Register | Login

Search results for gne-6776 site

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, Cheun
Thelial cells. Suppression of pancreatic cancer cell growth by Triphala in our model was due to induction of apoptosis, which in turn was associated with generation of ROS. Pretreatment of Capan-2 cells with antioxidant NAC blocked ROS generation and completely protected the cells from Triphalainduced apoptosis. Our results also demonstrate that Triphala treatment caused DNA damage resulting in t
Ine serum (FBS, Invitrogen, Carlsbad, CA) and 1 penicillin, streptomycin and amphotericin (Omega Scientific), with the addition of 5 g/ml of bovine insulin (Sigma-Aldrich, St. Louis, MO). All cell lines were mycoplasma free when periodically tested using a Mycoalert assay (Lonza, Rockland, ME).Oncogenic analysis of cell linesCell lines were analyzed for known oncogenic activating mutations and d
Les, CA, USA. 5 Millennium Pharmaceuticals, Inc., Cambridge, MA, USA. 6Division of Hematology-Oncology, 11?34 Factor Building, UCLA Medical Center, 10833 Le Conte Avenue, Los Angeles, CA 90095-1782, USA.Western blottingWestern blotting was performed as previously described [31]. Primary antibodies included pAkt (Ser473), pAkt (Thr308), Akt, pS6K (Thr389), S6K, pS6 (Ser235/236), S6, pMEK (Ser217/2
Thelial cells. Suppression of pancreatic cancer cell growth by Triphala in our model was due to induction of apoptosis, which in turn was associated with generation of ROS. Pretreatment of Capan-2 cells with antioxidant NAC blocked ROS generation and completely protected the cells from Triphalainduced apoptosis. Our results also demonstrate that Triphala treatment caused DNA damage resulting in t
Nium Pharmaceuticals, Inc., the manufacturer of TAK733. Acknowledgements This work was funded by The Seaver Institute, the Melanoma Research Foundation, the Melanoma Research Alliance, the Louise Belley and Richard Schnarr Fund, the Wesley Coyle Memorial Fund, the Garcia-Corsini Family Fund, the Keiter Family Foundation and the Caltech-UCLA Joint Center for Translational Medicine (all to A.R.). A
Les, CA, USA. 5 Millennium Pharmaceuticals, Inc., Cambridge, MA, USA. 6Division of Hematology-Oncology, 11?34 Factor Building, UCLA Medical Center, 10833 Le Conte Avenue, Los Angeles, CA 90095-1782, USA.Western blottingWestern blotting was performed as previously described [31]. Primary antibodies included pAkt (Ser473), pAkt (Thr308), Akt, pS6K (Thr389), S6K, pS6 (Ser235/236), S6, pMEK (Ser217/2
Ies were established from biopsies of metastatic melanoma of cutaneous origin as previously described [9] under the UCLA IRB approval #02-08-067 following the Declaration of Helsinki. SKMEL28, Wn1366 and SBCL2 were obtained from the American Type Culture Collection (ATCC, Rockville, MD). The uveal melanoma cell lines of the Mel20 series were established from fine needle aspirates of primary uveal
Thelial cells. Suppression of pancreatic cancer cell growth by Triphala in our model was due to induction of apoptosis, which in turn was associated with generation of ROS. Pretreatment of Capan-2 cells with antioxidant NAC blocked ROS generation and completely protected the cells from Triphalainduced apoptosis. Our results also demonstrate that Triphala treatment caused DNA damage resulting in t
Nium Pharmaceuticals, Inc., the manufacturer of TAK733. Acknowledgements This work was funded by The Seaver Institute, the Melanoma Research Foundation, the Melanoma Research Alliance, the Louise Belley and Richard Schnarr Fund, the Wesley Coyle Memorial Fund, the Garcia-Corsini Family Fund, the Keiter Family Foundation and the Caltech-UCLA Joint Center for Translational Medicine (all to A.R.). A
Les, CA, USA. 5 Millennium Pharmaceuticals, Inc., Cambridge, MA, USA. 6Division of Hematology-Oncology, 11?34 Factor Building, UCLA Medical Center, 10833 Le Conte Avenue, Los Angeles, CA 90095-1782, USA.Western blottingWestern blotting was performed as previously described [31]. Primary antibodies included pAkt (Ser473), pAkt (Thr308), Akt, pS6K (Thr389), S6K, pS6 (Ser235/236), S6, pMEK (Ser217/2
Led feedback inhibition of RAF-MEK signaling and elevated transcriptional output of the pathway. Proc Natl Acad Sci U S A 2009, 106:4519?524. Zuidervaart W, van Nieuwpoort F, Stark M, Dijkman R, Packer L, Borgstein AM, Pavey S, van der Velden P, Out C, Jager MJ, et al: Activation of the MAPK pathway is a common event in uveal melanomas although it rarely occurs through mutation of BRAF or RAS. Br
Xposed for varying time points to TAK733. A) The sensitive BRAFV600E mutated cutaneous melanoma cell line M229; B) The resistant BRAFV600E mutated cutaneous melanoma cell line M233.Cell proliferation and viability assaysMelanoma cell lines were treated with TAK-733 or parallel DMSO vehicle control at the given concentrations for 72 hours. Cell viability was measured using a tetrazolium compound [
Nium Pharmaceuticals, Inc., the manufacturer of TAK733. Acknowledgements This work was funded by The Seaver Institute, the Melanoma Research Foundation, the Melanoma Research Alliance, the Louise Belley and Richard Schnarr Fund, the Wesley Coyle Memorial Fund, the Garcia-Corsini Family Fund, the Keiter Family Foundation and the Caltech-UCLA Joint Center for Translational Medicine (all to A.R.). A


High PR Social Bookmarking Sites List 2018

Username:

Password:

Remember: