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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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Enhancer of the Kinase Suppressor of Ras-1), a regulator and binding partner of KSR1, is another scaffolding protein which is less understood. Its role in pancreatic cancer biology, or as a biomarker, remains to be explored. Current data suggests that CNKSR1 has multiple roles cancer biology, with some reports demonstrating that CNKSR1 interacts with tumor suppressors and othersdescribe its scaffo
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Inase suppressor of Ras 1 (CNKSR1)* Correspondence: rudloffu@mail.nih.gov Equal contributors 1 Thoracic and Gastrointestinal Oncology Branch, Gastrointestinal Oncology Section, Investigator Center for Cancer Research, National Cancer Institute, Building 10 - Hatfield CRC, Room 4-5950, Bethesda, MD 20892, USA Full list of author information is available at the end of the article?The Author(s). 201
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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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Thur GA, Hutson TE, Moschos SJ, Flaherty KT, et al: Survival in BRAF V600mutant advanced melanoma treated with vemurafenib. N Engl J Med 2012, 366:707?14. Lin WM, Baker AC, Beroukhim R, Winckler W, Feng W, Marmion JM, Laine E, Greulich H, Tseng H, Gates C, et al: Modeling genomic diversity and tumor dependency in malignant melanoma. Cancer Res 2008, 68:664?73. Haigis KM, Kendall KR, Wang Y, Cheung
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Time intervals in a time-dependent experiment. Expression and phosphorylation of ERK (Thr-202/Tyr204) and MEK-1 (Ser-217/221) was determined by western blotting. B) The effect of Triphala on the kinase activity of ERK was determined using a kit from Cell Signaling Technology, measuring the phosphorylation of Elk-1 at Ser-383. C, D) Effect of ERK inhibitor on Triphala induced apoptosis and activati
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Ns.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Toussaint et al. Molecular Cancer 2012, 11:32 http://www.molecular-cancer.com/content/11/1/Page 2 ofgrowth factor receptors [11] to effector metallo- [12,13] and serine- [14] proteases. Galectin-1 has also been identified as a key player in GBM cell mi
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Orithm. Galectin-1 was ranked at the top of this list. We thus took advantage of our own patient-derived glioblastoma xenograft model [25] in order to further decipher the roles of galectin-1 on GBM cell migration features. The system we have developed mitigates the effect of three important confounders from human samples. First, tissue is frozen within one minute of removal, ensuring high quality