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Patients for individualized clinical decision-making would fill an unmet clinical need. Activating somatic KRAS mutations are nearly omnipresent and a hallmark in the genetic make-up of pancreatic ductal adenocarcinoma (PDAC) [5]. While KRAS mutations themselves have been associated as prognostic markers, there is considerable and significant heterogeneity in the activation states of the downstrea
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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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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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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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Eration, Migration, Invasion, Galectin-Backgound In spite of recent advances in the treatment of patients with glioblastoma, the prognosis for those afflicted remains poor. Even when these tumors harbor a favorable gene methylation profile, the newest standard of care, including temozolomide as a chemotherapeutic [1],* Correspondence: Gtoussaint@medicine.tamhsc.edu 1 The Texas Brain and Spine Inst
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M solution and washed by Perm/Wash buffer according to fixation and pereabilization method recommended by BD bioscience, and then stained in sterile PBS containing 1.0 albumin bovine serum, 0.1 Nonidet P-40 (Sigma-Aldrich) and 3 M DAPI (4',6-diamidino-2-phenylindole). Flow cytometry was analyzed using FlowJo (Tree Star Inc, Asland, OR).Competing interests Erika von Euw, Mohammad Atefi, Narsis At
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Id tumors. J Clin Oncol 2010, 28:611s. Hall-Jackson CA, Eyers PA, Cohen P, Goedert M, Boyle FT, Hewitt N, Plant H, Hedge P: Paradoxical activation of Raf by a novel Raf inhibitor. Chem Biol 1999, 6:559?68. Su F, Viros A, Milagre C, Trunzer K, Bollag G, Spleiss O, Reis-Filho JS, Kong X, Koya RC, Flaherty KT, et al: RAS mutations in cutaneous squamous-cell carcinomas in patients treated with BRAF in

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