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Thelial cells. Suppression of pancreatic cancer cell growth by Triphala in our model was due to induction of apoptosis, which in turn was associated with generation of ROS. Pretreatment of Capan-2 cells with antioxidant NAC blocked ROS generation and completely protected the cells from Triphalainduced apoptosis. Our results also demonstrate that Triphala treatment caused DNA damage resulting in th
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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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Wski B, Glaspy JA, Comin-Anduix B, et al: Reversing melanoma cross-resistance to BRAF and MEK inhibitors by co-targeting the AKT/mTOR pathway. PLoS One 2011, 6:e28973. Prahallad A, Sun C, Huang S, Di Nicolantonio F, Salazar R, Zecchin D, Beijersbergen RL, Bardelli A, Bernards R: Unresponsiveness of colon cancer to BRAF(V600E) inhibition through feedback activation of EGFR. Nature 2012, 483:100?03.
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Xposed for varying time points to TAK733. A) The sensitive BRAFV600E mutated cutaneous melanoma cell line M229; B) The resistant BRAFV600E mutated cutaneous melanoma cell line M233.Cell proliferation and viability assaysMelanoma cell lines were treated with TAK-733 or parallel DMSO vehicle control at the given concentrations for 72 hours. Cell viability was measured using a tetrazolium compound [3
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Thotopically xenografted into the brains of immunocompromized mice. Invasive cells at the tumor periphery were isolated using laser capture microdissection. The mRNA expression profile of these cells was compared to expression at the tumor core, using normal mouse brain to control for host contamination. Galectin-1, a target identified by screening the resulting data, was stably over-expressed in
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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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Thotopically xenografted into the brains of immunocompromized mice. Invasive cells at the tumor periphery were isolated using laser capture microdissection. The mRNA expression profile of these cells was compared to expression at the tumor core, using normal mouse brain to control for host contamination. Galectin-1, a target identified by screening the resulting data, was stably over-expressed in
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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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