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Manuscript. Ethics approval and consent to participate The pancreatic TMA as well as pancreatic cancer biospecimens transferred under a Material Transfer Agreement (MTA) to NCI was approved by the Office of Human Subjects Research at the NIH and was found exempt from IRB review because it contained patient de-identified information. Consent for publication Not applicable. Competing interests The a
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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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Ed by the current ones, highlight a major role for galectin-1 in GBM invasiveness. The characteristic malignant phenotype of glioblastoma extends beyond aggressive invasion. This tumor develops resistance to chemo- and radio-therapy, it promotes neoangiogenesis, and it seems to benefit from immune privilege. Interestingly, galectin-1 may play a role in promoting each of these phenotypes. While gal
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Or his help with radial migration assays. Reagents used in preliminary pilot assays were kindly provided by Yoel Kloog Authors' contributions LGT and JHU conceived of the study and designed the assays. LGT performed tumor xenografting, cell culture, and laser capture microdissection. LGT, FL, and RK wrote and edited the manuscript. AN designed and performed all DNA vector construction and sequenci
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Ing glioblastoma cells to apoptosis. J Clin Oncol 2005, 23: 2411?422. Paulus W, Baur I, Beutler AS, Reeves SA: Diffuse brain invasion of glioma cells requires beta 1 integrins. Lab Invest 1996, 75:819?26. Uhm JH, Gladson CL, Rao JS: The role of integrins in the malignant phenotype of gliomas. Front Biosci 1999, 4:D188 199. Lipinski CA, Tran NL, Bay C, Kloss J, McDonough WS, Beaudry C, Berens ME, L
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Or his help with radial migration assays. Reagents used in preliminary pilot assays were kindly provided by Yoel Kloog Authors' contributions LGT and JHU conceived of the study and designed the assays. LGT performed tumor xenografting, cell culture, and laser capture microdissection. LGT, FL, and RK wrote and edited the manuscript. AN designed and performed all DNA vector construction and sequenci
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Activation of ERK with induction of apoptosis by various chemopreventive and chemotherapeutic agents [39-41]. In fact, oxidants have been shown to activate ERK by taking over the growth factor receptor signaling pathways [42-46]. Moreover, ERK may get activated in response to DNA damage and can phosphorylate p53 in vitro [23,24,47-49]. We found that exposure of Capan-2 or BxPC-3 cells with apoptos
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On problem with IRES vectors ?inability to transcribe the transcript following the IRES sequence if the first MCS is empty. The new pIRES2-acGFP1acGFP1 vector was used as a control for the pIRES2Gal1-acGFP1 construct. Both vectors were sequenced through their multiple cloning sites to ensure no PCRinduced mutations were present.Transfection and stable clone generationParental, control, and galecti