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Ge, stage, grade, race, resection and radiation. Sensitivity analyses were performed after excluding casesQuadri et al. BMC Cancer (2017) 17:Page 4 ofFig. 1 Representative photomicrographs of pancreatic cancer tissue microarray (TMA) cores illustrating intensities of CNKSR1 immunohistochemical staining scored as low: a, b no staining for CNKSR1 (score 0); c, d weak CNKSR1 (score 1+) staining; only
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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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Nonevent. All cases with missing information were included in proportional hazard ratio calculations after performing a sensitivity analysis which showed negligible effects of excluding missing data.ImmunohistochemistryImmunohistochemical staining for CNKSR1 (mouse monoclonal antibody CNKSR1 (clone 46), Santa Cruz Biotechnology, TX, USA, #sc-135,870; dilution 1:200) was performed on a Leica BOND-M
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Y intensity of p-ERK immunostaining. Figure 8C shows nuclear p-ERK expression levels (0, 1+, 2+, 3+)) by CNKSR1 cellular distribution (cytoplasmic CNKSR1 expression only vs cytoplasmic and nuclear) in pancreas cancer specimens of the SEER Pancreatic Cancer TMA (Mann Whitney U test; p = 0.017). To test whether expression levels of the two proteins are correlated as well, including if a possible neg
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Cal significance.Paraffin sections of our patient-derived glioblastoma xenografts (15 of 22 lines) were stained for galectin-1 expression. Around half of the xenografts tested showed preferential staining at the tumor-brain interface (Figure 3). A few tumors stained in their entirety, and another subset lacked significant staining. The 2 to 4 fold change in galectin-1 mRNA expression at the tumor
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Thanized and their brains removed and either frozen using Optimal Cutting Temperature (OCT) compound (Electron Microscopy Sciences, Fort Washington, PA) in cryomolds placed atop dry ice, or fixed in 10 buffered formalin and paraffin embedded for histopathological analysis. The symptom-free survival of nude mice harboring U87MG parental versus transfected xenografts was compared. Kaplan-Meyer surv
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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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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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