pAkt (Thr308), Akt, pS6K (Thr389), S6K, pS6 (Ser235/236), S6, pMEK (Ser217/22