4 results match your criteria: "From the Laura and Isaac Perlmutter Cancer Center at NYU Langone[Affiliation]"

Background: Hyperglycemia has been associated with worse survival in glioblastoma. Attempts to lower glucose yielded mixed responses which could be due to molecularly distinct GBM subclasses.

Methods: Clinical, laboratory, and molecular data on 89 IDH-wt GBMs profiled by clinical next-generation sequencing and treated with Stupp protocol were reviewed.

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Multiple combinational regimens have recently been approved and are now considered the standard of care for patients with advanced clear cell renal cell carcinoma (RCC). Several additional combinational regimens are deep in clinical assessment and are likely to soon join the crowded front-line therapeutic landscape. Most of these regimens are combinations of agents already approved as single-agents in RCC including tyrosine kinase inhibitors (TKI) and immune checkpoint inhibitors.

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The activity of the E3 ligase, SMURF2, is antagonized by an intramolecular, autoinhibitory interaction between its C2 and Hect domains. Relief of SMURF2 autoinhibition is induced by TGFβ and is mediated by the inhibitory SMAD, SMAD7. In a proteomic screen for endomembrane interactants of the RING-domain E3 ligase, RNF11, we identified SMURF2, among a cohort of Hect E3 ligases previously implicated in TGFβ signaling.

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Phase II study of sorafenib in children with recurrent or progressive low-grade astrocytomas.

Neuro Oncol

October 2014

NYU Comprehensive Neurofibromatosis Center, Division of Pediatric Hematology/Oncology, Department of Pediatrics and Laura and Isaac Perlmutter Cancer Center at NYU Langone Medical Center, New York, New York (M.A.K., G.L., A.M., J.C.A.); Division of Oncology, Children's Hospital of Philadelphia and the Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania (M.J.F., A.J.S.); Department of Radiology, NYU Langone Medical Center, New York, New York (S.S.M., M.C.B.); The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland (K.J.C.); Division of Pediatric Neurosurgery, Department of Neurosurgery, NYU Langone Medical Center, New York, New York (J.H.W., D.H.H.); Division of Biostatistics, Department of Population Health and The Laura and Isaac Perlmutter Cancer Center at NYU Langone Medical Center, New York, New York (J.D.G., T.H.); Department of Neurosurgery, Children's Hospital of Philadelphia and the Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania (A.C.R); Division of Hematology/Oncology, Children's Hospital Los Angeles, Los Angeles, California (G.D.); German Cancer Research Center and University Hospital, Heidelberg, Germany (D.T.W.J., A.K., S.M.P.); Division of Neuropathology, Department of Pathology, Johns Hopkins University, Baltimore, Maryland (C.G.E.); Division of Neuropathology, Department of Pathology, Department of Neurosurgery and Laura and Isaac Perlmutter Cancer Center at NYU Langone Medical Center, New York, New York (D.Z.).

Background: Activation of the RAS-RAF-MEK-ERK signaling pathway is thought to be the key driver of pediatric low-grade astrocytoma (PLGA) growth. Sorafenib is a multikinase inhibitor targeting BRAF, VEGFR, PDGFR, and c-kit. This multicenter phase II study was conducted to determine the response rate to sorafenib in patients with recurrent or progressive PLGA.

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