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Ns including phosphorylation of select sites of CNKSR1, appears in line with our findings of a correlation between the cellular distribution of CNKSR1 and nuclear p-ERK expression levels [30].Fig. 8 Cellular distribution of CNKSR1 is associated with p-ERK expression levels in pancreatic cancer specimens. a p-ERK cellular distribution and nuclear expression levels (scored as 1+, 2+, and 3+) in 86 c
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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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Ning (scored by 0, 1+, 2+, and 3+ intensity levels) compared to pancreatic cancers with cytoplasmic CNKSR1 staining only (Mann Whitney U test; 2-tailed). d Cytoplasmic CNKSR1 expression levels (scored semiquantitatively as 0, 1+, 2+, and 3+) and nuclear p-ERK expression levels (scored as positive cells) (Pearson's correlation coefficient test; 2-tailed). e Kaplan-Meier survival analysis of pancr
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Eased DTEC and reduction in TRDEC. To prove these statements, we have tested some biophysical characteristics as indices of collagen content of the regenerated tissues at 120 DPI. Compared to the ICTs, the ITTs had a higher dry matter content. They also showed almost similar patterns of water delivery and water uptake characteristics with their normal contralateral tendons. This bio-implant was no
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Ada L, Mirantes C, Santacana M, Pallares J, Macia A, Yeramian A, Encinas M, et al. KSR1 is Overexpressed in endometrial carcinoma and regulates proliferation and TRAIL-induced apoptosis by modulating FLIP levels. Am J Pathol. 2011;178(4):1529?3. 15. Wang L, Jiang CF, Li DM, Ge X, Shi ZM, Li CY, Liu X, Yin Y, Zhen LL, Liu LZ, et al. MicroRNA-497 inhibits tumor growth and increases chemosensitivity
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Action of the tumor [22,36]. Indeed, abrogating galectin-1 expression renders tumor cells more susceptible to temozolamide treatment [22,41]. Finally, galectin-1 induces apoptosis of activated T-cells [42-46], prevents host animals from mounting tumor vaccine-induced immunity [47], and may cooperate with TGF-beta in GBM-induced immunosuppression [48,49]. In sum, galectin-1 expression may inversely
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Action of the tumor [22,36]. Indeed, abrogating galectin-1 expression renders tumor cells more susceptible to temozolamide treatment [22,41]. Finally, galectin-1 induces apoptosis of activated T-cells [42-46], prevents host animals from mounting tumor vaccine-induced immunity [47], and may cooperate with TGF-beta in GBM-induced immunosuppression [48,49]. In sum, galectin-1 expression may inversely
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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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