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Rotein expression levels in pancreatic tumors compared to matched, uninvolved controls (p = 0.004).CNKSR1 expression levels are heterogeneous in pancreatic adenocarcinomaTo examine if CNKSR1 expression is dysregulated in pancreas cancer we first compared CNKSR1 expression measured by intensity of immunostaining in 13 randomly chosen matched tumor and normal pancreaticCombining cases from all three
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Rotein expression levels in pancreatic tumors compared to matched, uninvolved controls (p = 0.004).CNKSR1 expression levels are heterogeneous in pancreatic adenocarcinomaTo examine if CNKSR1 expression is dysregulated in pancreas cancer we first compared CNKSR1 expression measured by intensity of immunostaining in 13 randomly chosen matched tumor and normal pancreaticCombining cases from all three
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Thor(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.Quadri et al. BMC Cancer (2017) 17:Page 2 ofBackground While advances in the understanding of cancer biology, sc
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Ability was randomly developed and the peri-tendinous fibroblasts proliferated not only in the injured area, but also they randomly invaded into the peri-tendinous tissues such as skin, subcutaneous fascia and muscle and proliferated and manufactured a haphazard granulation tissue throughout these structures. Thus, the potential of the healing response of the ICTs was divided into different region
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AdeQuadri et al. BMC Cancer (2017) 17:Page 6 ofFig. 5 a Comparison of CNKSR1 expression of study cohort and secondary validation cohort. b Cellular distribution pattern of CNKSR1 showed primarily cytoplasmic expression in pancreatic cancer specimens. Nuclear staining of CNKSR1 was not associated with cytoplasmic CNKSR1 expression levels (0, 1+ vs 2+, 3+; p = 0.22; chi square test, 2-tailed)tumors
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Or cells, which was due to the activation of ERK and p53. To the best of our knowledge, this is the first study to report the molecular mechanism of the chemotherapeutic effects of Triphala against pancreatic cancer. Reactive oxygen species (ROS) are the known mediators of intracellular signaling cascades. Excessive production of ROS nonetheless leads to oxidative stress, loss of cell function and
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Galectin-1 transfectants. A population of GFP-sorted cells (the "Gal-1" bars in Figure 4A) was compared to its parental counterpart. The number of metabolically-active cells attached to fibronectin was no different between the two lines at eight hours. Changing the media at four hours reduced the number of cells left for labeling, but the effect was equal in both groups, suggesting a similar rate

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