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Erved association of CNKSR1 expression and survival outcome suggests scaffolding proteins of the RAS-MAPK pathway may account, in part, for the observed heterogeneity of PDAC biology, and clinically may aid in improved future patient stratification.MethodsStudy participants and tissue microarray (TMA) compositionDe-identified cancer tissues included in this analysis were confirmed to be pancreatic
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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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Ca, MA) and rested for 24 hours. 0.1 and 1 M of TAK733 or parallel DMSO vehicle control were added in triplicate for 20 hours. Cells were incubated for 1 hour with 2.0 Ci with metabolic tracers chosen as analogues of PET tracers: 3H-DDG (American Radiolabeled Chemicals Inc., St. Louis, MO) in glucose-free RPMI 1640 (Invitrogen), or methyl-3H-thymidine (thymidine, Moravek Biochemicals Inc., Brea, C
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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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Eration, Migration, Invasion, Galectin-Backgound In spite of recent advances in the treatment of patients with glioblastoma, the prognosis for those afflicted remains poor. Even when these tumors harbor a favorable gene methylation profile, the newest standard of care, including temozolomide as a chemotherapeutic [1],* Correspondence: Gtoussaint@medicine.tamhsc.edu 1 The Texas Brain and Spine Inst
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Id tumors. J Clin Oncol 2010, 28:611s. Hall-Jackson CA, Eyers PA, Cohen P, Goedert M, Boyle FT, Hewitt N, Plant H, Hedge P: Paradoxical activation of Raf by a novel Raf inhibitor. Chem Biol 1999, 6:559?68. Su F, Viros A, Milagre C, Trunzer K, Bollag G, Spleiss O, Reis-Filho JS, Kong X, Koya RC, Flaherty KT, et al: RAS mutations in cutaneous squamous-cell carcinomas in patients treated with BRAF 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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Ite were true: lowest relative expression value at the tumor edge compared to tumor core and normal brain. The genes meeting this ideal profile were ranked by pvalue (between core and edge).ImmunohistochemistryRaw data from chip hybridization experiments were normalized across chips and across probesets using a fast linear Loess routine [29], known as Fastlo. This normalization routine, in some re