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S N1) 65+ Years at Diagnosis Male Moderately Differentiated Poorly Differentiated Non-Palliative Radiation White AsianaHazard Ratio 1.611 Hazard Ratio 2.146 3.783 2.834 1.893 1.550 1.233 1.014 0.a95 Confidence Limits 1.057?.457 95 Confidence Limits 1.341?.434 2.089?.852 1.584?.069 1.206?.972 1.018?.359 0.821?.851 0.580?.772 0.508?.356 0.370?.231 0.288?.298 0.268?.p value 0.0.0014
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Xpressing tumors, patients did not show any difference in survival when stratified by resection status whereas patients with high CNKSR1 expression levels who underwent resection had significantly improved outcome compared to non-resected patients in this group. Combination of CNKSR1 expression levels with current clinicopathological prognostic features might improve risk stratification and treatm
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Yolk removal. Embryos with yolk (Y) were analysed in comparison with embryos after one-step deyolking (D) or after two additional wash steps (W). A. Total protein amount per embryo as determined by DC protein assay (Bio-Rad). B. Coomassie stain (0.5 embryos loaded per lane). C. Western blot against Tubulin and MEK (0.5 embryos loaded per lane). While yolk proteins were efficiently depleted, recove
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Esults. Embryos at high stage (3 1/3 hpf), 50 epiboly (5 1/4 hpf), 70 epiboly (7 hpf) and tailbud stage (10 hpf) were deyolked, separated by SDS-gel electrophoresis and Coomassie stained (A) or blotted and immunodetected with antibodies against Tubulin (55 kD) and Moesin (78/80 kD apparent molecular weight) (B). Note that total protein amount was lower in deyolked samples, therefore more embryos
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Esults. Embryos at high stage (3 1/3 hpf), 50 epiboly (5 1/4 hpf), 70 epiboly (7 hpf) and tailbud stage (10 hpf) were deyolked, separated by SDS-gel electrophoresis and Coomassie stained (A) or blotted and immunodetected with antibodies against Tubulin (55 kD) and Moesin (78/80 kD apparent molecular weight) (B). Note that total protein amount was lower in deyolked samples, therefore more embryos
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Ble cross-hybridizing host genes. The use of our animal model to identify mediators of glioma invasion has the potential pitfall of identifying artifacts of xenografting. That is, human glioma cells confronted with nude mouse brain rather than human brain may express genes specific to this setting. Two arguments can be made against this theory. First, there is no teleological reason for human cell
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Ioblastoma in general. In conclusion, the orthotopic glioblastoma xenograft model recapitulates not only the invasive phenotype, but also the regional expression profile reported in human samples of glioblastoma multiforme. The value of the model (i.e., abundant tissue, high-quality RNA, andToussaint et al. Molecular Cancer 2012, 11:32 http://www.molecular-cancer.com/content/11/1/Page 10 ofFigure
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R 100 mg/kg Triphala 5 times a week. Our results are consistent with previous studies where Triphala was shown to be effective in suppressing the growth ofPage 10 of(page number not for citation purposes)BMC Cancer 2008, 8:http://www.biomedcentral.com/1471-2407/8/.' .' .' .'0 0.5 1 2 4of cells with DCF fluorescenceS (5. 7KU 7U SS 6HU16 12 8 43 53 FOHDYHGFWLQTPL treatment (hours)1 P0 73/ J PO0.'