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R of proteins either indirectly or directly connected to MAPK/ERK signaling (Ras, ERBB2, Myc) [4, 31]. A limitation of this study was that the dataset did not include all clinical variables, such as complete TNM staging and chemotherapy treatment, and thus we could not evaluate all variables that might impact survival. While the HRs of known clinical (TNM system N and M stage) and pathological var
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E inflammatory response and tissue remodeling in tendon healing and also it revealed that; although the severe inflammatory reaction has been developed in response to the collagen implant, but this immune response was due to the remodeling effect of the collagen implant, not its rejection. It has been postulated that inflammation has a major role in tendon healing and if immune response does not p
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Rody JR, Rocha FG, Jia XY, Qin LX, D'Angelica MI, DeMatteo RP, et al. A novel survival-based tissue microarray of pancreatic cancer validates MUC1 and Mesothelin as biomarkers. PLoS One. 2012;7(7):10. 5. Jones S, Zhang XS, Parsons DW, Lin JCH, Leary RJ, Angenendt P, Mankoo P, Carter H, Kamiyama H, Jimeno A, et al. Core signaling pathways in human pancreatic cancers revealed by global genomic analy
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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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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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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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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