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He presence of higher transverse diameter and temperature in the injured area together with the higher infiltration of the inflammatory cells in the injured area of the treated lesions during the first 14 DPI, suggest that a higher inflammatory reaction has commenced, the healing response has been motivated by the collagen implant and the metabolism of the injured area has increased. At earlier st
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In TNFalpha-induced aromatase expression in breast adipose. Breast Cancer Res Treat. 2013;138(1):193-203. doi:10.1007/s10549-013-2413-5. PubMed 43. Windahl SH, Saxon L, Borjesson AE, Lagerquist MK, Frenkel B, Henning P, Lerner UH, Galea GL, Meakin LB, Engdahl C, Sjogren K, Antal MC, Krust A, Chambon P, Lanyon LE, Price JS, Ohlsson C. Estrogen receptor-alpha is required for the osteogenic response
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Tic cancer, there is considerable heterogeneity in the molecular make-up, MAPK/ERK pathway activation states, and clinical outcome in this disease. We analyzed the expression levels of CNKSR1, a scaffold that influences MAPK/ ERK pathway activity, in clinical pancreas cancer specimens and their impact on survival of patients with pancreatic cancer. Methods: Immunohistochemical staining for CNKSR1
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Ed migration and invasion in vitro. In vivo, tumors expressing high galectin-1 levels showed enhanced invasion and decreased host survival. Conclusions: In conclusion, cells at the margin of glioblastoma, in comparison to tumor core cells, have enhanced expression of mediators of invasion. Galectin-1 is likely one such mediator. Previous studies, along with the current one, have proven galectin-1
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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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Ting allows for harvesting of normal host brain from regions remote from the tumor, which serve as a control for possible contamination of samples microdissected at the tumor-brain interface. Galectin-1 was thus identified in this unsupervised method of analysis as a key marker of glioma invasion, while validating the novel filtering method (used to control for sample contamination) presented in t
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L resection is an important predictor of patient survival [3,4], local therapy for glioblastoma fails because microscopically invasive cells evade resection and eventually proliferate in spite of adjuvant chemoradiotherapy [5,6]. Controlling the invasive nature of this tumor may offer hope for more efficacious local therapy, improved quality of life, and perhaps better response to adjuvant therapi
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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

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