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Xpressing tumors, patients did not show any difference in survival when stratified by resection status whereas patients with high CNKSR1 expression levels who underwent resection had significantly improved outcome compared to non-resected patients in this group. Combination of CNKSR1 expression levels with current clinicopathological prognostic features might improve risk stratification and treatm
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Py, Black or Hispanic race/ethnicityQuadri et al. BMC Cancer (2017) 17:Page 10 ofFig. 7 Survival stratified by resection and CNKSR1 expression status. a Survival in limited subset of primary tumor biopsy specimens showing low CNKSR1 expression by resection status (p = 0.367). b Survival in patients with high CNKSR1 expression by resection status (p
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Ics, tumor characteristics, and treatment by CNKSR1 expression statusCNKSR1 Low (N = 34) Age group
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On by age, race, gender, grade, resection status, the TNM variables lymph node status (N0; No regional lymph node metastasis, N1; Regional lymph node metastasis, and NX;Quadri et al. BMC Cancer (2017) 17:Page 3 ofRegional lymph nodes cannot be assessed) and distant metastasis (M0; No distant metastasis, and M1; Distant metastasis), SEER stage (localized, regional, and distant), radiation, and prim
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S of pancreatic cancer. Nature. 2016;531(7592):47?2. 10. Kolch W. Coordinating ERK/MAPK signalling through scaffolds and inhibitors. Nat Rev Mol Cell Biol. 2005;6(11):827?7. 11. McKay MM, Morrison DK. Integrating signals from RTKs to ERK/MAPK. Oncogene. 2007;26(22):3113?1. 12. Kim M, Yan Y, Kortum RL, Stoeger SM, Sgagias MK, Lee K, Lewis RE, Cowan KH. Expression of kinase suppressor of Ras1 enhanc
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Ase) makes it a resource for identification, as well as preclinical targeting, of novel mediators of glioma invasion. Galectin-1 was identified in this manner, and has proven in vitro and in vivo to be important in the migration and invasion of glioblastoma cells. Previous work suggests an even greater role of galectin-1 in GBM neoangiogenesis, chemo- and radioresistence, and immune privilege. Tar
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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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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